The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
A family of intracellular CYSTEINE ENDOPEPTIDASES that play a role in regulating INFLAMMATION and APOPTOSIS. They specifically cleave peptides at a CYSTEINE amino acid that follows an ASPARTIC ACID residue. Caspases are activated by proteolytic cleavage of a precursor form to yield large and small subunits that form the enzyme. Since the cleavage site within precursors matches the specificity of caspases, sequential activation of precursors by activated caspases can occur.
Irreversible cessation of all bodily functions, manifested by absence of spontaneous breathing and total loss of cardiovascular and cerebral functions.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
The pathological process occurring in cells that are dying from irreparable injuries. It is caused by the progressive, uncontrolled action of degradative ENZYMES, leading to MITOCHONDRIAL SWELLING, nuclear flocculation, and cell lysis. It is distinct it from APOPTOSIS, which is a normal, regulated cellular process.
A short pro-domain caspase that plays an effector role in APOPTOSIS. It is activated by INITIATOR CASPASES such as CASPASE 9. Isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.
Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma.
Splitting the DNA into shorter pieces by endonucleolytic DNA CLEAVAGE at multiple sites. It includes the internucleosomal DNA fragmentation, which along with chromatin condensation, are considered to be the hallmarks of APOPTOSIS.
Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)
The segregation and degradation of damaged or unwanted cytoplasmic constituents by autophagic vacuoles (cytolysosomes) composed of LYSOSOMES containing cellular components in the process of digestion; it plays an important role in BIOLOGICAL METAMORPHOSIS of amphibians, in the removal of bone by osteoclasts, and in the degradation of normal cell components in nutritional deficiency states.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
A cell line derived from cultured tumor cells.
An in situ method for detecting areas of DNA which are nicked during APOPTOSIS. Terminal deoxynucleotidyl transferase is used to add labeled dUTP, in a template-independent manner, to the 3 prime OH ends of either single- or double-stranded DNA. The terminal deoxynucleotidyl transferase nick end labeling, or TUNEL, assay labels apoptosis on a single-cell level, making it more sensitive than agarose gel electrophoresis for analysis of DNA FRAGMENTATION.
Unexpected rapid natural death due to cardiovascular collapse within one hour of initial symptoms. It is usually caused by the worsening of existing heart diseases. The sudden onset of symptoms, such as CHEST PAIN and CARDIAC ARRHYTHMIAS, particularly VENTRICULAR TACHYCARDIA, can lead to the loss of consciousness and cardiac arrest followed by biological death. (from Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 7th ed., 2005)
Endogenous and exogenous compounds and that either inhibit CASPASES or prevent their activation.
A member of the Bcl-2 protein family and homologous partner of C-BCL-2 PROTO-ONCOGENE PROTEIN. It regulates the release of CYTOCHROME C and APOPTOSIS INDUCING FACTOR from the MITOCHONDRIA. Several isoforms of BCL2-associated X protein occur due to ALTERNATIVE SPLICING of the mRNA for this protein.
Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
A tumor necrosis factor receptor subtype found in a variety of tissues and on activated LYMPHOCYTES. It has specificity for FAS LIGAND and plays a role in regulation of peripheral immune responses and APOPTOSIS. Multiple isoforms of the protein exist due to multiple ALTERNATIVE SPLICING. The activated receptor signals via a conserved death domain that associates with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.
A state of prolonged irreversible cessation of all brain activity, including lower brain stem function with the complete absence of voluntary movements, responses to stimuli, brain stem reflexes, and spontaneous respirations. Reversible conditions which mimic this clinical state (e.g., sedative overdose, hypothermia, etc.) are excluded prior to making the determination of brain death. (From Adams et al., Principles of Neurology, 6th ed, pp348-9)
Inhibitors of SERINE ENDOPEPTIDASES and sulfhydryl group-containing enzymes. They act as alkylating agents and are known to interfere in the translation process.
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
Established cell cultures that have the potential to propagate indefinitely.
Elements of limited time intervals, contributing to particular results or situations.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
A large group of proteins that control APOPTOSIS. This family of proteins includes many ONCOGENE PROTEINS as well as a wide variety of classes of INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS such as CASPASES.
Death of the developing young in utero. BIRTH of a dead FETUS is STILLBIRTH.
Cytochromes of the c type that are found in eukaryotic MITOCHONDRIA. They serve as redox intermediates that accept electrons from MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III and transfer them to MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX IV.
A long pro-domain caspase that contains a death effector domain in its pro-domain region. Caspase 8 plays a role in APOPTOSIS by cleaving and activating EFFECTOR CASPASES. Activation of this enzyme can occur via the interaction of its N-terminal death effector domain with DEATH DOMAIN RECEPTOR SIGNALING ADAPTOR PROTEINS.
Enzymes that catalyze the transfer of multiple ADP-RIBOSE groups from nicotinamide-adenine dinucleotide (NAD) onto protein targets, thus building up a linear or branched homopolymer of repeating ADP-ribose units i.e., POLY ADENOSINE DIPHOSPHATE RIBOSE.
A long pro-domain caspase that contains a caspase recruitment domain in its pro-domain region. Caspase 9 is activated during cell stress by mitochondria-derived proapoptotic factors and by CARD SIGNALING ADAPTOR PROTEINS such as APOPTOTIC PROTEASE-ACTIVATING FACTOR 1. It activates APOPTOSIS by cleaving and activating EFFECTOR CASPASES.
A transmembrane protein belonging to the tumor necrosis factor superfamily that was originally discovered on cells of the lymphoid-myeloid lineage, including activated T-LYMPHOCYTES and NATURAL KILLER CELLS. It plays an important role in immune homeostasis and cell-mediated toxicity by binding to the FAS RECEPTOR and triggering APOPTOSIS.
Exogenous and endogenous compounds which inhibit CYSTEINE ENDOPEPTIDASES.
A member of the bcl-2 protein family that plays a role in the regulation of APOPTOSIS. Two major isoforms of the protein exist due to ALTERNATIVE SPLICING of the BCL2L1 mRNA and are referred to as Bcl-XS and Bcl-XL.
Conceptual response of the person to the various aspects of death, which are based on individual psychosocial and cultural experience.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
The voltage difference, normally maintained at approximately -180mV, across the INNER MITOCHONDRIAL MEMBRANE, by a net movement of positive charge across the membrane. It is a major component of the PROTON MOTIVE FORCE in MITOCHONDRIA used to drive the synthesis of ATP.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. A mutant or absent p53 protein has been found in LEUKEMIA; OSTEOSARCOMA; LUNG CANCER; and COLORECTAL CANCER.
A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials.
A flavoprotein that functions as a powerful antioxidant in the MITOCHONDRIA and promotes APOPTOSIS when released from the mitochondria. In mammalian cells AIF is released in response to pro-apoptotic protein members of the bcl-2 protein family. It translocates to the CELL NUCLEUS and binds DNA to stimulate CASPASE-independent CHROMATIN condensation.
A family of cell surface receptors that signal via a conserved domain that extends into the cell CYTOPLASM. The conserved domain is referred to as a death domain due to the fact that many of these receptors are involved in signaling APOPTOSIS. Several DEATH DOMAIN RECEPTOR SIGNALING ADAPTOR PROTEINS can bind to the death domains of the activated receptors and through a complex series of interactions activate apoptotic mediators such as CASPASES.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.
Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
The process by which chemical compounds provide protection to cells against harmful agents.
A multi-domain mitochondrial membrane protein and member of the bcl-2 Protein family. Bak protein interacts with TUMOR SUPPRESSOR PROTEIN P53 and promotes APOPTOSIS.
A protein of the annexin family isolated from human PLACENTA and other tissues. It inhibits cytosolic PHOSPHOLIPASE A2, and displays anticoagulant activity.
A CELL LINE derived from human T-CELL LEUKEMIA and used to determine the mechanism of differential susceptibility to anti-cancer drugs and radiation.
A member of the Bcl-2 protein family that reversibly binds MEMBRANES. It is a pro-apoptotic protein that is activated by caspase cleavage.
The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE.
A long pro-domain caspase that has specificity for the precursor form of INTERLEUKIN-1BETA. It plays a role in INFLAMMATION by catalytically converting the inactive forms of CYTOKINES such as interleukin-1beta to their active, secreted form. Caspase 1 is referred as interleukin-1beta converting enzyme and is frequently abbreviated ICE.
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
A conserved class of proteins that control APOPTOSIS in both VERTEBRATES and INVERTEBRATES. IAP proteins interact with and inhibit CASPASES, and they function as ANTI-APOPTOTIC PROTEINS. The protein class is defined by an approximately 80-amino acid motif called the baculoviral inhibitor of apoptosis repeat.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
A family of serine-threonine kinases that plays a role in intracellular signal transduction by interacting with a variety of signaling adaptor proteins such as CRADD SIGNALING ADAPTOR PROTEIN; TNF RECEPTOR-ASSOCIATED FACTOR 2; and TNF RECEPTOR-ASSOCIATED DEATH DOMAIN PROTEIN. Although they were initially described as death domain-binding adaptor proteins, members of this family may contain other protein-binding domains such as those involving caspase activation and recruitment.
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
The first continuously cultured human malignant CELL LINE, derived from the cervical carcinoma of Henrietta Lacks. These cells are used for VIRUS CULTIVATION and antitumor drug screening assays.
Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
A short pro-domain caspase that plays an effector role in APOPTOSIS. It is activated by INITIATOR CASPASES such as CASPASE 3 and CASPASE 10. Several isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.
Quaternary ammonium analog of ethidium; an intercalating dye with a specific affinity to certain forms of DNA and, used as diiodide, to separate them in density gradients; also forms fluorescent complexes with cholinesterase which it inhibits.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
A subgroup of mitogen-activated protein kinases that activate TRANSCRIPTION FACTOR AP-1 via the phosphorylation of C-JUN PROTEINS. They are components of intracellular signaling pathways that regulate CELL PROLIFERATION; APOPTOSIS; and CELL DIFFERENTIATION.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
The B-cell leukemia/lymphoma-2 genes, responsible for blocking apoptosis in normal cells, and associated with follicular lymphoma when overexpressed. Overexpression results from the t(14;18) translocation. The human c-bcl-2 gene is located at 18q24 on the long arm of chromosome 18.
Within a eukaryotic cell, a membrane-limited body which contains chromosomes and one or more nucleoli (CELL NUCLEOLUS). The nuclear membrane consists of a double unit-type membrane which is perforated by a number of pores; the outermost membrane is continuous with the ENDOPLASMIC RETICULUM. A cell may contain more than one nucleus. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
ENDOPEPTIDASES which have a cysteine involved in the catalytic process. This group of enzymes is inactivated by CYSTEINE PROTEINASE INHIBITORS such as CYSTATINS and SULFHYDRYL REAGENTS.
A long pro-domain caspase that contains a caspase recruitment domain in its pro-domain region. Activation of this enzyme can occur via the interaction of its caspase recruitment domain with CARD SIGNALING ADAPTOR PROTEINS. Caspase 2 plays a role in APOPTOSIS by cleaving and activating effector pro-caspases. Several isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.
A gene silencing phenomenon whereby specific dsRNAs (RNA, DOUBLE-STRANDED) trigger the degradation of homologous mRNA (RNA, MESSENGER). The specific dsRNAs are processed into SMALL INTERFERING RNA (siRNA) which serves as a guide for cleavage of the homologous mRNA in the RNA-INDUCED SILENCING COMPLEX. DNA METHYLATION may also be triggered during this process.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
Transport proteins that carry specific substances in the blood or across cell membranes.
An indolocarbazole that is a potent PROTEIN KINASE C inhibitor which enhances cAMP-mediated responses in human neuroblastoma cells. (Biochem Biophys Res Commun 1995;214(3):1114-20)
A pro-apoptotic protein and member of the Bcl-2 protein family that is regulated by PHOSPHORYLATION. Unphosphorylated Bad protein inhibits the activity of BCL-XL PROTEIN.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
A CARD signaling adaptor protein that plays a role in the mitochondria-stimulated apoptosis (APOPTOSIS, INTRINSIC PATHWAY). It binds to CYTOCHROME C in the CYTOSOL to form an APOPTOSOMAL PROTEIN COMPLEX and activates INITIATOR CASPASES such as CASPASE 9.
A transmembrane-protein belonging to the TNF family of intercellular signaling proteins. It is a widely expressed ligand that activates APOPTOSIS by binding to TNF-RELATED APOPTOSIS-INDUCING LIGAND RECEPTORS. The membrane-bound form of the protein can be cleaved by specific CYSTEINE ENDOPEPTIDASES to form a soluble ligand form.
Glycoproteins found on the membrane or surface of cells.
A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.
High molecular weight proteins found in the MICROTUBULES of the cytoskeletal system. Under certain conditions they are required for TUBULIN assembly into the microtubules and stabilize the assembled microtubules.
Microscopy of specimens stained with fluorescent dye (usually fluorescein isothiocyanate) or of naturally fluorescent materials, which emit light when exposed to ultraviolet or blue light. Immunofluorescence microscopy utilizes antibodies that are labeled with fluorescent dye.
Intracellular signaling adaptor proteins that bind to the cytoplasmic death domain region found on DEATH DOMAIN RECEPTORS. Many of the proteins in this class take part in intracellular signaling from TUMOR NECROSIS FACTOR RECEPTORS.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
A group of cytochromes with covalent thioether linkages between either or both of the vinyl side chains of protoheme and the protein. (Enzyme Nomenclature, 1992, p539)
Cysteine proteinase found in many tissues. Hydrolyzes a variety of endogenous proteins including NEUROPEPTIDES; CYTOSKELETAL PROTEINS; proteins from SMOOTH MUSCLE; CARDIAC MUSCLE; liver; platelets; and erythrocytes. Two subclasses having high and low calcium sensitivity are known. Removes Z-discs and M-lines from myofibrils. Activates phosphorylase kinase and cyclic nucleotide-independent protein kinase. This enzyme was formerly listed as EC
Members of the class of neutral glycosphingolipids. They are the basic units of SPHINGOLIPIDS. They are sphingoids attached via their amino groups to a long chain fatty acyl group. They abnormally accumulate in FABRY DISEASE.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
Ubiquitous, inducible, nuclear transcriptional activator that binds to enhancer elements in many different cell types and is activated by pathogenic stimuli. The NF-kappa B complex is a heterodimer composed of two DNA-binding subunits: NF-kappa B1 and relA.
Electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (OXIDATION-REDUCTION).
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
A system of cisternae in the CYTOPLASM of many cells. In places the endoplasmic reticulum is continuous with the plasma membrane (CELL MEMBRANE) or outer membrane of the nuclear envelope. If the outer surfaces of the endoplasmic reticulum membranes are coated with ribosomes, the endoplasmic reticulum is said to be rough-surfaced (ENDOPLASMIC RETICULUM, ROUGH); otherwise it is said to be smooth-surfaced (ENDOPLASMIC RETICULUM, SMOOTH). (King & Stansfield, A Dictionary of Genetics, 4th ed)
Naturally occurring or synthetic substances that inhibit or retard the oxidation of a substance to which it is added. They counteract the harmful and damaging effects of oxidation in animal tissues.
The two lipoprotein layers in the MITOCHONDRION. The outer membrane encloses the entire mitochondrion and contains channels with TRANSPORT PROTEINS to move molecules and ions in and out of the organelle. The inner membrane folds into cristae and contains many ENZYMES important to cell METABOLISM and energy production (MITOCHONDRIAL ATP SYNTHASE).
The number of CELLS of a specific kind, usually measured per unit volume or area of sample.
Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.
All deaths reported in a given population.
Cell surface receptors that bind TUMOR NECROSIS FACTORS and trigger changes which influence the behavior of cells.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
Various physiological or molecular disturbances that impair ENDOPLASMIC RETICULUM function. It triggers many responses, including UNFOLDED PROTEIN RESPONSE, which may lead to APOPTOSIS; and AUTOPHAGY.
A protein-serine-threonine kinase that is activated by PHOSPHORYLATION in response to GROWTH FACTORS or INSULIN. It plays a major role in cell metabolism, growth, and survival as a core component of SIGNAL TRANSDUCTION. Three isoforms have been described in mammalian cells.
Postmortem examination of the body.
A CELL LINE derived from a PHEOCHROMOCYTOMA of the rat ADRENAL MEDULLA. PC12 cells stop dividing and undergo terminal differentiation when treated with NERVE GROWTH FACTOR, making the line a useful model system for NERVE CELL differentiation.
Diseases of plants.
A short pro-domain caspase that plays an effector role in APOPTOSIS. It is activated by INITIATOR CASPASES such as CASPASE 7; CASPASE 8; and CASPASE 10. Isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.
A condition of decreased oxygen content at the cellular level.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
The action of a drug in promoting or enhancing the effectiveness of another drug.
Immunologic method used for detecting or quantifying immunoreactive substances. The substance is identified by first immobilizing it by blotting onto a membrane and then tagging it with labeled antibodies.
Refers to animals in the period of time just after birth.
The N-acetyl derivative of CYSTEINE. It is used as a mucolytic agent to reduce the viscosity of mucous secretions. It has also been shown to have antiviral effects in patients with HIV due to inhibition of viral stimulation by reactive oxygen intermediates.
The process of moving proteins from one cellular compartment (including extracellular) to another by various sorting and transport mechanisms such as gated transport, protein translocation, and vesicular transport.
A class of morphologically heterogeneous cytoplasmic particles in animal and plant tissues characterized by their content of hydrolytic enzymes and the structure-linked latency of these enzymes. The intracellular functions of lysosomes depend on their lytic potential. The single unit membrane of the lysosome acts as a barrier between the enzymes enclosed in the lysosome and the external substrate. The activity of the enzymes contained in lysosomes is limited or nil unless the vesicle in which they are enclosed is ruptured. Such rupture is supposed to be under metabolic (hormonal) control. (From Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.
Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept.
A superfamily of PROTEIN-SERINE-THREONINE KINASES that are activated by diverse stimuli via protein kinase cascades. They are the final components of the cascades, activated by phosphorylation by MITOGEN-ACTIVATED PROTEIN KINASE KINASES, which in turn are activated by mitogen-activated protein kinase kinase kinases (MAP KINASE KINASE KINASES).
Proteins encoded by the mitochondrial genome or proteins encoded by the nuclear genome that are imported to and resident in the MITOCHONDRIA.
Proteins found in the nucleus of a cell. Do not confuse with NUCLEOPROTEINS which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus.
An inhibitor of apoptosis protein that is translated by a rare cap-independent mechanism. It blocks caspase-mediated cellular destruction by inhibiting CASPASE 3; CASPASE 7; and CASPASE 9.
Electron microscopy in which the ELECTRONS or their reaction products that pass down through the specimen are imaged below the plane of the specimen.
A member of the myeloid leukemia factor (MLF) protein family with multiple alternatively spliced transcript variants encoding different protein isoforms. In hematopoietic cells, it is located mainly in the nucleus, and in non-hematopoietic cells, primarily in the cytoplasm with a punctate nuclear localization. MLF1 plays a role in cell cycle differentiation.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A tripeptide with many roles in cells. It conjugates to drugs to make them more soluble for excretion, is a cofactor for some enzymes, is involved in protein disulfide bond rearrangement and reduces peroxides.
Proteins prepared by recombinant DNA technology.
Tumor necrosis factor receptor family members that are widely expressed and play a role in regulation of peripheral immune responses and APOPTOSIS. The receptors are specific for TNF-RELATED APOPTOSIS-INDUCING LIGAND and signal via conserved death domains that associate with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.
A tetrameric enzyme that, along with the coenzyme NAD+, catalyzes the interconversion of LACTATE and PYRUVATE. In vertebrates, genes for three different subunits (LDH-A, LDH-B and LDH-C) exist.
Proteins and peptides that are involved in SIGNAL TRANSDUCTION within the cell. Included here are peptides and proteins that regulate the activity of TRANSCRIPTION FACTORS and cellular processes in response to signals from CELL SURFACE RECEPTORS. Intracellular signaling peptide and proteins may be part of an enzymatic signaling cascade or act through binding to and modifying the action of other signaling factors.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.
Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.
A light microscopic technique in which only a small spot is illuminated and observed at a time. An image is constructed through point-by-point scanning of the field in this manner. Light sources may be conventional or laser, and fluorescence or transmitted observations are possible.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.
Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
Compounds which inhibit the synthesis of proteins. They are usually ANTI-BACTERIAL AGENTS or toxins. Mechanism of the action of inhibition includes the interruption of peptide-chain elongation, the blocking the A site of ribosomes, the misreading of the genetic code or the prevention of the attachment of oligosaccharide side chains to glycoproteins.
Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.
Proteins that originate from insect species belonging to the genus DROSOPHILA. The proteins from the most intensely studied species of Drosophila, DROSOPHILA MELANOGASTER, are the subject of much interest in the area of MORPHOGENESIS and development.
A plant genus of the family SOLANACEAE. Members contain NICOTINE and other biologically active chemicals; its dried leaves are used for SMOKING.
Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
A type of CELL NUCLEUS division by means of which the two daughter nuclei normally receive identical complements of the number of CHROMOSOMES of the somatic cells of the species.
An infant during the first month after birth.
An inhibitory T-lymphocyte receptor that has specificity for CD274 ANTIGEN and PROGRAMMED CELL DEATH 1 LIGAND 2 PROTEIN. Signaling by the receptor limits T cell proliferation and INTERFERON GAMMA synthesis. The receptor also may play an essential role in the regulatory pathway that induces PERIPHERAL TOLERANCE.
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
Expanded structures, usually green, of vascular plants, characteristically consisting of a bladelike expansion attached to a stem, and functioning as the principal organ of photosynthesis and transpiration. (American Heritage Dictionary, 2d ed)
A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.
A diazo-naphthalene sulfonate that is widely used as a stain.
A broad category of carrier proteins that play a role in SIGNAL TRANSDUCTION. They generally contain several modular domains, each of which having its own binding activity, and act by forming complexes with other intracellular-signaling molecules. Signal-transducing adaptor proteins lack enzyme activity, however their activity can be modulated by other signal-transducing enzymes
A mitogen-activated protein kinase subfamily that regulates a variety of cellular processes including CELL GROWTH PROCESSES; CELL DIFFERENTIATION; APOPTOSIS; and cellular responses to INFLAMMATION. The P38 MAP kinases are regulated by CYTOKINE RECEPTORS and can be activated in response to bacterial pathogens.
A promyelocytic cell line derived from a patient with ACUTE PROMYELOCYTIC LEUKEMIA. HL-60 cells lack specific markers for LYMPHOID CELLS but express surface receptors for FC FRAGMENTS and COMPLEMENT SYSTEM PROTEINS. They also exhibit phagocytic activity and responsiveness to chemotactic stimuli. (From Hay et al., American Type Culture Collection, 7th ed, pp127-8)
A class of statistical procedures for estimating the survival function (function of time, starting with a population 100% well at a given time and providing the percentage of the population still well at later times). The survival analysis is then used for making inferences about the effects of treatments, prognostic factors, exposures, and other covariates on the function.
The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action during the developmental stages of an organism.
A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.
A CCAAT-enhancer binding protein that is induced by DNA DAMAGE and growth arrest. It serves as a dominant negative inhibitor of other CCAAT-enhancer binding proteins.
Protein analogs and derivatives of the Aequorea victoria green fluorescent protein that emit light (FLUORESCENCE) when excited with ULTRAVIOLET RAYS. They are used in REPORTER GENES in doing GENETIC TECHNIQUES. Numerous mutants have been made to emit other colors or be sensitive to pH.
Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.
A subtype of caspases that contain long pro-domain regions that regulate the activation of the enzyme. The pro-domain regions contain protein-protein interaction motifs that can interact with specific signaling adaptor proteins such as DEATH DOMAIN RECEPTORS; DED SIGNALING ADAPTOR PROTEINS; and CARD SIGNALING ADAPTOR PROTEINS. Once activated, the initiator caspases can activate other caspases such as the EFFECTOR CASPASES.
Interruption or suppression of the expression of a gene at transcriptional or translational levels.
An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.
The entity of a developing mammal (MAMMALS), generally from the cleavage of a ZYGOTE to the end of embryonic differentiation of basic structures. For the human embryo, this represents the first two months of intrauterine development preceding the stages of the FETUS.
Hereditary and sporadic conditions which are characterized by progressive nervous system dysfunction. These disorders are often associated with atrophy of the affected central or peripheral nervous system structures.
Methods of investigating the effectiveness of anticancer cytotoxic drugs and biologic inhibitors. These include in vitro cell-kill models and cytostatic dye exclusion tests as well as in vivo measurement of tumor growth parameters in laboratory animals.
The unfavorable effect of environmental factors (stressors) on the physiological functions of an organism. Prolonged unresolved physiological stress can affect HOMEOSTASIS of the organism, and may lead to damaging or pathological conditions.
Eukaryotic cell line obtained in a quiescent or stationary phase which undergoes conversion to a state of unregulated growth in culture, resembling an in vitro tumor. It occurs spontaneously or through interaction with viruses, oncogenes, radiation, or drugs/chemicals.
A common neoplasm of early childhood arising from neural crest cells in the sympathetic nervous system, and characterized by diverse clinical behavior, ranging from spontaneous remission to rapid metastatic progression and death. This tumor is the most common intraabdominal malignancy of childhood, but it may also arise from thorax, neck, or rarely occur in the central nervous system. Histologic features include uniform round cells with hyperchromatic nuclei arranged in nests and separated by fibrovascular septa. Neuroblastomas may be associated with the opsoclonus-myoclonus syndrome. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2099-2101; Curr Opin Oncol 1998 Jan;10(1):43-51)
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
A compound obtained from the bark of the white willow and wintergreen leaves. It has bacteriostatic, fungicidal, and keratolytic actions.
Proteins whose abnormal expression (gain or loss) are associated with the development, growth, or progression of NEOPLASMS. Some neoplasm proteins are tumor antigens (ANTIGENS, NEOPLASM), i.e. they induce an immune reaction to their tumor. Many neoplasm proteins have been characterized and are used as tumor markers (BIOMARKERS, TUMOR) when they are detectable in cells and body fluids as monitors for the presence or growth of tumors. Abnormal expression of ONCOGENE PROTEINS is involved in neoplastic transformation, whereas the loss of expression of TUMOR SUPPRESSOR PROTEINS is involved with the loss of growth control and progression of the neoplasm.
Quaternary salts derived from tetrazoles. They are used in tests to distinguish between reducing sugars and simple aldehydes, for detection of dehydrogenase in tissues, cells, and bacteria, for determination of corticosteroids, and in color photography. (From Mall's Dictionary of Chemistry, 5th ed, p455)
Derivatives of phosphatidic acids in which the phosphoric acid is bound in ester linkage to a serine moiety. Complete hydrolysis yields 1 mole of glycerol, phosphoric acid and serine and 2 moles of fatty acids.
A plant genus of the family BRASSICACEAE that contains ARABIDOPSIS PROTEINS and MADS DOMAIN PROTEINS. The species A. thaliana is used for experiments in classical plant genetics as well as molecular genetic studies in plant physiology, biochemistry, and development.
A large multisubunit complex that plays an important role in the degradation of most of the cytosolic and nuclear proteins in eukaryotic cells. It contains a 700-kDa catalytic sub-complex and two 700-kDa regulatory sub-complexes. The complex digests ubiquitinated proteins and protein activated via ornithine decarboxylase antizyme.
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.

Low resting potential and postnatal upregulation of NMDA receptors may cause Cajal-Retzius cell death. (1/11751)

Using in situ patch-clamp techniques in rat telencephalic slices, we have followed resting potential (RP) properties and the functional expression of NMDA receptors in neocortical Cajal-Retzius (CR) cells from embryonic day 18 to postnatal day 13, the time around which these cells normally disappear. We find that throughout their lives CR cells have a relatively depolarized RP (approximately -50 mV), which can be made more hyperpolarized (approximately -70 mV) by stimulation of the Na/K pump with intracellular ATP. The NMDA receptors of CR cells are subjected to intense postnatal upregulation, but their similar properties (EC50, Hill number, sensitivity to antagonists, conductance, and kinetics) throughout development suggest that their subunit composition remains relatively homogeneous. The low RP of CR cells is within a range that allows for the relief of NMDA channels from Mg2+ blockade. Our findings are consistent with the hypothesis that CR cells may degenerate and die subsequent to uncontrolled overload of intracellular Ca2+ via NMDA receptor activation by ambient glutamate. In support of this hypothesis we have obtained evidence showing the protection of CR cells via in vivo blockade of NMDA receptors with dizocilpine.  (+info)

Ischemic tolerance in murine cortical cell culture: critical role for NMDA receptors. (2/11751)

Murine cortical cultures containing both neurons and glia (days in vitro 13-15) were exposed to periods of oxygen-glucose deprivation (5-30 min) too brief to induce neuronal death. Cultures "preconditioned" by sublethal oxygen-glucose deprivation exhibited 30-50% less neuronal death than controls when exposed to a 45-55 min period of oxygen-glucose deprivation 24 hr later. This preconditioning-induced neuroprotection was specific in that neuronal death induced by exposure to excitotoxins or to staurosporine was not attenuated. Neuroprotection was lost if the time between the preconditioning and severe insult were decreased to 7 hr or increased to 72 hr and was blocked if the NMDA antagonist 100 microM 3-((D)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid was applied during the preconditioning insult. This was true even if the duration of preconditioning was increased as far as possible (while still remaining sublethal). A similar preconditioning effect was also produced by sublethal exposure to high K+, glutamate, or NMDA but not to kainate or trans-1-aminocyclopentane-1, 3-dicarboxylic acid.  (+info)

Fas/Apo [apoptosis]-1 and associated proteins in the differentiating cerebral cortex: induction of caspase-dependent cell death and activation of NF-kappaB. (3/11751)

The developing cerebral cortex undergoes a period of substantial cell death. The present studies examine the role of the suicide receptor Fas/Apo[apoptosis]-1 in cerebral cortical development. Fas mRNA and protein are transiently expressed in subsets of cells within the developing rat cerebral cortex during the peak period of apoptosis. Fas-immunoreactive cells were localized in close proximity to Fas ligand (FasL)-expressing cells. The Fas-associated signaling protein receptor interacting protein (RIP) was expressed by some Fas-expressing cells, whereas Fas-associated death domain (FADD) was undetectable in the early postnatal cerebral cortex. FLICE-inhibitory protein (FLIP), an inhibitor of Fas activation, was also expressed in the postnatal cerebral cortex. Fas expression was more ubiquitous in embryonic cortical neuroblasts in dissociated culture compared to in situ within the developing brain, suggesting that the environmental milieu partly suppresses Fas expression at this developmental stage. Furthermore, FADD, RIP, and FLIP were also expressed by subsets of dissociated cortical neuroblasts in culture. Fas activation by ligand (FasL) or anti-Fas antibody induced caspase-dependent cell death in primary embryonic cortical neuroblast cultures. The activation of Fas was also accompanied by a rapid downregulation of Fas receptor expression, non-cell cycle-related incorporation of nucleic acids and nuclear translocation of the RelA/p65 subunit of the transcription factor NF-kappaB. Together, these data suggest that adult cortical cell number may be established, in part, by an active process of receptor-mediated cell suicide, initiated in situ by killer (FasL-expressing) cells and that Fas may have functions in addition to suicide in the developing brain.  (+info)

Microvessels from Alzheimer's disease brains kill neurons in vitro. (4/11751)

Understanding the pathogenesis of Alzheimer's disease is of widespread interest because it is an increasingly prevalent disorder that is progressive, fatal, and currently untreatable. The dementia of Alzheimer's disease is caused by neuronal cell death. We demonstrate for the first time that blood vessels isolated from the brains of Alzheimer's disease patients can directly kill neurons in vitro. Either direct co-culture of Alzheimer's disease microvessels with neurons or incubation of cultured neurons with conditioned medium from microvessels results in neuronal cell death. In contrast, vessels from elderly nondemented donors are significantly (P<0.001) less lethal and brain vessels from younger donors are not neurotoxic. Neuronal killing by either direct co-culture with Alzheimer's disease microvessels or conditioned medium is dose- and time-dependent. Neuronal death can occur by either apoptotic or necrotic mechanisms. The microvessel factor is neurospecific, killing primary cortical neurons, cerebellar granule neurons, and differentiated PC-12 cells, but not non-neuronal cell types or undifferentiated PC-12 cells. Appearance of the neurotoxic factor is decreased by blocking microvessel protein synthesis with cycloheximide. The neurotoxic factor is soluble and likely a protein, because its activity is heat labile and trypsin sensitive. These findings implicate a novel mechanism of vascular-mediated neuronal cell death in Alzheimer's disease.  (+info)

Rapid death of adoptively transferred T cells in acquired immunodeficiency syndrome. (5/11751)

Human immunodeficiency virus (HIV)-specific cytotoxic T lymphocytes (CTL) probably play the major role in controlling HIV replication. However, the value of adoptive transfer of HIV-specific CTL expanded in vitro to HIV+ patients has been limited: this contrasts with the success of CTL therapy in treating or preventing Epstein-Barr virus and cytomegalovirus disease after bone marrow transplantation (BMT). We investigated the fate of expanded HIV-specific CTL clones in vivo following adoptive transfer to a patient with acquired immunodeficiency syndrome (AIDS). Two autologous CTL clones specific for HIV Gag and Pol were expanded to large numbers (>10(9)) in vitro and infused into an HIV-infected patient whose viral load was rising despite antiretroviral therapy. The fate of one clone was monitored by staining peripheral blood mononuclear cells (PBMCs) with T-cell receptor-specific tetrameric major histocompatibility complex (MHC)-peptide complexes. Although the CTL transfer was well tolerated, there were no significant changes in CD4 and CD8 lymphocyte counts and virus load. By tracking an infused clone using soluble MHC-peptide complexes, we show that cells bearing the Gag-specific T-cell receptors were rapidly eliminated within hours of infusion through apoptosis. Thus, the failure of adoptively transferred HIV-specific CTL to reduce virus load in AIDS may be due to rapid apoptosis of the infused cells, triggered by a number of potential mechanisms. Further trials of adoptive transfer of CTL should take into account the susceptibility of infused cells to in vivo apoptosis.  (+info)

Role of hypoxia-induced Bax translocation and cytochrome c release in reoxygenation injury. (6/11751)

We investigated mechanisms of cell death during hypoxia/reoxygenation of cultured kidney cells. During glucose-free hypoxia, cell ATP levels declined steeply resulting in the translocation of Bax from cytosol to mitochondria. Concurrently, there was cytochrome c release and caspase activation. Cells that leaked cytochrome c underwent apoptosis after reoxygenation. ATP depletion induced by a mitochondrial uncoupler resulted in similar alterations even in the presence of oxygen. Moreover, inclusion of glucose during hypoxia prevented protein translocations and reoxygenation injury by maintaining intracellular ATP. Thus, ATP depletion, rather than hypoxia per se, was the cause of protein translocations. Overexpression of Bcl-2 prevented cytochrome c release and reoxygenation injury without ameliorating ATP depletion or Bax translocation. On the other hand, caspase inhibitors did not prevent protein translocations, but inhibited apoptosis during reoxygenation. Nevertheless, they could not confer long-term viability, since mitochondria had been damaged. Omission of glucose during reoxygenation resulted in continued failure of ATP production, and cell death with necrotic morphology. In contrast, cells expressing Bcl-2 had functional mitochondria and remained viable during reoxygenation even without glucose. Therefore, Bax translocation during hypoxia is a molecular trigger for cell death during reoxygenation. If ATP is available during reoxygenation, apoptosis develops; otherwise, death occurs by necrosis. By preserving mitochondrial integrity, BCL-2 prevents both forms of cell death and ensures cell viability.  (+info)

Elevated expression of the CD4 receptor and cell cycle arrest are induced in Jurkat cells by treatment with the novel cyclic dinucleotide 3',5'-cyclic diguanylic acid. (7/11751)

The effect of the novel, naturally occurring nucleotide cyclic diguanylic acid (c-di-GMP) on the lymphoblastoid CD4+ Jurkat cell line was studied. When exposed to 50 microM c-di-GMP, Jurkat cells exhibited a markedly elevated expression of the CD4 receptor of up to 6.3-fold over controls. C-di-GMP also causes blockage of the cell cycle at the S-phase, characterized by increased cellular thymidine uptake, reduction in G2/M-phase cells, increase in S-phase cells and decreased cell division. Additionally c-di-GMP naturally enters these cells and binds irreversibly to the P21ras protein. The effects described appear to be unique for c-di-GMP.  (+info)

Glutamate receptor signaling interplay modulates stress-sensitive mitogen-activated protein kinases and neuronal cell death. (8/11751)

Glutamate receptors modulate multiple signaling pathways, several of which involve mitogen-activated protein (MAP) kinases, with subsequent physiological or pathological consequences. Here we report that stimulation of the N-methyl-D-aspartate (NMDA) receptor, using platelet-activating factor (PAF) as a messenger, activates MAP kinases, including c-Jun NH2-terminal kinase, p38, and extracellular signal-regulated kinase, in primary cultures of hippocampal neurons. Activation of the metabotropic glutamate receptor (mGluR) blocks this NMDA-signaling through PAF and MAP kinases, and the resultant cell death. Recombinant PAF-acetylhydrolase degrades PAF generated by NMDA-receptor activation; the hetrazepine BN50730 (an intracellular PAF receptor antagonist) also inhibits both NMDA-stimulated MAP kinases and neuronal cell death. The finding that the NMDA receptor-PAF-MAP kinase signaling pathway is attenuated by mGluR activation highlights the exquisite interplay between glutamate receptors in the decision making process between neuronal survival and death.  (+info)

Initiating discussions about fungal cell death is challenged by the lack of a vocabulary with generally agreed-upon definitions. The definition of programmed cell death also holds layers of complexity. The concept of physiological cell death arose in the 19th and 20th centuries when investigators observed the systematic disappearance of cells in various developing animal models (8). With the discovery of lysosomes in 1955 (9), some researchers in the cell death field became occupied with the idea that leakage of hydrolases from these suicide bags was to blame, while others argued that unleashed hydrolases were a consequence rather than a cause of cell death (10). These ideas have been revisited and extended more recently both in human disease (11) and in yeast cell death (12).. In pursuit of the components that control developmental cell death, Richard Lockshin and his PhD adviser Carroll Williams at Harvard published a series of papers in 1964 to 1965 applying the term programmed cell ...
Nonapoptotic forms of cell death may facilitate the selective elimination of some tumor cells or be activated in specific pathological states. The oncogenic RAS-selective lethal small molecule erastin triggers a unique iron-dependent form of nonapoptotic cell death that we term ferroptosis. Ferropto …
TY - JOUR. T1 - Nitric oxide-GAPDH-Siah. T2 - a novel cell death cascade.. AU - Hara, Makoto R.. AU - Snyder, Solomon H. PY - 2006/7. Y1 - 2006/7. N2 - 1. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is an extremely abundant glycolytic enzyme, and exemplifies the class of proteins with multiple, seemingly unrelated functions. Recent studies indicate that it is a major intracellular messenger mediating apoptotic cell death. This paper reviews the GAPDH cell death cascade and discusses its clinical relevance. 2. A wide range of apoptotic stimuli activate NO formation, which S-nitrosylates GAPDH. The S-nitrosylation abolishes catalytic activity and confers upon GAPDH the ability to bind to Siah, an E3-ubiquitin-ligase, which translocates GAPDH to the nucleus. In the nucleus, GAPDH stabilizes the rapidly turning over Siah, enabling it to degrade selected target proteins and affect apoptosis. 3. The cytotoxicity of mutant Huntingtin (mHtt) requires nuclear translocation which appears to be ...
The concept of programmed cell death has evolved over the years to include both apoptotic and non-apoptotic death mechanisms. This study describes a novel form of non-apoptotic cell death induced as a result of dysregulated macropinocytosis. We have named this cell death methuosis. Methuosis is observed when the activated form of Ras GTPase is over-expressed in glioblastoma cells. It is accompanied by the accumulation of large phase-lucent cytoplasmic vacuoles, followed by rounding up, detachment, and disintegration of the cells. The vacuoles quickly take up extracellular fluid-phase tracers, a hallmark of macropinosomes. Our studies also show that the Ras-induced vacuoles are not acidic and are negative for LC3-II (a marker for autophagosomes), transferrin and EEA1 (endosomal markers). These observations rule out the vacuoles originating from autophagosomal, endosomal or lysosomal compartments. Even though caspase activation is observed in dying cells, death is not prevented by zVAD-fmk, a ...
In the context of pulmonary infection, both hosts and pathogens have evolved a multitude of mechanisms to regulate the process of host cell death. The host aims to rapidly induce an inflammatory response at the site of infection, promote pathogen clearance, quickly resolve inflammation, and return to tissue homeostasis. The appropriate modulation of cell death in respiratory epithelial cells and pulmonary immune cells is central in the execution of all these processes. Cell death can be either inflammatory or anti-inflammatory depending on regulated cell death (RCD) modality triggered and the infection context. In addition, diverse bacterial pathogens have evolved many means to manipulate host cell death to increase bacterial survival and spread. The multitude of ways that hosts and bacteria engage in a molecular tug of war to modulate cell death dynamics during infection emphasizes its relevance in host responses and pathogen virulence at the host pathogen interface. This narrative review outlines
Animals and plants diverged over one billion years ago and evolved unique mechanisms for many cellular processes, including cell death. One of the most well-studied cell death programmes in animals, apoptosis, involves gradual cell dismantling and engulfment of cellular fragments, apoptotic bodies, through phagocytosis. However, rigid cell walls prevent plant cell fragmentation and thus apoptosis is not applicable for executing cell death in plants. Furthermore, plants are devoid of the key components of apoptotic machinery, including phagocytosis as well as caspases and Bcl-2 family proteins. Nevertheless, the concept of plant
It has been described that in mammalian cells, growth and integrity are directly influenced by changes in cell membrane composition occurring when PtdCho biosynthesis has been perturbed by mutations, inhibition, or nutrient deficiency (Cui et al., 1996). We also found that the reduced primary root growth in XPL1 Arabidopsis mutants is related to a 50% reduction in cell elongation. Because PEAMT plays a pivotal role in the PtdCho biosynthetic pathway in plants, reduced root growth and epidermal cell death in xipotl could also be because of perturbation in the synthesis of PtdCho in the root meristem. However, the observation that PA can alleviate cell death suggests that some of cellular phenotypes observed in xipotl are not because of a direct effect in the reduction of PtdCho levels (Figure 9).. Cell death has been classified into physiological cell death and nonphysiological cell death (Vaux and Korsmeyer, 1999). Physiological cell death refers to the process of programmed cell death, in which ...
TY - JOUR. T1 - Programmed cell death in fission yeast. AU - Rodriguez-Menocal, Luis. AU - DUrso, Gennaro. N1 - Funding Information: We would like to thank Bill Burhans and Frank Madeo for valuable discussions. G.D. is supported by NIH1R01CA099034-01. L.R.M is supported by a post-doctoral fellowship from the American Heart Association.. PY - 2004/11. Y1 - 2004/11. N2 - Recently a metacaspase, encoded by YCA1, has been implicated in a primitive form of apoptosis or programmed cell death in yeast. Previously it had been shown that over-expression of mammalian pro-apoptotic proteins can induce cell death in yeast, but the mechanism of how cell death occurred was not clearly established. More recently, it has been shown that DNA or oxidative damage, or other cell cycle blocks, can result in cell death that mimics apoptosis in higher cells. Also, in fission yeast deletion of genes required for triacylglycerol synthesis leads to cell death and expression of apoptotic markers. A metacaspase sharing ...
Different cell-death mechanisms control many physiological and pathological processes in humans. Mitochondria play important roles in cell death through the release of pro-apoptotic factors such as cytochrome c and apoptosis-inducing factor (AIF), which activate caspase-dependent and caspase-independent cell death, respectively. Poly(ADP-ribose) polymerase 1 (PARP-1) is emerging as an important activator of caspase-independent cell death. PARP-1 generates the majority of long, branched poly(ADP-ribose) (PAR) polymers following DNA damage. Overactivation of PARP-1 initiates a nuclear signal that propagates to mitochondria and triggers the release of AIF. AIF then shuttles from mitochondria to the nucleus and induces peripheral chromatin condensation, large-scale fragmentation of DNA and, ultimately, cytotoxicity. Identification of the pro-death and pro-survival signals in the PARP-1-mediated cell-death program might provide novel therapeutic targets in human diseases.
bcl-x is a member of the bcl-2 gene family, which may regulate programmed cell death. Mice were generated that lacked Bcl-x. The Bcl-x-deficient mice died around embryonic day 13. Extensive apoptotic cell death was evident in postmitotic immature neurons of the developing brain, spinal cord, and dorsal root ganglia. Hematopoietic cells in the liver were also apoptotic. Analyses of bcl-x double-knockout chimeric mice showed that the maturation of Bcl-x-deficient lymphocytes was diminished. The life-span of immature lymphocytes, but not mature lymphocytes, was shortened. Thus, Bcl-x functions to support the viability of immature cells during the development of the nervous and hematopoietic systems. ...
TY - JOUR. T1 - Activation of caspase-8 and Erk-1/2 in domes regulates cell death induced by confluence in MDCK cells. AU - Chang, Yung Heng. AU - Lin, Hsi Hui. AU - Wang, Yang Kao. AU - Chiu, Wen Tai. AU - Su, Hsiao Wen. AU - Tang, Ming Jer. PY - 2007/4/1. Y1 - 2007/4/1. N2 - Under normal culture conditions, cells adhere to culture dish, spread out, proliferate, and finally cover all areas and reach confluence. During the confluent stage, cell proliferation ceases and differentiation is enhanced. Meanwhile, cell death also appears as the monolayer confluence proceeds. To delineate the mechanism of cell death induced by the confluent process, we employed Madin-Darby canine kidney (MDCK) cells. When approaching confluence, MDCK cells exhibited increase the levels of caspase-2 and enhanced the activity of caspase-8. Using various caspase inhibitors to block apoptosis, we found that only z-VAD-fmk and z-IETD-fmk can inhibit confluent cell death, indicating that confluent cell death is mediated by ...
BACKGROUND: High levels of ex vivo CD4 T-cell death and the accumulation of highly differentiated and/or immunosenescent T cells have been associated with poor CD4 T-cell recovery in treated HIV-infected individuals. However, the relationship between cell death and T-cell differentiation is still unclear. METHODS: We have analyzed cell death, immunosenescence and differentiation parameters in HAART-treated subjects (VL |50 copies/mL for more than 2 years) with CD4 T-cell count |350 cells/μL (immunodiscordant, n = 23) or |400 cells/μL (immunoconcordant, n = 33). We included 11 healthy individuals as reference. RESULTS: As expected, suboptimal CD4 T-cell recovery was associated with low frequencies of naïve cells, high frequencies of transitional and effector memory cells and a subsequent low ratio of central/transitional memory cells in the CD4 compartment. These alterations correlated with spontaneous CD4 T-cell death. A deeper analysis of cell death in CD4 T-cell subsets showed increased cell death
The life/death decisions in the cell are controlled by the balance between apoptotic and anti-apoptotic signaling pathways such as DNA repair. Despite the fact these pathways have been studied relatively well, their quantitative regulation until recently has been poorly understood. This situation has dramatically changed in the last years. Creation of mathematical models of apoptotic and non-apoptotic signaling pathways led to an enormous progress in the quantitative understanding of the network regulation and provided fascinating insights into the mechanisms of life/death control. Moreover, it led to the identification of targets within the cell death networks followed by the drug discovery. In this Research topic, the computational models of apoptotic and non-apoptotic signaling and their biological implications will be addressed. Central attention will be given to the cross-talk between cell death and DNA repair pathways defining cell fate. Additionally, we also welcome methodology-related
Bax inhibitor-1 (BI-1) was initially identified for its ability to inhibit BAX-induced apoptosis in yeast cells and is the founding member of a family of highly hydrophobic proteins localized in diverse cellular membranes. It is evolutionarily conserved and orthologues from plants can substitute for …
Programmed Cell Death Pcd Plays Pivotal Roles In Tumor Progression Cancer Therapeutics And Resistance Of Tumor Cells To Therapy With The Discovery Of Key Mechanisms That Are Involved In Mediating Pcd And In Promoting Resistance To Therapy Design Of Therapeutic Approaches For Promoting Tumor Selective Cell Death Has Risen Dramatically
Cell death and differentiation is a monthly research journal focused on the exciting field of programmed cell death and apoptosis. It provides a single accessible source of information for both scientists and clinicians, keeping them up-to-date with advances in the field. It encompasses programmed cell death, cell death induced by toxic agents, differentiation and the interrelation of these with cell proliferation.
Cel-lu-lar deci-sions to live or die are fun-da-men-tal to devel-op-ment and adult home-osta-sis, play-ing roles in a wide vari-ety of phys-i-o-log-i-cal and patho-log-i-cal processes. These include can-cer, degen-er-a-tive dis-ease, innate and adap-tive immu-nity, ischemia-​reperfusion injury, and infec-tious disease. Over the past decades, the fun-da-men-tal mol-e-c-u-lar mech-a-nisms under-ly-ing one form of cell death, apop-to-sis, have been largely defined. Other forms of cell death, such as pro-grammed necro-sis or autophagic cell death, are not as well understood. In this meet-ing, the path-ways that impact on a cells deci-sion to live or die will be pre-sented in the con-text of phys-i-ol-ogy and dis-ease, and ways to influ-ence that deci-sion ther-a-peu-ti-cally will be explored. The con-se-quence of cell death for the body is also of great inter-est, as the clear-ance of dying cells impacts on other phys-i-o-log-i-cal processes. ...
Ferroptosis is a non-apoptotic form of regulated cell death. It is distinct from other regulated cell death phenotypes, such as apoptosis and necroptosis. Ferroptosis is characterized by extensive lipid peroxidation, which can be suppressed by iron chelators or lipophilic antioxidants. Mechanistically, Ferroptosis inducers are divided into two classes: (1) inhibitors of cystine import via system xc− (e.g., Erastin), which subsequently causes depletion of glutathione (GSH), and (2) covalent inhibitors (e.g., (1S, 3R)-RSL3) of glutathione peroxidase 4 (GPX4). Since GPX4 reduces lipid hydroperoxides using GSH as a co-substrate, both compound classes ultimately result in loss of GPX4 activity, followed by elevated levels of lipid reactive oxygen species (ROS) and consequent cell death. Ferroptosis is an iron- and ROS-dependent form of regulated cell death (RCD). Misregulated Ferroptosis has been implicated in multiple physiological and pathological processes, including cancer cell death, ...
Cell death has been recognized in the cardiovascular system for centuries. In Virchows 1858 lectures, he described atherosclerosis as producing new tissue, followed by cell death: Thus, we have here an active process which really produces new tissues, but then hurries on to destruction in consequence of its own development.1 Degraded and dying cells are found in both myocardial infarction and in atherosclerosis, and until the last 20 years were classified as necrosis. Death was considered a passive phenomenon due to ischemic or other insult, resulting in cell membrane dissolution and leakage of proinflammatory contents. The consequences of cell death resulted from loss of the function of the live cells and subsequent inflammation.. This scenario changed with the description of apoptosis in the 1970s,2 and the subsequent detailed description of the mechanisms underlying this form of programmed cell death. The presence of apoptosis in atherosclerotic plaques has been confirmed by a number of ...
The robust and rapid induction of innate immune signaling is a hallmark of the host response to microbial infection. Successful pathogens subvert, thwart, or dismantle these defensive measures. Growing evidence suggests that the host recognizes these disruptive efforts, eliciting effective backup measures. Cell death processes, including apoptosis and pyroptosis, are integral components of the host response to infection. Multiprotein inflammasome complexes sense the presence of pathogens and activate inflammatory caspases, typically caspase-1 or caspase-11, leading to pyroptotic cell death and maturation of the inflammatory cytokines interleukin-1β (IL-1β) and IL-18. Pyroptosis is an inflammasome-driven cytotoxic process that occurs in macrophages after limited proteolysis of gasdermin D (GSDMD). The generation of an N-terminally cleaved fragment then creates large oligomeric membrane pores and causes lytic cell death (1-7). At present, caspase-1 and caspase-11 are the only known regulators of ...
SIRT1 ameliorates oxidative stress induced neural cell death and is down-regulated in Parkinsons disease. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Sortilin (∼95 kDa) is a member of the recently discovered family of Vps10p-domain receptors, and is expressed in a variety of tissues, notably brain, spinal cord and muscle. It acts as a receptor for neurotensin, but predominates in regions of the nervous system that neither synthesize nor respond to this neuropeptide, suggesting that sortilin has additional roles. Sortilin is expressed during embryogenesis in areas where nerve growth factor (NGF) and its precursor, proNGF, have well-characterized effects. These neurotrophins can be released by neuronal tissues, and they regulate neuronal development through cell survival and cell death signalling. NGF regulates cell survival and cell death via binding to two different receptors, TrkA and p75NTR (ref. 10). In contrast, proNGF selectively induces apoptosis through p75NTR but not TrkA. However, not all p75NTR-expressing cells respond to proNGF, suggesting that additional membrane proteins are required for the induction of cell death. Here we report that
TY - JOUR. T1 - Role of apoptosis in pancreatic β-cell death in diabetes. AU - Chandra, Joya. AU - Zhivotovsky, Boris. AU - Zaitsev, Sergei. AU - Juntti-Berggren, Lisa. AU - Berggren, Per Olof. AU - Orrenius, Sten. PY - 2001. Y1 - 2001. N2 - Apoptosis is a physiological form of cell death that occurs during normal development, and critical mediators of this process include caspases, reactive oxygen species, and Ca2+. Excessive apoptosis of the pancreatic β-cell has been associated with diabetes. Consequently, apoptosis research has focused on how infiltrating macrophages or cytotoxic T-cells might kill pancreatic β-cells using cytokines or death receptor triggering. Meanwhile, the intracellular events in the target β-cell have been largely ignored. Elucidation of such targets might help develop improved treatment strategies for diabetes. This article will outline recent developments in apoptosis research, with emphasis on mechanisms that may be relevant to β-cell death in type 1 and type 2 ...
Near East University Experimental Health Sciences Research Center (DESAM) board members and doctoral students represented our country in collaboration with the Marmara University, Genetic and Metabolic Diseases Research and Application Center (GEMHAM) and Cell Death Research Association (HÖAD) at...
BOC lecture - 7 Cell Death 1. The Biology of Cancer Chapter 9: p53 and Apoptosis: Master Guardian and Executioner Cell Death 2. Apoptosis Autophagy Necrosis Programmed cell death. Death cycle is programmed by the cell itself Self-eating Catabolic process involving lysosomes.
DESCRIPTION (provided by applicant): The reduction of oxygen occurring as a result of advanced vascular diseases poses severe clinical problems including massive cell death and resultant tissue loss. Compared to pharmacological methods of therapeutic angiogenesis, cell-based strategies represent a direct approach to generate a capillary network. Endothelial colony forming cells (ECFCs) are a subpopulation of endothelial progenitor cells that exhibit robust angiogenic potential under hypoxic conditions and can form functional vascular networks in vivo. Adipose- derived stem cells (ASCs) are a promising cell population for promoting angiogenesis and potentially stabilizing new vessels. However, the success of cell-based therapies is limited by rapid cell death due to apoptosis upon implanting cells into ischemic tissue environments, dramatically reducing the number of cells available to participate in vasculogenesis. Additionally, recent data suggest that cells derived from older donors are more ...
Galluzzi L, Vitale I, Abrams JM, Alnemri ES, Baehrecke EH, Blagosklonny MV, Dawson TM, Dawson VL, El-Deiry WS, Fulda S, Gottlieb E, Green DR, Hengartner MO, Kepp O, Knight RA, Kumar S, Lipton SA, Lu X, Madeo F, Malorni W, Mehlen P, Nunez G, Peter ME, Piacentini M, Rubinsztein DC, Shi Y, Simon HU, Vandenabeele P, White E, Yuan J, Zhivotovsky B, Melino G, Kroemer G (2012). Molecular definitions of cell death subroutines: recommendations of the Nomencla- ture Committee on Cell Death 2012.Cell Death Differ 19, 107-120. ...
Although the antitumor properties of cannabinoids were first observed more than 30 years ago, when Munson et al (27) demonstrated that Δ9-tetrahydrocannabinoid (THC) inhibits lung adenocarcinoma cell growth in vivo, the elucidation of mechanisms employed by cannabinoids for influencing cancer cell proliferation and death was developed in the last two decades. However, there are still many obscure sides on death pathways activated by these compounds and, in particular, on the different contribution of apoptosis and autophagy in cell death.. The anticancer potential of this class of compounds can be very different in the various tumor systems. This depends on the mechanism used by cannabinoids to interact with the cells, i.e. the class of receptors to which they bind or on the specific intracellular activated pathways.. Regarding the interaction with the target cell, it has been demonstrated that cannabinoids can interact with the specific type 1 or 2 cannabinoid receptors (CB1 and CB2), which ...
Ren, Y.; Lv, Q.; Yue, W.; Liu, B.; Zou, Z., 2019: The programmed cell death protein-1/programmed cell death ligand 1 expression, CD3+ T cell infiltration, NY-ESO-1 expression, and microsatellite instability phenotype in primary cutaneous melanoma and mucosal melanoma and their clinical significance and prognostic value: a study of 89 consecutive cases
Cell death and Differentiation provides an accessible source of up-to-date information for scientists and clinicians. It covers programmed cell death, cell death induced by toxic agents, differentiation and their relation to cell proliferation.
Death receptors are activated, for example, in the case of infections when white blood cells that have combatted a virus are to be removed. It was previously known that death receptors in the blood can be measured, but not whether an elevated level was linked to increased cell death in type 2 diabetes and arteriosclerosis. The aim of the study was therefore to investigate whether death receptors could be used as a marker that could be linked to ongoing tissue damage and if this could be used to predict the risk of developing diseases. The results show that increased cell death can be linked to increased levels in the blood of three different members of the same death receptor family (TNFR-1, TRAILR-2 and Fas). Increased cell death is seen in type 2 diabetes as well as arteriosclerosis. High blood sugar and blood fats (low levels of HDL, the good cholesterol) subject the bodys blood vessels and insulin-producing beta cells to stress. Long-term stress damages the cells and can cause the ...
Cell Death and Immunity symposium will provide a unique opportunity to bring together researchers in the cell death and immunology communities, as well as scientists studying host-pathogen interactions, who are focused on understanding the molecular and cellular mechanisms that link cell death and the immune response.. Visit the website to know more.
Cell Death and Immunity symposium will provide a unique opportunity to bring together researchers in the cell death and immunology communities, as well as scientists studying host-pathogen interactions, who are focused on understanding the molecular and cellular mechanisms that link cell death and the immune response.. Visit the website to know more.
BioAssay record AID 729817 submitted by ChEMBL: Induction of apoptosis in human DG75 cells assessed as cell death at 2.5 uM after 24 hrs by flow cytometry (Rvb = 0.8 +/- 0.25%).
Billions of cells in our body die every day. Damaged, infected or superfluous cells are thus disposed of to keep our bodies healthy. It is thought that most of these cells die by a process called apoptosis. However, we have shown that cells in the breast, following lactation, do not die by apoptosis but by a novel mechanism that requires organelles called lysosomes. These tend to be thought of as cellular waste bins since they digest cellular components and recycle them. However, we have discovered that during regression of the breast, enzymes called cathepsins leak out of the lysosomes into the cell and induce a process that we call lysosomal-mediated programmed cell death (LM-PCD). This is the first time that this type of cell death has been shown to occur in a normal mammalian organism. Furthermore, we have shown that a transcription factor, Stat3, that is often associated with breast cancer, is responsible for executing LM-PCD as it induces high levels of cathepsins while suppressing ...
Originally aired: Wednesday, December 6, 2017. The mechanisms of cell death play a fundamental role in neurodegenerative disorders such as Alzheimers disease, Parkinsons disease, and Huntingtons disease. Caspase activity, cathepsin activity, and oxidative stress all contribute to cell death in the forms of apoptosis, pyroptosis, and necrosis. ICT offers a reliable and accurate line of fluorescent reagents to help neuroscience researchers detect cell death in their samples using flow cytometry, fluorescence microscopy, or a fluorescence plate reader. In this webinar, we will discuss different types of cell death, the role of cell death in neurodegenerative diseases, and methods to assess cell death in cell cultures.. ...
Big Pharma has been accused of selling drugs that are so dangerous they cause death and drugs that cause the. some direct toxicity that causes death or
My lab is interested in understanding the mechanisms by which normal and malignant cells regulate programmed cell death. Multicellular organisms have devised a tightly regulated, genetically programmed mechanism of cell suicide to maintain homeostasis and to prevent propagation of genetically damaged cells. The discovery of the BCL-2 family of genes uncovered the underlying genetic mechanism of this regulation, as well as a class of oncogenes that governs cell death rather than cell proliferation. There are two major pathways that regulation programmed cell death: apoptosis and programmed necrosis. Simply, apoptotic cells implode in a relatively immune silent manner. Necrotic cells explode, releasing cellular contents and inciting an immune response- beneficial in settings of infection, but detrimental in settings of chronic damage, where the inflammation elicited by necrotic cell death amplifies cellular damage. Current studies focus on how programmed cell death regulates homeostasis in
Purpose: TUNEL assay is widely used to evaluate cell death. Quantification of TUNEL-positive (TUNEL+) cells in tissue sections is usually performed manually, ideally by two masked observers. This process is time consuming, prone to measurement errors, and not entirely reproducible. In this paper, we describe an automated quantification approach to address these difficulties. Methods: We developed an ImageJ macro to quantitate cell death by TUNEL assay in retinal cross-section images. The script was coded using IJ1 programming language. To validate this tool, we selected a dataset of TUNEL assay digital images, calculated layer area and cell count manually (done by two observers), and compared measurements between observers and macro results. Results: The automated macro segmented outer nuclear layer (ONL) and inner nuclear layer (INL) successfully. Automated TUNEL+ cell counts were in-between counts of inexperienced and experienced observers. The intraobserver coefficient of variation (COV) ...
TY - JOUR. T1 - Connexin 43 channels protect osteocytes against oxidative stress-induced cell death. AU - Kar, Rekha. AU - Riquelme, Manuel A.. AU - Werner, Sherry. AU - Jiang, Jean X.. PY - 2013/7. Y1 - 2013/7. N2 - The increased osteocyte death by oxidative stress (OS) during aging is a major cause contributing to the impairment of bone quality and bone loss. However, the underlying molecular mechanism is largely unknown. Here, we show that H2O2 induced cell death of primary osteocytes and osteocytic MLO-Y4 cells, and also caused dose-dependent decreased expression of gap junction and hemichannel-forming connexin 43 (Cx43). The decrease of Cx43 expression was also demonstrated with the treatment of other oxidants, rotenone and menadione. Antioxidant reversed the effects of oxidants on Cx43 expression and osteocyte cell death. Cx43 protein was also much lower in the osteocytes from 20-month-old as opposed to the 5-week-old or 20-week old mice. Dye transfer assay showed that H2O2 reduced the gap ...
(−)-Epigallocatechin-3-gallate (EGCG) is the most extensive studied tea polyphenol for its anti-cancer function. In this study, we report a novel mechanism of action for EGCG-mediated cell death by identifying the critical role of lysosomal membrane permeabilization (LMP). First, EGCG-induced cell death in human cancer cells (both HepG2 and HeLa) was found to be caspase-independent and accompanied by evident cytosolic vacuolization, only observable when cells were treated in serum-free medium. The cytosolic vacuolization observed in EGCG-treated cells was most probably caused by lysosomal dilation. Interestingly, EGCG was able to disrupt autophagic flux at the degradation stage by impairment of lysosomal function, and EGCG-induced cell death was independent of Atg5 or autophagy. The key finding of this study is that EGCG is able to trigger LMP, as evidenced by Lyso-Tracker Red staining, cathepsin D cytosolic translocation and cytosolic acidification. Consistently, a lysosomotropic agent, chloroquine,
TY - JOUR. T1 - How Do Cardiomyocytes Die? Apoptosis and Autophagic Cell Death in Cardiac Myocytes. AU - Kunapuli, Sanjay. AU - Rosanio, Salvatore. AU - Schwarz, Ernst R.. PY - 2006/6/1. Y1 - 2006/6/1. N2 - Background: Cell death constitutes one of the key events in biology. Historically, apoptosis and necrosis have been considered to represent the 2 fundamental forms of cell death. Apoptosis is a tightly regulated, energy-dependent process in which cell death follows a programmed set of events. Necrosis refers to the sum of degenerative changes that follow any type of cell death. Methods and Results: The role of apoptosis in development of ischemic heart disease, hypertensive heart disease, and end-stage heart failure has been well documented. Recent evidence suggests the potential role of a third mechanism of cell death, autophagy, in loss of cardiac myocytes. Autophagic cell death has been recently documented in myocardial cells from hypertrophied, failing, and hibernating myocardium. ...
P2X7 is an ATP-gated ion channel that is highly expressed by leukocytes, such as macrophages. Here, it has been demonstrated to be involved in the regulation of various cell death pathways; including apoptosis, pyroptosis, necrosis, and autophagy. However, cell death induction via P2X7 is complex and is reliant upon the nature of the stimulus, the duration of the stimulus, and the cell type investigated. Previous reports state that high extracellular ATP concentrations promote osmotic lysis, but whether positive allosteric modulation of P2X7 in the presence of lower concentrations of ATP condemns cells to the same fate is unknown. In this study, we compared cell death induced by high ATP concentrations, to cell death induced by compound K, a recently identified and potent positive allosteric modulator of P2X7. Based on our observations, we propose that high ATP concentrations induce early cell swelling, loss of mitochondrial membrane potential, plasma membrane rupture, and LDH release. ...
Programmed cell death (or apoptosis) is usually an evolutionarily conserved, genetically controlled suicide mechanism for cells that, when deregulated, can lead to developmental defects, cancers, and degenerative diseases [1, 2]. for germ cell death. We confirmed this initial observation by performing a dose-response analysis of the deletion mutant. In contrast to wild-type animals, deletion mutants did not exhibit an increase in germ cell apoptosis after exposure to increasing doses of IR (Physique?1C; see also Figure?S1 available online). This was reminiscent of loss-of-function (lf) mutants that are also resistant to IR-induced apoptosis. Therefore, we examined whether regulates germ cell death specifically, like and mutants. We found that developmental cell death was unaffected in mutants, suggesting that the rules of cell death by is usually specific to germ cells, like (Physique?1D). Finally, to determine whether the allele is usually a null, we performed a deficiency analysis by crossing ...
Programmed cell death (PCD) is a deliberate cellular suicide process. Dysfunction of PCD is implicated in various human diseases, including developmental and neurodegenerative disorders, cancer and autoimmune diseases [1]. PCD can be categorized by morphological criteria [2]. Type I cell death, known as apoptosis, is characterized by cell shrinkage, nuclear condensation, membrane blebbing, mitochondria dysfunction, loss of selectivity in membrane permeabilization, and nuclear DNA fragmentation. Lastly, cells are rapidly eliminated by phagocytosis [3]. Type II PCD refers to autophagic cell death (ACD). Autophagy is a catabolic process that disposes of various cytoplasmic components, including protein aggregates and organelles [4]. The components are sequestered by autophagosomes, which fuse with lysosomes for degradation. This process usually occurs in response to cellular stress to protect the cells. However, prolonged autophagy can cause ACD [5]. Type III cell death, called necrosis, is best ...
Hot pepper is one of the economically important crops in Asia. A large number of gene sequences, including expressed sequence tag (EST) and genomic sequences are publicly available. However, it is still a daunting task to determine gene function due to difficulties in genetic modification of a pepper plants. Here, we show the application of the virus-induced gene silencing (VIGS) repression for the study of 459 pepper ESTs selected as non-host pathogen-induced cell death responsive genes from pepper microarray experiments in Nicotiana benthamiana. Developmental abnormalities in N. benthamiana plants are observed in the 32 (7%) pepper ESTs-silenced plants. Aberrant morphological phenotypes largely comprised of three groups: stunted, abnormal leaf, and dead. In addition, by employing the combination of VIGS and Agrobacterium-mediated transient assays, we identified novel pepper ESTs that involved in Bax or INF1-mediated cell death responses. Silencing of seven pepper ESTs homologs suppressed Bax or INF1
The p38 mitogen-activated protein kinase (p38 MAPK) family, which is comprised of four protein isoforms, p38α, p38β, p38γ and p38δ, forms one of the key MAPK pathways. The p38 MAPKs are implicated in many cellular processes including inflammation, differentiation, cell growth, cell cycle and cell death. The function of p38 MAPKs in mitotic entry has been well established, but their role in mitotic progression has remained controversial. We identify p38γ MAPK as a modulator of mitotic progression and mitotic cell death. In HeLa cells, loss of p38γ results in multipolar spindle formation and chromosome misalignment, which induce a transient M phase arrest. The majority of p38γ-depleted cells die at mitotic arrest or soon after abnormal exit from M-phase. We show that p38 MAPKs are activated at the kinetochores and spindle poles throughout mitosis by kinase(s) that are stably bound to these structures. Finally, p38γ is required for the normal kinetochore localization of polo-like kinase 1 ...
Molecular deletion of transglutaminase 2 (TG2) has been shown to improve function and survival in a host of neurological conditions including stroke, Huntingtons disease, and Parkinsons disease. However, unifying schemes by which these cross-linking or polyaminating enzymes participate broadly in neuronal death have yet to be presented. Unexpectedly, we found that in addition to TG2, TG1 gene expression level is significantly induced following stroke in vivo or due to oxidative stress in vitro. Forced expression of TG1 or TG2 proteins is sufficient to induce neuronal death in Rattus norvegicus cortical neurons in vitro. Accordingly, molecular deletion of TG2 alone is insufficient to protect Mus musculus neurons from oxidative death. By contrast, structurally diverse inhibitors used at concentrations that inhibit TG1 and TG2 simultaneously are neuroprotective. These small molecules inhibit increases in neuronal transamidating activity induced by oxidative stress; they also protect neurons ...
Autophagy is a process in which cells digest their own organelles and proteins in response to nutritional starvation. Yu et al. describe a form of cell death that bears similarities to autophagy. Unlike apoptosis, which depends on activation of proteases in the caspase family, autophagic cell death in a mouse cell line was actually inhibited by caspase-8. Inhibition of expression of two genes known to function in autophagy, ATG7 and beclin 1, reduced cell death caused by inhibition of caspase-8. These findings could impact strategies for combating unwanted apoptosis that use caspase inhibitors to prevent cell death.. L. Yu, A. Alva, H. Su, P. Dutt, E. Freundt, S. Welsh, E. H. Baehrecke, M. J. Lenardo, Regulation of an ATG7-beclin 1 program of autophagic cell death by caspase-8. Science 304, 1500-1502 (2004). [Abstract] [Full Text]. ...
TY - JOUR. T1 - Therapeutic implications of disorders of cell death signalling. T2 - membranes, micro-environment, and eicosanoid and docosanoid metabolism. AU - Davidson, Jillian. AU - Rotondo, D. AU - Rizzo, Maria. AU - Leaver, Anne. PY - 2012/6/6. Y1 - 2012/6/6. N2 - Disruptions of cell death signalling occur in pathological processes, such as cancer and degenerative disease. Increased knowledge of cell death signalling has opened new areas of therapeutic research, and identifying key mediators of cell death has become increasingly important. Early triggering events in cell death may provide potential therapeutic targets, whereas agents affecting later signals may be more palliative in nature. A group of primary mediators are derivatives of the highly unsaturated fatty acids (HUFAs), particularly oxygenated metabolites such as prostaglandins. HUFAs, esterified in cell membranes, act as critical signalling molecules in many pathological processes. Currently, agents affecting HUFA metabolism ...
TY - JOUR. T1 - The wound response in fresh-cut lettuce involves programmed cell death events. AU - Iakimova, Elena T.. AU - Woltering, Ernst J.. PY - 2018/7. Y1 - 2018/7. N2 - In this work, the involvement of programmed cell death (PCD) in the wound-induced postharvest browning disorder and senescence in butterhead lettuce (Lactuca sativa L.) fresh-cuts was studied. At the wounded (cut, bruised) sites, rapid browning, loss of chlorophyll and massive cell death, accompanied with accumulation of reactive oxygen species and increased electrolyte leakage occurred in a narrow strip of tissue adjacent the injury. The dead cell morphology (protoplast and nuclei shrinkage) together with the biochemical and physiological changes resembled necrotic PCD type. With a slight delay post-wounding, senescence associated with similar cell death features was initiated in distant non-wounded sites. In addition to necrotic PCD, both in wounded and senescing tissue, the appearance of empty cell corpses was ...
At the beginning of neurogenesis, massive brain cell death occurs and more than 50% of cells are eliminated by apoptosis along with neuronal differentiation. However, few studies were conducted so far regarding the regulation of neural progenitor cells (NPCs) death during development. Because of the physiological role of cell death during development, aberration of normal apoptotic cell death is detrimental to normal organogenesis. Apoptosis occurs in not only neuron but also in NPCs and neuroblast. When growth and survival signals such as EGF or LIF are removed, apoptosis is activated as well as the induction of differentiation. To investigate the regulation of cell death during developmental stage, it is essential to investigate the regulation of apoptosis of NPCs. Neural progenitor cells were cultured from E14 embryonic brains of Sprague-Dawley rats. For in vivo VPA animal model, pregnant rats were treated with VPA (400 mg/kg S.C.) diluted with normal saline at E12. To analyze the cell death, we
Oxygen glucose deprivation (OGD)/re-oxygenation (OGDR) induces profound oxidative injury and neuronal cell death. It mimics ischemia-reperfusion neuronal injury. CPI-1189 is a novel tumor necrosis factor alpha-inhibiting compound with potential neuroprotective function. Here in SH-SY5Y neuronal cells and primary murine cortical neurons, CPI-1189 pretreatment potently inhibited OGDR-induced viability reduction and cell death. In OGDR-stimulated neuronal cells, p38 phosphorylation was blocked by CPI-1189. In addition, CPI-1189 alleviated OGDR-induced reactive oxygen species production, lipid peroxidation, and glutathione consumption. OGDR-induced neuronal cell apoptosis was also inhibited by CPI-1189 pretreatment. Furthermore, in SH-SY5Y cells and cortical neurons, CPI-1189 alleviated OGDR-induced programmed necrosis by inhibiting mitochondrial p53-cyclophilin D-adenine nucleotide translocase 1 association, mitochondrial depolarization, and lactate dehydrogenase release to the medium. In summary, CPI-1189
Cell death is the event of a biological cell ceasing to carry out its functions. This may be the result of the natural process of old cells dying and being replaced by new ones, or may result from such factors as disease, localized injury, or the death of the organism of which the cells are part. Kinds of cell death include the following: Programmed cell death (or PCD) is cell death mediated by an intracellular program. PCD is carried out in a regulated process, which usually confers advantage during an organisms life-cycle. For example, the differentiation of fingers and toes in a developing human embryo occurs because cells between the fingers apoptose; the result is that the digits are separate. PCD serves fundamental functions during both plant and metazoa (multicellular animals) tissue development. Apoptosis or Type I cell-death, and autophagy or Type II cell-death are both forms of programmed cell death, while necrosis is a non-physiological process that occurs as a result of infection or ...
Cancer cells increase glucose metabolism to support aerobic glycolysis. However, only some cancer cells are acutely sensitive to glucose withdrawal, and the underlying mechanism of this selective sensitivity is unclear. We showed that glucose deprivation initiates a cell death pathway in cancer cells that is dependent on the kinase RIPK1. Glucose withdrawal triggered rapid plasma membrane depolarization and an influx of extracellular calcium into the cell through the L-type calcium channel Cav1.3 (CACNA1D), followed by activation of the kinase CAMK1. CAMK1 and the demethylase PPME1 were required for the subsequent demethylation and inactivation of the catalytic subunit of the phosphatase PP2A (PP2Ac) and the phosphorylation of RIPK1. Plasma membrane depolarization, PP2Ac demethylation, and cell death were prevented by glucose and, unexpectedly, by its nonmetabolizable analog 2-deoxy-d-glucose (2-DG), a glycolytic inhibitor. These findings reveal a previously unknown function of glucose as a ...
Most schemes for TGs role in acute and chronic neurodegeneration have centered around the ability of these enzymes to cross-link mutated and/or accumulated proteins in a host of diseases, including AD, HD, and PD (Caccamo et al., 2010). And while this model unifies diseases associated with proteotoxicity, it fails to account for the benefits of molecular or pharmacological TG deletion in ischemic (Hwang et al., 2009; Colak et al., 2011) or hemorrhagic stroke (Okauchi et al., 2009). Indeed, exciting new data on the role of TG in autophagosome formation (DEletto et al., 2009), in inhibiting axonal transport of growth factors such as BDNF (Borrell-Pagès et al., 2006), in repressing adaptive gene expression (McConoughey et al., 2010), and on influencing nuclear actin dynamics (Munsie et al., 2011) have focused attention on biological roles of these fascinating enzymes other than cross-linking. Here, we demonstrate that TG is a necessary component of oxidative stress-induced death signaling in ...
During development, large numbers of cells die by a nonpathological process referred to as programmed cell death. In many tissues, dying cells display similar changes in morphology and chromosomal DNA organization, which has been termed apoptosis. Apoptosis is such a widely documented phenomenon that many authors have assumed all programmed cell deaths occur by this process. Two well-characterized model systems for programmed cell death are (i) the death of T cells during negative selection in the mouse thymus and (ii) the loss of intersegmental muscles of the moth Manduca sexta at the end of metamorphosis. In this report we compare the patterns of cell death displayed by T cells and the intersegmental muscles and find that they differ in terms of cell-surface morphology, nuclear ultrastructure, DNA fragmentation, and polyubiquitin gene expression. Unlike the T cells, which are known to die via apoptosis, we find that the intersegmental muscles display few of the features that characterize ...
Lesion mimic mutants spontaneously produce disease spots in the absence of biotic or abiotic stresses. Analyzing lesion mimic mutants sheds light on the mechanisms underlying programmed cell death and defense-related responses in plants. Here, we isolated and characterized the rice (Oryza sativa) spotted leaf 36 (spl36) mutant, which was identified from an ethyl methanesulfonate-mutagenized japonica cultivar Yundao population. spl36 displayed spontaneous cell death and enhanced resistance to rice bacterial pathogens. Gene expression analysis suggested that spl36 functions in the disease response by upregulating the expression of defense-related genes. Physiological and biochemical experiments indicated that more cell death occurred in spl36 than the wild type and that plant growth and development were affected in this mutant. We isolated SPL36 by map-based cloning. A single base substitution was detected in spl36, which results in a cysteine-to-arginine substitution in SPL36. SPL36 is predicted to
BNIP3 is a cell death-inducing mitochondrial protein that is part of a Bcl-2 subfamily with NIX and ceBNIP3. BNIP3-induced cell death morphologically resembles necrosis that is characterized by rapid plasma membrane damage and mitochondrial dysfunction in the early stages, followed by DNA fragmentation and chromatin condensation characteristic of apoptotic cell death in the later stages. DNA fragmentation during most types of apoptosis is predominantly due to caspase-3 activation. However, BNIP3-induced cell death is independent of caspase-3 activity, thus the mechanism of BNIP3-induced DNA fragmentation remains unknown. Co-immunoprecipitation analysis revealed an interaction between BNIP3, NIX, and caspase-2. The interaction is unique in that it is not mediated through the caspase-2 prodomain. Caspases-1, -8, and -9, which have homologous prodomains to caspase-2, do not bind BNIP3 or NIX, indicating specificity for caspase-2. Further structural analysis indicated that the transmembrane domain ...
TY - JOUR. T1 - The role of vacuole in plant cell death. AU - Hara-Nishimura, I.. AU - Hatsugai, N.. N1 - Funding Information: Acknowledgements. We are grateful to the Ministry of Education, Culture, Sports, Science, and Technology of Japan (MEXT) for Grants-in-Aid for Scientific Research (no. 22000014) and for the Global Center of Excellence Program Formation of a Strategic Base for Biodiversity and Evolutionary Research: from Genome to Ecosystem.. PY - 2011/8. Y1 - 2011/8. N2 - Almost all plant cells have large vacuoles that contain both hydrolytic enzymes and a variety of defense proteins. Plants use vacuoles and vacuolar contents for programmed cell death (PCD) in two different ways: for a destructive way and for a non-destructive way. Destruction is caused by vacuolar membrane collapse, followed by the release of vacuolar hydrolytic enzymes into the cytosol, resulting in rapid and direct cell death. The destructive way is effective in the digestion of viruses proliferating in the cytosol, ...
Cell death can occur through 3 mechanisms: apoptosis, autophagy, and necrosis. Apoptosis, or programmed cell death, results in controlled cell shrinkage and nuclear fragmentation via the action of caspases, as well as an anti-inflammatory cytokine release. In contrast, necrosis signals via RIPK1 (RIP1), leading to cell swelling, lysis, and a pro-inflammatory cytokine release. Autophagy destroys the cells damaged proteins and organelles via an intracellular catabolic process in the lysosome. Multiple physiological processes require the removal of specific cells by a controlled cell-death program. For example, tissue remodeling activates apoptosis, whereas energy metabolism and growth regulation responses rely on autophagy. Developmental processes often activate apoptosis, while bodily injuries or infection more commonly induce necrosis. The molecular mechanisms behind these cell death pathways overlap, and can be co-activated during some cellular functions. Apoptosis and necrosis both signal ...
FIG. 2. Dose- and time-dependent effects of SERCA inhibition on CHOP expression, caspase-3 activation, and cell death. Cell death was assayed in real-time by propidium iodide incorporation in MIN6 cells. A: Images illustrating the progressive propidium iodide incorporation in a field of MIN6 cells exposed to 1 μmol/l thapsigargin (Tg). B: Representative time course of cell death in response to various concentrations of thapsigargin. ○, Control; ▪, 0.01 μmol/l thapsigargin; ▴, 0.1 μmol/l thapsigargin; •, 1 μmol/l thapsigargin. C: Dose dependence of the thapsigargin-induced MIN6 cell death, quantified as the area under the curves (IAUC) of the first 24 h of the propidium iodide incorporation profiles (n = 3). D: Induction of CHOP (∼31-kDa band) and cleaved caspase-3 (∼17- to 19-kDa band) in MIN6 cells cultured for 24 h in DMEM containing 25 mmol/l glucose and increasing concentrations of thapsigargin (n = 3). E: Representative real-time imaging of caspase-3 activation in living ...
The present study aimed to investigate anti-proliferative and apoptotic effects of quercetin on human leukemia cells and effects of quercetin-induced cell death on a nov..
Programmed cell death (or PCD) is the death of a cell in any form, mediated by an intracellular program. PCD is carried out in a biological process, which usually confers advantage during an organisms life-cycle. For example, the differentiation of fingers and toes in a developing human embryo occurs because cells between the fingers apoptose; the result is that the digits are separate. PCD serves fundamental functions during both plant and animal tissue development. Apoptosis and autophagy are both forms of programmed cell death, but necrosis was long seen as a non-physiological process that occurs as a result of infection or injury. Necrosis is the death of a cell caused by external factors such as trauma or infection and occurs in several different forms. Recently a form of programmed necrosis, called necroptosis, has been recognized as an alternate form of programmed cell death. It is hypothesized that necroptosis can serve as a cell-death backup to apoptosis when the apoptosis signaling is ...
Excitotoxic cell death, the end for many cells after ischemic brain injury and in some neurodegenerative diseases, is triggered by glutamate-induced calcium influx. Downstream, activation of the p38α map kinase leads to apoptosis, but just how calcium and p38 connect has been an open question. New results from Michael Courtneys lab at the University of Kuopio in Finland show that the small GTPase Rho is the missing link. Their work, published in the March 18 online edition of Nature Neuroscience, establishes Rho activation by calcium influx as a necessary and sufficient event to turn on p38 and cause cell death in primary neurons.. Their results open up a potential new target for drugs to block excitotoxicity, and may have some additional relevance to Alzheimer disease. Inhibitors of Rho and its downstream kinase Rock can modulate amyloid-β (Aβ) peptide production (Zhou et al., 2003; Leuchtenberger et al., 2006). In addition, Rho is farnesylated, and changes in Rho/Rock pathway activity have ...
Cell death is not only an essential phenomenon in normal development and homeostasis, but also crucial in various pathologies. It is now clear that many types of cell death can be regulated by pharmacological or genetic interventions. These were largely achieved by identifying the molecular mechanisms underlying the regulated cell death (RCD). While in the immune system, RCD needs to be facilitated to help the clearance of pathogens and tumors, in healthy cells, especially the terminally differentiated neurons in the nervous system, it is more desirable to protect cells from dying due to stress under pathological conditions. Thus, understating the inhibitory and the activating signals for RCD in different systems is important. In this thesis, I will discuss the study of two key molecules involved in RCD: programmed death 1 (PD-1, as inhibitor for RCD) and serine/threonine kinase receptor interaction protein 3 (RIP3, as promoter for RCD) in two different systems. First, I studied the role of PD-1
Dive into the research topics of Neuronal death in amyotrophic lateral sclerosis is apoptosis: Possible contribution of a programmed cell death mechanism. Together they form a unique fingerprint. ...
Although it is well established that IFNγ causes cell death in a variety of cell types (Deiss et al., 1995; Ossina et al., 1997; Wen et al., 1997; Ruiz-Ruiz et al., 2000; Trautmann et al., 2000; Horiuchi et al., 2006), the signal transduction downstream of STAT1 remains largely unknown (Barber, 2000). Unraveling the role of IFNγ in apoptosis remains a challenge because IFNγ may prime cells to apoptosis and through induction of many genes can concomitantly elicit an antiproliferative and a proliferative state (Xiang et al., 2008). The decision between life and death may depend on possible costimuli or the cell type. Enhanced expression and translocation of Diablo into the cytosol play a critical role in the promotion of IFNγ-induced apoptosis of IFNγ-sensitive B cells (Yoshikawa et al., 2001). Th1 cells that secrete high levels of IFNγ are more susceptible to activation-induced cell death than Th2 cells because Th2 cells express Fas-associated phosphatase, FAP-1 (Zhang et al., 1997). In ...
03.05.2016 The Gutenberg Research College (GRC) of Johannes Gutenberg University Mainz (JGU) has chosen to give the 2016 Gutenberg Research Award to American biomedical researcher Dr. Vishva Dixit for his groundbreaking work in the field of programmed cell death. His findings have contributed significantly to the understanding of the actual mechanisms involved in the crucial process that is also known as apoptosis. At the same time, Dixit is also helping to convert the information obtained into a form that can be employed in clinical applications. In the person of Dr. Vishva Dixit, the Gutenberg Research College is bestowing the Gutenberg Research Award on an internationally acclaimed top-level researcher. His groundbreaking findings on cell death have provided important clues that help us understand in much more detail the processes associated with the immune system, emphasized the Director of the Gutenberg Research College, Professor Matthias Neubert. Programmed cell death is actually a ...
TY - JOUR. T1 - Comparative analysis of the role of small G proteins in cell migration and cell death. T2 - Cytoprotective and promigratory effects of RalA. AU - Jeon, Hyejin. AU - Zheng, Long Tai. AU - Lee, Shinrye. AU - Lee, Won Ha. AU - Park, Nammi. AU - Park, Jae-Yong. AU - Heo, Won Do. AU - Lee, Myung Shik. AU - Suk, Kyoungho. PY - 2011/1/1. Y1 - 2011/1/1. N2 - Small G protein superfamily consists of more than 150 members, and is classified into six families: the Ras, Rho, Rab, Arf, Ran, and RGK families. They regulate a wide variety of cell functions such as cell proliferation/differentiation, cytoskeletal reorganization, vesicle trafficking, nucleocytoplasmic transport and microtubule organization. The small G proteins have also been shown to regulate cell death/survival and cell shape. In this study, we compared the role of representative members of the six families of small G proteins in cell migration and cell death/survival, two cellular phenotypes that are associated with ...
Balakireva A. V., Zamyatnin Jr A. A. Cutting out the gaps between proteases and programmed cell death // Frontiers in plant science. - 2019. - Vol. 10. - P. 704. To date, many animal models for programmed cell death (PCD) have been extensively characterized and classified while such efforts in plant types of PCD still remain poorly understood. However, despite a wide range of functional differences between PCD types in animals and plants, it is certain that all of them are regulated through the recruitment of proteases. Most importantly, proteases are able to perform proteolysis that results in a gain or loss of protein function. This principle relies on the presence of proteolytic cascades where proteases are activated upon various upstream stimuli and which lead to repetitive cell death. While protease activation, proteolytic cascades and targeted substrates are described in detail mainly for nematode, human, and mice models of apoptosis, for plants, only fragmentary knowledge of protease ...
Finland Deaths Stats, NationMaster. Retrieved from Finland Deaths Stats, NationMaster. 1948-2012. ,,.. Finland Deaths Stats, NationMaster, ,, [assessed 1948-2012]. Finland Deaths Stats, NationMaster [Internet]. 1948-2012. Avaliable from: ,,.. Finland Deaths Stats, NationMaster. Avaliable at: Assessed 1948-2012.. Finland Deaths Stats, NationMaster, (assessed 1948-2012). Finland Deaths Stats, NationMaster, (last visited 1948-2012). Finland Deaths Stats, NationMaster, (as ...
Scale?bars denote 50 m. Open in a separate window Figure 7 Correlation among cell death, nitric oxide (NO) and autophagy in tobacco BY-2 cells after 24 h of toxin (AaT) exposure. After 24 h, AaT facilitated Ca2+ influx with an accumulation of reactive oxidant intermediates and NO, to manifest necrotic cell death. Inhibition of NO accumulation by 2-(4-Carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) decreased the level of necrotic cell death, and induced autophagy, which suggests NO accumulation represses autophagy and facilitates necrotic cell death at 24 h. Application of N-acetyl-L-cysteine at 3 h, 666-15 confirmed ROS to be the key initiator of autophagy, and together with cPTIO for 24 h, revealed the combined effects of NO and ROS is required for necrotic HR cell death. and plants with silenced or knocked-out (Fr.) Keissler causes a serious worldwide depletion of economic yield30. In (tobacco), the pathogen has been reported to inculcate lethal symptoms like anthracnose, ...
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Glioma-initiating cells (GIC) are considered the underlying cause of recurrences of aggressive glioblastomas, replenishing the tumor population and undermining the efficacy of conventional chemotherapy. Here we report the discovery that inhibiting T-type voltage-gated Ca2+ and KCa channels can effectively induce selective cell death of GIC and increase host survival in an orthotopic mouse model of human glioma. At present, the precise cellular pathways affected by the drugs affecting these channels are unknown. However, using cell-based assays and integrated proteomics, phosphoproteomics, and transcriptomics analyses, we identified the downstream signaling events these drugs affect. Changes in plasma membrane depolarization and elevated intracellular Na+, which compromised Na+-dependent nutrient transport, were documented. Deficits in nutrient deficit acted in turn to trigger the unfolded protein response and the amino acid response, leading ultimately to nutrient starvation and GIC cell death. ...
During development of the nervous system, as many as half of all neurons generated are ultimately eliminated by a process known as programmed cell death. Much of this cell death occurs as newly differentiated neurons compete for limiting amounts of survival-promoting neurotrophic factors. Though counterintuitive, the selective death of neurons at specific times during development is critical for sculpting a properly wired nervous system. While programmed cell death is essential for normal development, too much or too little cell death later in life is a confounding factor in diseases ranging from Alzheimers disease and stroke to brain cancer. Research in the Freeman laboratory is aimed at characterizing the mechanisms that regulate cell death in the mammalian nervous system. More specifically, we aim to identify and understand the critical cell signaling events that, if left unchecked, commit a neuron to die ...
JUPITER, FL - January 27, 2015 - In a pair of related studies, scientists from the Florida campus of The Scripps Research Institute (TSRI) have shown their drug candidates can target biological...
1. Lipid-induced cell death - Investigation of the mechanism leading to lipotoxicity. 2. Meiotic Processes within the regulation of aging - characterization of the mechanism leading to longevity in yeast and mammalian cells. 3. Autophagy (self-eating) in dying cells - Interconnection of apoptosis and autophagy via a new Bcl-2 family-protein. 4. Identification of a novel yeast caspase - Functional analysis of the raptor- protein regarding the regulation of autophagy and apoptosis. 5. Yeast as a model for neurodegeneration - Parkinson´s, Alzheimer`s, and Huntington`s disease. 6. Caspase independent regulation of cell death - implications of apoptosis-inducing factor AIF1 and its interactom in aging and apoptosis. Contact: Prof. Dr. Frank Madeo. ...
Drug resistance has been mostly explained by molecular changes, such as overexpression of p-glycoprotein or O6-methylguanine-DNA-methyltransferase, which interfere with drug actions on the targets (1 , 2) . Because most anticancer agents, regardless of their diverse targets, exert effects by inducing apoptosis via activation of apoptotic pathways common to many cellular stresses, any antiapoptotic changes disrupting the common intrinsic pathways to execute physiological cell death can also make malignant cells resistant to chemotherapy (3) . Such alterations opposing apoptosis are routinely observed in malignant tumors, including both the functional loss of tumor suppressors p53, Bax, or PTEN and deregulated hyperfunction of oncogenic proteins, such as Ras, Bcl-2, and PI3K 2 ,(3) .. In tumor cells with an aberrantly activated PI3K/Akt survival pathway, the increased antiapoptotic signals overcome apoptotic signals of anticancer drugs, confer drug resistance on the tumor cells, and result in a ...
Cells of the Monocyte / Macrophage lineage are key players in innate and adaptive immunity. They eliminate pathogens through their phagocytic and antimicrobial properties, secretion of inflammatory and immunoregulatory cytokines, as well as their capacity to present foreign antigens to T lymphocytes in lymphoid tissues. The importance of M/Ms in the immune response require them to undergo strict regulation, which occurs, at least in part, through the control of monocytic cell survival. Autophagy is a ubiquitous cellular process by which cells degrade intracellular, cytoplasmic components via a network of interconnected vacuoles to carry out a variety of functions. Autophagy typically functions in maintaining cellular homeostasis and mitigating stresses. However, more recent studies have shown that autophagy may play a role in cell death. Our laboratory has previously found that the cytokine IFNγ can induce cell death in human monocytes in an autophagy-dependent manner. Conversely, IL-10 ...
Inflammasome Lab researchers, Associate Professor Kate Schroder and Dr Dave Boucher, are looking forward to the 2nd Japan Australia Meeting on Cell Death, in Tokyo 22-23 May 2018.
Roscoff, May 17th, 2021. SeaBeLife, a pharmaceutical company focused on identifying a new class of drug candidates able to deprogram regulated cell death, announces its second seed money fundraising with several Business Angels networks.. The companys disruptive technology is based on inhibiting simultaneously two kinds of necrotic cell deaths. The therapeutic potential is major because simultaneous activation has been recently pointed as an explanation for acute pathologies, which have limited therapeutic options and are notoriously hard to treat.. In particular SeaBeLife has confirmed the promising in vivo preliminary results obtained in 2020 for two indications: acute renal failure and liver failure. Beyond acute pathologies, SeaBeLife is also looking into chronical diseases such as Parkinsons, Alzheimers, or AMD (retinal degeneration). Encouraging preliminary results were generated in vitro for all these three chronic indications. The team is presently performing in vivo ...
Extensive programmed cell death (PCD) occurs in the developing nervous system. Neuronal death occurs, at least in part, because neurons are produced in excess during development and compete with each other for the limited amounts of the survival-promoting trophic factors secreted by target tissues. Neuronal death is apoptotic and utilizes components that are conserved in other PCD pathways. In this review, we discuss the mechanism of trophic factor-dependent neuronal cell death by focusing on the pathway of nerve growth factor (NGF) deprivation-induced sympathetic neuronal death. We describe the biochemical and genetic events that occur in NGF-deprived sympathetic neurons undergoing PCD. Participation of the Bcl-2 family of proteins and the interleukin-1β-converting enzyme family of proteases (caspases) in this and other models of neuronal death is also examined. The order and importance of these components during NGF deprivation-induced sympathetic neuronal death are discussed.. ...
The role of these enzymes in programmed cell death was first identified in 1993, with their functions in apoptosis well characterised. This is a form of programmed cell death, occurring widely during development, and throughout life to maintain cell homeostasis. Activation of caspases ensures that the cellular components are degraded in a controlled manner, carrying out cell death with minimal effect on surrounding tissues.[3]. Caspases have other identified roles in programmed cell death such as pyroptosis and necroptosis. These forms of cell death are important for protecting an organism from stress signals and pathogenic attack. Caspases also have a role in inflammation, whereby it directly processes pro-inflammatory cytokines such as pro-IL1β. These are signalling molecules that allow recruitment of immune cells to an infected cell or tissue. There are other identified roles of caspases such as cell proliferation, tumour suppression, cell differentiation, neural development and axon ...
Mitochondrial regulation of cell death: a phylogenetically conserved control - Mitochondria are fundamental for eukaryotic cells as they participate in critical catabolic and anabolic pathways. Moreover, mitochondria play a key role in the signal transduction cascades that precipitate many (but not all) regulated variants of cellular demise. In this short review, we discuss the differential implication of mitochondria in the major forms of regulate cell death.
Cellular decisions to live or die are fundamental to development and adult homeostasis, playing roles in a wide variety of physiological and pathological processes. These include cancer, degenerative disease, innate and adaptive immunity, ischemia-reperfusion injury, and infectious disease. As the study of cell death moves beyond the central mechanisms of apoptosis to wider issues of regulation and other forms of cell death, this vibrant area of research widens its influence and importance for human health and disease.
The MAP kinase p38 is activated by noncanonical BMP signaling, and also by cellular stress, with p38 activity providing a second readout of intrinsic and extrinsic function. If Gdf6a promotes apoptosis by increasing cell stress, upregulated p38 activity would be observed in mutants, while the converse would occur if p38 is a mediator of Gdf6a signaling. Compared with gdf6a+/+ siblings (Fig. 4A), gdf6a−/− embryos exhibit markedly increased ocular p38 MAP kinase phosphorylation assessed with whole-mount IHC using phospho-specific (Thr180/Tyr182) p38 MAP kinase antibodies (Fig. 4B). If such increased levels of phosphorylated-p38 MAP kinases activate apoptosis, inhibition of this kinase would be expected to rescue the gdf6a −/− cell death phenotype. To test this, we applied a pharmacologic inhibitor of p38 MAP kinase (SB203580 [60 μM]) to zebrafish embryos and examined apoptosis using caspase-3 IHC. Treatment with SB203580 partially inhibits the increased ocular caspase-3 activation of ...
Intra-cellular processes: cell motility and division; cell death; intra-cellular transport; secretion. Extra-cellular processes ... Metabolism: Anabolic and catabolic processes; cell maintenance and homeostasis; secondary metabolism. ... inter-, extr-cellular processes like cell adhesion; organismal process like blood clotting or the immune system. General: ...
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... and causes cell death in cultured cells". J. Biol. Chem. 275 (4): 2647-53. doi:10.1074/jbc.275.4.2647. PMID 10644725. Li PF, Li ... "Calcium binding of ARC mediates regulation of caspase 8 and cell death". Mol. Cell. Biol. 24 (22): 9763-70. doi:10.1128/MCB. ... "Inhibition of both the extrinsic and intrinsic death pathways through nonhomotypic death-fold interactions". Mol. Cell. 15 (6 ... Cell Death Differ. 12 (6): 682-6. doi:10.1038/sj.cdd.4401631. PMID 15861191. Rual JF, Venkatesan K, Hao T, Hirozane-Kishikawa T ...
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Shaul Y (2000). "c-Abl: activation and nuclear targets". Cell Death Differ. 7 (1): 10-6. doi:10.1038/sj.cdd.4400626. PMID ... cell division, cell adhesion, and stress response such as DNA repair. Activity of ABL1 protein is negatively regulated by its ... a site for phosphorylation in leukaemia cells". Genes to Cells. 9 (9): 781-90. doi:10.1111/j.1365-2443.2004.00772.x. PMID ... Cell. 6 (6): 1413-23. doi:10.1016/S1097-2765(00)00138-6. PMID 11163214. Yoshida K, Komatsu K, Wang HG, Kufe D (May 2002). "c- ...
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... synuclein-mediated apoptotic cell death". Cell Death & Differentiation. 22 (12): 2107-2122. doi:10.1038/cdd.2015.79. ISSN 1476- ...
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Cell Death & Disease. 6 (8): e1856. doi:10.1038/cddis.2015.211. PMC 4558504. PMID 26270350. "The Immune System and Primary ... These cells include T lymphocytes (T cells), that primarily mediate the immune system, B lymphocytes (B cells) and Natural ... Hematopoietic stem cells give rise to blood cells. Differentiation and proliferation of hematopoietic stem cells require a lot ... Stem cells are taken from an affected child's blood or bone marrow. Then in laboratory conditions the stem cells are ...
Cell Death Discovery. 3 (1): 17071. doi:10.1038/cddiscovery.2017.71. ISSN 2058-7716. PMC 5683310. PMID 29152378. Gommans, ... induction of pluripotent stem cells from somatic cells by Oct4, Sox2, Myc and Klf4". Cell Research. 17 (7): 578-580. doi: ... The change in cell state demonstrates that ATFs can replace traditional transcription factors in cell reprogramming. Angelman ... Directing cell differentiation and reprogramming cell fate have traditionally been achieved via a mixture of transcription ...
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Ceramide mediates many cell-stress responses, including the regulation of programmed cell death (apoptosis) and cell aging ( ... whereby the cells differentiated into white blood cells called macrophages. Treatment of the same cells by exogenous Sph caused ... This results in a substantial decrease in insulin responsiveness (i.e. to glucose) and in the death of insulin-producing cells ... Obeid, L. M., Linardic, C. M., Karolak, L. A. & Hannun, Y. A. (1993) Programmed cell death induced by ceramide. Science. 259, ...
... polymerase activation attenuates beta-lapachone-induced necrotic cell death in human osteosarcoma cells". Toxicol. Appl. ... Cell Death Differ. 9 (11): 1172-84. doi:10.1038/sj.cdd.4401094. PMID 12404116. S2CID 38809690. Strausberg RL, Feingold EA, ... Cell. Biol. 24 (12): 5314-23. doi:10.1128/MCB.24.12.5314-5323.2004. PMC 419898. PMID 15169895. v t e (Articles with short ... V. The coding sequences of 40 new genes (KIAA0161-KIAA0200) deduced by analysis of cDNA clones from human cell line KG-1". DNA ...
... virus replication and protection from cell death require ER stress (PERK) pathway activation". Cell Death & Disease. 7 (e2127 ... PERK dimerizes with BiP in resting cells and oligomerizes in ER-stressed cells. Although this is traditionally the accepted ... This also produces translational attenuation of the protein machinery involved in running the cell cycle, producing cell cycle ... Cell. 75 (4): 717-28. doi:10.1016/0092-8674(93)90492-9. PMID 7902213. Brewer JW, Diehl JA (November 2000). "PERK mediates cell- ...
"Phospho-ΔNp63α/miR-885-3p axis in tumor cell life and cell death upon cisplatin exposure". Cell Cycle. 10 (22): 3938-47. doi: ... Cell Death Differ. 18 (6): 974-84. doi:10.1038/cdd.2010.164. PMC 3131937. PMID 21233845. Huang X, Xu S, Gao J, Liu F, Yue J, ... Chen T, Wu B (October 2011). "miRNA expression profiling identifies DSPP regulators in cultured dental pulp cells". Int. J. Mol ... "MicroRNA-885-3p inhibits the growth of HT-29 colon cancer cell xenografts by disrupting angiogenesis via targeting BMPR1A and ...
"The role of phosphatidylserine in recognition of apoptotic cells by phagocytes". Cell Death Differ. 5 (7): 551-62. doi:10.1038/ ... During programmed cell death a protein called a scramblase equilibrates this distribution, displaying phosphatidylserine on the ... These membranes are flat sheets that form a continuous barrier around all cells. The cell membranes of almost all organisms and ... This procedure is now used extensively, for example by fusing B-cells with myeloma cells. The resulting "hybridoma" from this ...
Cell Death Differ. 17 (1): 68-77. doi:10.1038/cdd.2009.84. PMC 2818775. PMID 19557014. Rotin D, Kumar S (Jun 2009). " ... "Patch-clamp studies on epithelial sodium channels in salivary duct cells". Cell Biochem. Biophys. 36 (2-3): 105-13. doi:10.1385 ... "Androgens differentially regulate the expression of NEDD4L transcripts in LNCaP human prostate cancer cells". Mol. Cell. ... Cell. 36 (3): 457-68. doi:10.1016/j.molcel.2009.09.043. PMC 2796330. PMID 19917253. Zhang Y, Ding Y, Chen YG, Tao Q (Aug 1, ...
June 2002). "ASK1 is essential for endoplasmic reticulum stress-induced neuronal cell death triggered by expanded polyglutamine ... Cell Death & Disease. 10 (11): 800. doi:10.1038/s41419-019-2039-6. PMC 6805898. PMID 31641108. Montibeller L, de Belleroche J ( ... Huang ZM, Tan T, Yoshida H, Mori K, Ma Y, Yen TS (September 2005). "Activation of hepatitis B virus S promoter by a cell type- ... July 2012). "Identification of Toyocamycin, an agent cytotoxic for multiple myeloma cells, as a potent inhibitor of ER stress- ...
Cell Death Differ. 18 (11): 1702-10. doi:10.1038/cdd.2011.28. PMC 3190106. PMID 21455217. Kulkarni S, Savan R, Qi Y, Gao X, ... Haflidadóttir BS, Bergsteinsdóttir K, Praetorius C, Steingrímsson E (2010). "miR-148 regulates Mitf in melanoma cells". PLOS ... "Combined mRNA and microRNA profiling reveals that miR-148a and miR-20b control human mesenchymal stem cell phenotype via EPAS1 ... "miR-148a is an androgen-responsive microRNA that promotes LNCaP prostate cell growth by repressing its target CAND1 expression ...
... an essential role of mitochondrial complex I in the interferon-beta and retinoic acid-induced cancer cell death". Cell Death ... Huang G, Chen Y, Lu H, Cao X (2007). "Coupling mitochondrial respiratory chain to cell death: ... Cytogenet Cell Genet. 82 (1-2): 115-9. doi:10.1159/000015082. PMID 9763677. S2CID 46818955. Mao M, Fu G, Wu JS, Zhang QH, Zhou ... hematopoietic stem/progenitor cells by expressed sequence tags and efficient full-length cDNA cloning". Proc Natl Acad Sci U S ...
Cell Death Dis. 5 (3): e1153. doi:10.1038/cddis.2014.118. PMC 3973230. PMID 24675471. v t e (Articles with short description, ... Cell. 25 (6): 917-31. doi:10.1016/j.molcel.2007.02.017. PMID 17386267. Rizvi F, Shukla S, Kakkar P (2014). "Essential role of ...
Celsi F, Pizzo P, Brini M, Leo S, Fotino C, Pinton P, Rizzuto R (May 2009). "Mitochondria, calcium and cell death: a deadly ... Filadi R, Pendin D, Pizzo P (February 2018). "Mitofusin 2: from functions to disease". Cell Death & Disease. 9 (3): 330. doi: ... Among different cell types, neurons are particularly sensitive to MFN2 defects: to work properly, these cells need functional ... Vyas S, Zaganjor E, Haigis MC (July 2016). "Mitochondria and Cancer". Cell. 166 (3): 555-566. doi:10.1016/j.cell.2016.07.002. ...
"Tumor treating fields increases membrane permeability in glioblastoma cells". Cell Death Discovery. 4: 113. doi:10.1038/s41420- ... This division is uncontrolled in cancer cells. The TTFields electric charge prevents the cancer cell from dividing, thereby ... where the majority of normal cells are non-proliferating. During cell division, a structure called a spindle self-assembles ... The spindle attaches to the 23 chromosomes and pulls the DNA into two new cells. The proteins in the spindle have a positive ...
Cell Death Dis. 5 (5): e1226. doi:10.1038/cddis.2014.168. PMC 4047874. PMID 24832598. Lu H, Shamanna RA, Keijzers G, Anand R, ... "Werner protein protects nonproliferating cells from oxidative DNA damage". Mol. Cell. Biol. 25 (23): 10492-506. doi:10.1128/MCB ... Cell. 46 (1): 43-53. doi:10.1016/j.molcel.2012.02.020. PMC 3328772. PMID 22500736. Séguéla-Arnaud M, Crismani W, Larchevêque C ... So S, Adachi N, Lieber MR, Koyama H (2004). "Genetic interactions between BLM and DNA ligase IV in human cells". J. Biol. Chem ...
Cell Death & Disease. 1 (10): e82. doi:10.1038/cddis.2010.59. PMC 3035901. PMID 21368855. Rabouille C, Linstedt AD (2016). " ... Yoshimura S, Yoshioka K, Barr FA, Lowe M, Nakayama K, Ohkuma S, Nakamura N (June 2005). "Convergence of cell cycle regulation ... The Journal of Cell Biology. 155 (4): 557-70. doi:10.1083/jcb.200107045. PMC 2198855. PMID 11706049. Lane JD, Lucocq J, Pryde J ... The Journal of Cell Biology. 156 (3): 495-509. doi:10.1083/jcb.200110007. PMC 2173349. PMID 11815631. Cheng JP, Betin VM, Weir ...
"FKHRL1-mediated expression of Noxa and Bim induces apoptosis via the mitochondria in neuroblastoma cells". Cell Death Differ. ... Kim JY, Ahn HJ, Ryu JH, Suk K, Park JH (2004). "BH3-only protein Noxa is a mediator of hypoxic cell death induced by hypoxia- ... "The molecular mechanism of Noxa-induced mitochondrial dysfunction in p53-mediated cell death". J. Biol. Chem. 278 (48): 48292-9 ... "Proteasome inhibitor PS-341 induces apoptosis in cisplatin-resistant squamous cell carcinoma cells by induction of Noxa". J. ...
... because these cells have severe chromosomal abnormalities, they eventually stop dividing or undergo cell death. A novel ... In Drosophila cells, Aurora B depletion disrupts chromosome structure and compaction. In these cells, the condensin complex ... Inhibition of Aurora B kinase by BI811283 in cancer cells leads to the formation of cells with severely abnormal numbers of ... Nigg EA (2001). "Mitotic kinases as regulators of cell division and its checkpoints". Nat. Rev. Mol. Cell Biol. 2 (1): 21-32. ...
Cell Death & Disease. 4 (10): e889. doi:10.1038/cddis.2013.399. PMC 3920944. PMID 24176847. Pathania, Anup Singh; Guru, Santosh ... "Regulation of Breast Cancer Stem Cells by Mesenchymal Stem Cells in the Metastatic Niche". Principles of Stem Cell Biology and ... He is known for his studies on investigating the regulatory mechanisms of Cancer Stem Cells during tumor metastasis. His ... doi:10.1007/978-981-10-4298-0_1. ISBN 978-981-10-4297-3. Korkaya, Hasan; Malik, Fayaz (2013). "Breast Cancer Stem Cells: ...
For example, it has been reported that immunoglobulin therapy can block Fas-mediated cell death. Perhaps a more popular theory ... Indeed, it is becoming more clear that immunoglobulin can bind to a number of membrane receptors on T cells, B cells, and ... Cell Death & Disease. 11 (1): 50. doi:10.1038/s41419-020-2249-y. PMC 6978335. PMID 31974400. Trinath J, Hegde P, Sharma M, ... a cancer of a type of white blood cell) or myeloma (a cancer of another type of white blood cell) and who have frequent ...
Cell Death & Differentiation. 28 (1): 35-51. doi:10.1038/s41418-020-0565-5. ISSN 1476-5403. PMC 7852529. PMID 32494027. Vazquez ... One of these changes are to the uterine natural killer cells (uNK). NK cells, part of the innate immune system, are cytotoxic ... In the first trimester of pregnancy, uNK cells are among the most abundant leukocytes present, but the number of uNK cells ... An increase in prevalence of proinflammatory cells and natural killer cells can be found in women experiencing a miscarriage. ...
Macon had a structured duraluminum hull with three interior keels.[5] The airship was kept aloft by 12 helium-filled gas cells ... The crew to the Macon were floating around in rubber floats and almost froze to death. I had to read about the Akron disaster, ... Pieces of structure punctured the rear gas cells and caused gas leakage. The commander, acting rapidly and on fragmentary ...
... to be held in a private cell in the maximum-security Vroom Building.[8] He remained incarcerated there until his death in 2009 ... "Walk of Death." Unruh was found to be criminally insane and died in 2009 after a lengthy illness at the age of 88 following ... on the 60th anniversary of the mass murder and just one month before Unruh's death).[21] ...
... and therefore cause the death of the cell at an early stage. However, some mutations are seen with one notable example being ... "Cell. 126 (1): 107-120. doi:10.1016/j.cell.2006.05.036. PMID 16839880. S2CID 15006256.. ... All cells contain the enzyme hexokinase, which catalyzes the conversion of glucose that has entered the cell into glucose-6- ... Hexokinase is inhibited by high levels of G6P in the cell. Thus the rate of entry of glucose into cells partially depends on ...
"Sheriff of Wall Street' pursues case linked to death of Russian lawyer". Retrieved March 22, 2017.. ... and within a year he was found dead in his prison cell-a suspicious circumstance.[46] Bharara and his office stated that some ... "Death to My Hometown" at an October 2012 concert in Hartford, Connecticut.[147] ...
"UNEP and Daimler Call for Infrastructure for Electric and Fuel-cell Vehicles". 4 July 2008. Archived from the ... "refused to lead and instead sought to bribe and bully developing nations to sign up to the equivalent of a death warrant."[128] ... "effectively signed a death warrant for many of the world's poorest children. Up to 250,000 children from poor communities could ...
These are found in all cell membranes and the membranes of most cell organelles.[2] Phosphatidylcholines are structurally ... In knockout mice, their dysfunction results easily in death with cyanosis and paralysis.[17] ... Choline is stored in the cell membranes and organelles as phospholipids, and inside cells as phosphatidylcholines and ... Acetylcholine is even present in the placenta and may help control cell proliferation and differentiation (increases in cell ...
Granger supported embryonic stem-cell research and voted against banning "chemically induced abortions."[30][31][32][33] She ... filling a vacancy left by the death of Jennifer Dunn.[5] In a statement to the press following her endorsement, she said that ... "House votes to expand stem cell research". Houston Chronicle. Retrieved April 14, 2019 ...
... the death of neural stem cells or neurons, or a combination of these factors.[58] Research in animal models such as rodents has ... "Cell Stem Cell. 18 (5): 591-6. doi:10.1016/j.stem.2016.03.012. PMC 4860115. PMID 27038591.. ... "Cell Stem Cell. 19 (1): 120-6. doi:10.1016/j.stem.2016.04.017. PMID 27179424.. ... For example, the Notch pathway genes regulate the balance between stem cell proliferation and neurogenesis in the stem cell ...
Death[edit]. Banzer died of lung cancer at a medical clinic in Santa Cruz de la Sierra on 5 May 2002, aged 75, five days before ... "Hidden cells reveal Bolivia's dark past". BBC News. 5 March 2009. Retrieved 4 May 2010.. ... Argentina where five years later he was kidnapped and assassinated by right-wing death squads associated with the Videla ...
a b c „Exposure of {alpha}2,6-sialylated lactosaminic chains marks apoptotic and necrotic death in different cell types"; ... Tateno H, Uchiyama N, Kuno A, Togayachi A, Sato T, Narimatsu H, Hirabayashi J."A novel strategy for mammalian cell surface ... "O-acetyl sialic acid binding lectin as a probe for detection of subtle change on cell surface induced during acute ...
Following the death of Yosef Levy during the Battle of Jaffa, he became district commander. Was later Herut founder, serving as ... He was sent to Europe to create Irgun cells in Europe, and was in charge of the Irgun's 1946 bombing of the British Embassy in ... Captured in an arms raid in Sarafand military camp and sentenced to death together with Irgun member Yosef Simchon. After the ... At the time of his death, he was the last surviving participant in the Sergeants affair.[5] ...
... programmed cell death) kareng makamateng cancer cells. Agpang kareng talasalugsug a lupung ing citral iya ing bage a makamate ... Ikit da iti ing agagawa ning citral kareng alang sirang cells ampng makamateng cancer cells a peparagul da keng petri dish. Ing ... Agiang ing citral pete no reng cancer cells, pepaburen no retang masaleseng cells a ela ninanu. Iting ikit da mengapamulala la ... Dudai N, Weinstein Y, Krup M, Rabinski T, Ofir R (May 2005). "Citral is a new inducer of caspase-3 in tumor cell lines". Planta ...
1,723 civilian deaths[4] ≈1,050 SLA militiamen deaths[5]. 91,105 total Arab deaths[6]. ... The cells were equipped with bombs and firearms, which they used to kill Jewish settlers in the area, as well as engaging in a ... "Lebanon Sees More Than 1,000 War Deaths". AP via Archived from the original on 6 February 2012. Retrieved 25 November ... The war ended following Gamal Abdel Nasser's death in 1970. Once Sadat took over, he tried to forge positive relations with the ...
Upon the death of Sir George Downing, 3rd Baronet in 1749, the wealth left by his grandfather, Sir George Downing, 1st Baronet ...
Cell death. *Necrosis *Avascular necrosis. *Coagulative necrosis. *Liquefactive necrosis. *Gangrenous necrosis. *Caseous ... The American Way of Death, by Jessica Mitford. References[edit]. .mw-parser-output .reflist{font-size:90%;margin-bottom:0.5em; ...
... and located by tracking his cell phone.[53] On October 26, Sayoc was arrested in the parking lot of an AutoZone store in ... reported that he was the subject of death threats from Sayoc made on Facebook in April 2018. According to Somin, after he ...
Programmed cell death. *Avian flight. *Biological complexity. *Cooperation. *Color vision *in primates ...
Most deaths from anhydrous ammonia are caused by severe damage to the throat and lungs from a direct blast to the face. An ... The ammonia extracts the fluid and destroys eye cells and tissue in minutes. ...
... death occurred 19 days to 3 weeks after ingestion.[16] The presenting symptoms of button cell ingestion may be misdiagnosed and ... Button cells are single cells, usually disposable primary cells. Common anode materials are zinc or lithium. Common cathode ... Wider variants are usually called coin cells. Devices using button cells are usually designed around a cell giving a long ... A button cell, watch battery, or coin battery is a small single-cell battery shaped as a squat cylinder typically 5 to 25 mm ( ...
Cell》 89: 263-73. PMID 9108481. 2009년 3월 31일에 확인함.. CS1 관리 - 여러 이름 (링크) ... Concerted Action on SeroConversion to AIDS and Death in Europe". 》Lancet》 355 (9210): 1131-7. 2000년 4월. doi:10.1016/S0140-6736( ... Clapham PR, McKnight A. (2001). "HIV-1 receptors and cell tropism". 》Br Med Bull.》 58 (4): 43-59. doi:10.1093/bmb/58.1.43. PMID ... Garcia JV, Miller AD (1991년 4월). "Serine phosphorylation-independent downregulation of cell-surface CD4 by nef". 》Nature》 350 ( ...
"Ammonia for fuel cells". Retrieved 5 September 2019.. *^ "Survey reveals aluminum remains fastest growing automotive ... Carl Benz remained a member of the board of directors of Daimler-Benz until his death in 1929, and at times, his two sons also ... Traffic collisions are the largest cause of injury-related deaths worldwide.[12] Mary Ward became one of the first documented ... Traffic collisions are the largest cause of injury-related deaths worldwide.[12] ...
Cell phone reception can be sporadic and, when available, signal strength and clarity is poor. Although the surrounding ... A moratorium on three-axles trucks was imposed in 2009 following the deaths of two people when a tractor trailer lost control ...
Untreated, diabetes leads to coma and then death. Diabetic emergencies[edit]. Too little insulin over time can cause tissue ... β-cell dysfunction and insulin resistance.[6] Factors which contribute to insulin resistance include obesity and endocrine ... which is caused by damage to the myelin sheath of the peripheral nerves due to glucose toxicity and cell starvation, which are ... At this point the size difference in human and animal red blood cells can create inaccurate readings.[24] ...
... the alcohol in hand sanitizers may not have the 10-15 seconds exposure time required to denature proteins and lyse cells.[4] In ... permanent damage to the nervous system or death".[87] Products suspected of manufacture by Eskbiochem SA with excessive ... "Serious Adverse Health Events, Including Death, Associated with Ingesting Alcohol-Based Hand Sanitizers Containing Methanol - ...
For uses in the natural sciences, see Cell culture and Tissue culture. For other uses, see Culture (disambiguation). ... in order to deny the animal insignificance and death that Homo sapiens became aware of when they acquired a larger brain.[12][ ...
Triple H in a Hell in a Cell match at Wrestlemania XXVIII)[২৭] ... "The Demon of Death Valley". *"The Lord of Darkness". *"The Best Pure Striker in Sports-Entertainment History" ...
... killer T cell, or cytotoxic T-lymphocyte (CTL)) are a sub-group of T cells that induce the death of cells that are infected ... Gamma delta T cellsEdit. Main article: Gamma delta T cell. Gamma delta T cells (γδ T cells) possess an alternative T cell ... When B cells and T cells are activated some become memory B cells and some memory T cells. Throughout the lifetime of an animal ... The cells that carry out the adaptive immune response are white blood cells known as lymphocytes. B cells and T cells, two ...
The process by which a ka became an akh was not automatic upon death; it involved a 70-day journey through the duat, or ... Cell Biology, vol 51 (3), pp. 200-204. ... Park, Chang-Won (2010). Cultural Blending in Korean Death Rites ... Ancient Filipinos believed that upon death, the soul of a person travels (usually by boat) to a spirit world.[30][31][32] There ... Paganito can be used to appease or banish them.[30][33][35] Ancestor spirits also figured prominently during illness or death, ...
74,0 74,1 «Small-cell carcinoma of the prostate»։ Journal of the Royal Society of Medicine 90 (6): 340-1։ June 1997։ PMC ... reported no clear evidence that screening for prostate cancer decreases the risk of death from prostate cancer» ... 75,0 75,1 «[Clinicopathological characterization of prostatic small cell carcinoma: a case report and review of the literature ... Expression of prostate-specific membrane antigen (PSMA), increases cell folate uptake and proliferation and suggests a novel ...
"No life without death, no death without life': laureate's tribute to Keats". Write Out Loud. 22 February 2021. Retrieved 29 ... For Summer has o'er-brimm'd their clammy cells. First stanza of "To Autumn",[86]. September 1819. ... Hunt blamed his death on the Quarterly Review's scathing attack of "Endymion". As Byron quipped in his narrative poem Don Juan ... Kottoor, Gopikrishnan (1994). The Mask of Death: The Final Days of John Keats, (A Radio Play). Writers WorkShop Kolkata, 1994 ...
Apoptosis or Type I cell-death, and autophagy or Type II cell-death are both forms of programmed cell death, while necrosis is ... "non-apoptotic programmed cell-death" (or "caspase-independent programmed cell-death"), these alternative routes to death are as ... Ischemic cell death, or oncosis, is a form of accidental, or passive cell death that is often considered a lethal injury. The ... Activation-induced cell death (AICD) is a programmed cell death caused by the interaction of Fas receptor (Fas, CD95)and Fas ...
Organisms that carry disease can travel through the blood stream into the liver and form an abscess, a collection of infected tissue and pus.
The researchers found higher death rates among people with SCD than previous estimates that used other methods. Read the key ... by matching up data from studies that monitor all people with SCD in a population with state death records. ... This study estimated death rates among people with sickle cell disease (SCD) ... Sickle Cell Disease is a group of genetic (inherited) red blood cell disorders. Healthy red blood cells are round and they move ...
This form of cell death is dependent on iron and oxidative stress. It has been identified as a key player in kidney diseases. ... Protected from a form of cell death, women are more resilient to kidney disease Researchers find a root cause for a difference ... Souma and colleagues conducted studies in mice focusing on a form of cell death called ferroptosis, which was only recently ... In females, NRF2 is highly active, keeping cell death in check. In males, however, the sex hormone testosterone reduces the ...
Cell Death & Differentiation (Cell Death Differ) ISSN 1476-5403 (online) ISSN 1350-9047 (print) ... And when one thinks of cell death, one thinks of apoptosis. The concept of cell death, and the concept that it was an important ... Molecular mechanisms of cell death in neurological diseases. Cell Death Differ. 2021;28:2029-44. ... Programmed cell death 50 (and beyond). Cell Death Differ. 2016;23:10-7. ...
... induces acute cell death in CLL cells. Our mechanistic studies reveal that increased AKT activity upon inhibition of SHIP1 ... resulting in cell death in CLL with immunogenic features. Our results demonstrate that CLL cells critically depend on ... allowing sustained proliferation and survival but avoid ROS-induced cell death and suggest transient SHIP1-inhibition as an ... signaling pathway may be leveraged to trigger CLL cell death. Though counterintuitive, our data show that genetic ...
Programmed cell death and apoptosis.. in: Tomei L.D. Cope F.O. Apoptosis: The Molecular Basis of Cell Death. Cold Spring Harbor ... A quantitative lifespan study of changes in cell number, cell division and cell death in various regions of the mouse forebrain ... Cell death and control of cell survival in the oligodendrocyte lineage. *. B.A. Barres. B.A. Barres ... Dead cells are observed in many developing animal tissues, but the causes of these normal cell deaths are mostly unknown. We ...
NYC Correction captain probed for response to jail suicide attempt linked to previous cell death resulting in $1.5 million ... At the Kross Center, Gonzalez was placed in an intake cell packed with 25 others at 2:40 a.m. where he continued to beg for ... The probers also found that officers failed to perform CPR and first aid as Gonzalez died on the floor of the intake cell. Some ... Henry and eight other officers, as well as two city EMS workers, saw Feliciano hanging in the cell - but did not act for nearly ...
Find methods information, sources, references or conduct a literature review on PROGRAMMED CELL DEATH ... The programmed cell death ligand 1 (PD-L1) and its receptor programmed cell death 1 (PD-1) deliver inhibitory signals to ... Cancer cells can escape T cell-mediated cellular cytotoxicity by exploiting the inhibitory programmed cell-death protein 1 (PD- ... Background Clinical studies have shown that the efficacy of programmed cell death receptor-1/programmed cell death ligand-1 (PD ...
View the Xuejun Jiang Lab page for Ferroptotic Lipid Signaling: Stronger than Cell Death.
... Acta Otolaryngol. 2012 May; ...
... is due to a series of highly regulated processes that lead to cell death, thus is a form of programmed cell death (PCD; van ... Relationship between petal abscission and programmed cell death in Prunus yedoensis and Delphinium belladonna *Tetsuya Yamada1 ... Wilting at the end of petal life is due to programmed cell death (PCD). It is not known whether the abscission of turgid petals ... Yamada, T., Ichimura, K. & van Doorn, W.G. Relationship between petal abscission and programmed cell death in Prunus yedoensis ...
... Plant Physiol. 2018 Oct;178(2):907-922. doi: 10.1104/ ... Surprisingly, a strong hypersensitive response (HR) cell death was observed when soybean MAPK KINASE KINASE1 (GmMEKK1), a ... The involvement of GmMPK4 kinase activity in cell death and in flg22- or SA-triggered defense responses in soybean requires ...
Few of us would ever think that the very thing we love so much could one day lead to our death. In fact, more people are now ... Its not possible to know from cell phone records if the driver was typing, reaching for the phone, or reading a text at the ... Such deaths have been reported in China and Nepal. Representatives from each of the phone companies involved reported ... Federal investigators said that the pickup truck drivers cell phone records revealed that hed sent five text messages at the ...
Woman donates stem cells 13 years after holding drives to find bone marrow match for her dad, a late Morristown firefighter ...
Apoptotic cells are identified by their altered morphology, caspase activation, and the presence of damaged DNA. ... Apoptosis is a type of programmed cell death that occurs normally throughout the lifespan and can also occur in response to ... Types of Cell Death. Cell death mechanisms include:. *Apoptosis - programmed cell death that occurs during growth and ... Different assays can be used to determine the mechanism of cell death or rule out a mechanism of cell death within a cellular ...
... working at Nokias assembly plant here was crushed to death after her head and neck got jammed in a machine last night. MORE ... CHENNAI, India-A 22-year-old woman, working at Nokias assembly plant here was crushed to death after her head and neck got ...
A woman is born with just so many egg cells, called oocytes. When she begins ovulating, she has about 400. Even though that may ... Cell death in eggs traced to smoking. Researchers discover new type of cancer ... A woman is born with just so many egg cells, called oocytes. When she begins ovulating, she has about 400. Even though that may ...
Cracking the Cell Death Code. Carla V. Rothlin and Sourav Ghosh. Phagocyte Responses to Cell Death in Flies. Andrew J. Davidson ... Regulation of Cell Death and Immunity by XIAP. Philipp J. Jost and Domagoj Vucic. Cell Death and Neurodegeneration. Benjamin J ... Cell Death in Plant Immunity. Eugenia Pitsili, Ujjal J. Phukan, and Nuria S. Coll. Dysregulation of Cell Death in Human Chronic ... Cell Survival and Cell Death, Second Edition. Book Series: A Cold Spring Harbor Perspectives in Biology Collection. Subject ...
Programmed cell death, or apoptosis, is the process whereby certain cells are induced to activate their own death or cell ... Apoptosis, unlike necrosis, is mediated by the active participation of dying cells. In another words, the dying cells ... suggesting the occurence of an evolutionarily preserved common programmed cell death mechanism among multicellular organisms. ... Apoptosis has been described in a wide variety of cell and tissue types from nematodes to mammals. ...
Cancer cell death via necroptosis can actually promote tumor growth, as this process can result in suppression of the bodys ... New Way of Cell Death Identified in a Tiny Worm Offers Clues on Neurodegeneration Apoptosis, one form of programmed cell ... The study results revolve around carefully regulated cell dell death mechanisms that, by killing defective cells or those ... thrives in the presence of neighboring tumor cells undergoing a particular form of "orchestrated cell death." This is according ...
... C2C12 cells exposed to Bothrops venoms. ... Photobiomodulation reduces cell death and cytokine production in C2C12 cells exposed to Bothrops venoms. - GreenMedInfo Summary ... Photobiomodulation reduces cell death and cytokine production in C2C12 cells exposed to Bothrops venoms. ... Our results showed that the application of PBM increases cell viability and decreases cell death byapoptosis and necrosis. ...
Mitochondrial calcium uptake underlies ROS generation during aminoglycoside-induced hair cell death. ... Mitochondrial calcium uptake underlies ROS generation during aminoglycoside-induced hair cell death. ... suggesting that mitochondrial calcium drives ROS generation during aminoglycoside-induced hair cell death. Furthermore, ... The increased oxidation observed in both mitochondria and cytoplasm of dying hair cells was highly correlated with ...
Cell-Free Hemoglobin-Based Blood Substitutes and Risk of Myocardial Infarction and Death. JAMA. 2008;299(19):2304-2312. ... Cell-Free Hemoglobin-Based Blood Substitutes and Risk of Myocardial Infarction and Death. ... Hemoglobin-Based Blood Substitutes and Risk of Myocardial Infarction and Death-Reply. JAMA 2008;300:1298-9. ...
Here, we review the latest research progress on the mechanisms of nitrosative stress-mediated cell death, primarily involving ... Here, we review the latest research progress on the mechanisms of nitrosative stress-mediated cell death, primarily involving ... Accordingly, an in-depth study of the relationship between nitrosative stress and cell death has important practical ... Accordingly, an in-depth study of the relationship between nitrosative stress and cell death has important practical ...
With outages bringing down cell service - despite promises from wireless companie... ... "Having a functional cell phone isnt about checking the latest Facebook status, its literally about life or death. Cell phones ... Life or death: Cell service outage could mean fire alerts dont go through. ... Hundreds of cell sites were down. In Marin County, 35% of cell sites were down. In Sonoma County, it was 22%; Napa County: 15 ...
But for the infrastructure workers who maintain cell towers, the industry... ... The Occupational Safety and Health Administration is calling the 2013 rate of cell tower worker deaths "alarming." The group is ... and cell towers between 2003 and 2011-fifty of them at cell towers. The report found that many of the incidents occurred ... Working on cell towers is more dangerous than working in construction.. Photo by Gary Lerude/Flickr.. ...
On the morning of Jeffrey Epsteins death there was shouting and shrieking from his jail cell, a source familiar with the ... Shrieking heard from Jeffrey Epsteins jail cell the morning he died. August 13, 2019 / 7:25 AM. / CBS News ... She claims his cell was regularly left unlocked and she saw him move freely through the dormitory area - sometimes completely ...
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  • Apoptosis or Type I cell-death, and autophagy or Type II cell-death are both forms of programmed cell death, while necrosis is a non-physiological process that occurs as a result of infection or injury. (
  • Apoptosis is the process of programmed cell death (PCD) that may occur in multicellular organisms. (
  • There is some evidence that certain symptoms of "apoptosis" such as endonuclease activation can be spuriously induced without engaging a genetic cascade, however, presumably true apoptosis and programmed cell death must be genetically mediated. (
  • Called "non-apoptotic programmed cell-death" (or "caspase-independent programmed cell-death"), these alternative routes to death are as efficient as apoptosis and can function as either backup mechanisms or the main type of PCD. (
  • Immunogenic cell death or immunogenic apoptosis is a form of cell death caused by some cytostatic agents such as anthracyclines, oxaliplatin and bortezomib, or radiotherapy and photodynamic therapy (PDT). (
  • And when one thinks of cell death, one thinks of apoptosis. (
  • The concept of cell death, and the concept that it was an important biological phenomenon, has a long history, but the image and biology of apoptosis now dominate all previous concepts. (
  • Whether one considers death to be programmed, to be an alternate form of death-necroptosis, ferroptosis, and several other variants, apoptosis is the standard by which they are evaluated. (
  • Apoptosis - programmed cell death that occurs during growth and development and can also occur in response to harmful environmental stimuli. (
  • Apoptosis is a highly regulated form of programmed cell death that occurs in multicellular organisms during development, throughout the lifespan, and in response to cellular stress. (
  • Apoptosis is a form of programmed cell death mediated by caspases and a host of other proteins. (
  • Apoptosis, one form of programmed cell suicide, is well described-scientists know which molecules induce it and the processes that take place in the cell. (
  • 280 nm UV LED irradiation inhibits proliferation and induces apoptosis and necrosis in cultured HL-60 human leukemia cells. (
  • The rates of cell proliferation and apoptosis, the cell cycle profiles and the mRNA expression of B‑cell lymphoma 2 (Bcl‑2) were detected using cell counting kit‑8, multicaspase assays, propidium iodide staining and reverse transcription‑quantitative polymerase chain reaction, respectively. (
  • UV LED at 8‑30 J/m2 induced dose‑dependent apoptosis and G0/G1 cell cycle arrest, and inhibited theexpression of Bcl‑2 mRNA, while UV LED at 60 J/m2 induced necrosis. (
  • In conclusion, 280 nm UV LED irradiation inhibits proliferation and induces apoptosis and necrosis in cultured HL‑60 cells. (
  • In addition, the cell cycle arrest at the G0/G1 phase and the downregulation of Bcl‑2 mRNA expression were shown to be involved in UV LED-induced apoptosis. (
  • Written and edited by experts in the field, this collection from Cold Spring Harbor Perspectives in Biology provides a comprehensive update on the cell signaling that underlies the main cell death programs (apoptosis, pyroptosis, and necroptosis) and how this knowledge is driving the development of therapeutic drugs to treat some human diseases. (
  • Programmed cell death, or apoptosis, is the process whereby certain cells are induced to activate their own death or cell suicide. (
  • Apoptosis has been described in a wide variety of cell and tissue types from nematodes to mammals. (
  • Apoptosis, unlike necrosis, is mediated by the active participation of dying cells. (
  • It has been found that apoptosis related genes have high homology in terms of DNA sequences, suggesting the occurence of an evolutionarily preserved common programmed cell death mechanism among multicellular organisms. (
  • Here, we review the latest research progress on the mechanisms of nitrosative stress-mediated cell death, primarily involving several regulated cell death processes, including apoptosis, autophagy, ferroptosis, pyroptosis, NETosis, and parthanatos, highlighting nitrosative stress as a unique mechanism in cardiovascular diseases. (
  • Mechanisms of Apoptosis in Crustacea: What Conditions Induce Versus Suppress Cell Death? (
  • Mechanisms that serve to depress apoptosis include the inhibition of caspase activity by high potassium in energetically healthy cells, alterations in nucleotide abundance during energy-limited states like diapause and anoxia, resistance to opening of the calcium-induced MPTP, and viral accommodation during persistent viral infection. (
  • Characterization of the players, pathways, and their significance in the core machinery of crustacean apoptosis is revealing new insights for the field of cell death. (
  • To answer these questions, the scientists engineered a mouse model where they could turn on apoptosis and catch phagocytes in the act of sampling dying cells. (
  • One million cells in our bodies die every second-they commit suicide by a mechanism known as apoptosis. (
  • In Means To An End, Douglas Green provides a clear and comprehensive view of apoptosis and other cell death mechanisms. (
  • Green outlines the roles of apoptosis and death mechanisms such as necrosis in embryogenesis, neuronal selection, and the development of self-tolerance in the immune system. (
  • In addition, he explains how cell death defends the body against cancer and traces the evolutionary origins of the apoptosis machinery back over a billion years. (
  • As a leader in the field of cell death since the late 1980s, Dr. Green s contribution has been pivotal, particularly in defining the process of activation-induced apoptosis in T cells. (
  • This is an important publication for researchers on the fringes of the cell death field, or anyone who wants a more global perspective on apoptosis. (
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a transmembrane cytokine that is a promising anticancer agent as it selectively induces apoptosis in various types of tumor cells. (
  • TRAIL has the ability to selectively induce apoptosis in a wide range of tumor cells but does not induce toxicity in most normal cells ( 2 ). (
  • Previous studies indicate that genistein exerts anticancer properties that include the inhibition of tumor cell proliferation, enhanced tumor cell differentiation triggering cell cycle arrest, and the induction of apoptosis in some cell types ( 9 - 11 ). (
  • For other entries pertaining to cell death mechanisms see also the Apoptosis and Cell Death Dictionary section of this encyclopedia. (
  • The researchers injected miR-29 into young mice neurons and found that the neurons became resistant to apoptosis and to multiple programmed cell death signals. (
  • Researchers at the University of North Carolina at Chapel Hill have discovered a molecule that can make brain cells resistant to programmed cell death or apoptosis. (
  • There is the real possibility that this molecule could be used to block the cascade of events known as apoptosis that eventually causes brain cells to break down and die," said senior study author Mohanish Deshmukh , PhD, associate professor of cell and developmental biology . (
  • Most of the deaths are apoptotic and are identified by techniques used to recognize apoptosis, but techniques identifying lysosomes (whether in dying or involuting cells or in the phagocytes that invade the tissue) also reveal patterns of cell death. (
  • Programmed cell death in peripheral lymphocytes from HIV-infected persons: increased susceptibility to apoptosis of CD4 and CD8 T cells correlates with lymphocyte activation and with disease progression. (
  • To study the relationship between the increased apoptosis in HIV infection and the activation state of the immune system, we analyzed cell surface expression of activation markers on apoptotic and nonapoptotic cells. (
  • We found that in the chronic phase of HIV infection, 50 to 60% of the apoptotic cells exhibited an activated phenotype (they were HLA-DR+, CD38+, CD45RO+, and Fas+), and interestingly, the CD45RO+ subset appeared to be more prone to apoptosis in HIV-positive persons. (
  • However, a significant correlation was found between the intensity of anti-CD3-induced apoptosis in both CD4 and CD8 T cells from HIV-infected persons and their in vivo expression of CD45RO and HLA-DR molecules. (
  • Altogether these observations indicate that the increased susceptibility to apoptosis of peripheral T cells from HIV-infected persons correlates with disease progression and support the hypothesis that the chronic activation of the immune system occurring throughout HIV infection is the primary mechanism responsible for this cell deletion process. (
  • The most common cell death pathway is called apoptosis and constitutes a tightly regulated program that results in cell shrinkage and the formation of apoptotic bodies, which are engulfed and digested by phagocytic cells, like macrophages. (
  • Stress-induced NO can be protective, produce physiological disorders, DNA damage, and programmed cell death (apoptosis). (
  • Apoptosis, or modified cell passing, advanced as a quick and irreversible prepare to proficiently dispense with broken cells. (
  • A trademark of cancer is the capacity of harmful cells to avoid apoptosis. (
  • Cancer cells anticipate MOMP by intensification of anti- apoptotic BCL-2 family proteins and hindrance of one or different anti-apoptotic BCL-2 family proteins cause apoptosis in cancer cells, but not in sound ordinary cells - it is regularly said that cancer cells are prepared to passing or dependent to anti-apoptotic BCL-2 family. (
  • In multicellular life forms, cells that are now not required or are a risk to the living being are annihilated by a firmly controlled cell suicide handle known as modified cell passing, or apoptosis. (
  • Research performed over the past decade has transformed apoptosis from a distinctive form of cell death known only by its characteristic morphology and genomic destruction to an increasingly well understood cellular disassembly pathway remarkable for its complex and multifaceted regulation. (
  • They moved on to do experiments showing that that MCP-1 plays a critical role in mediating photoreceptor apoptosis (cell death) in an experimental (mouse) model of RD. RD led to increased MCP-1 expression in the Müller glia and increased CD11b+ macrophage/microglia in the detached retina. (
  • The Nobel Prize for Medicine or Physiology of 2002 was awarded to Sydney Brenner, H. Robert Horvitz and John E. Sulston for their discovery regarding gene regulation of organ development and programmed cell death or apoptosis. (
  • During the process of bodily growth, organ development and continuous cellular division which are all constructive processes, there is also a co-occurring destructive process called programmed cell death or apoptosis. (
  • It is now well established that cancer cells exhibit a number of genetic defects in the machinery that governs programmed cell death and that sabotage of apoptosis is one of the principal factors aiding in the evolution of the carcinogenic phenotype. (
  • Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induces apoptotic cell death in a variety of tumor cells without significant cytotoxicity on normal cells. (
  • The development of the form and structure of the endocardial cushion is accompanied by precise patterns of abundant cell death having the morphological features of programmed cell death (apoptosis), which plays an important role in the elimination of redundant cells and in changes of phenotypic composition during histogenesis. (
  • The clarification of the role of the apoptosis regulatory genes constitutes a major task in future studies of cell death in the developing heart. (
  • Apoptosis is a distinct form of cell death that plays an important role in various physiological processes in mammals. (
  • We investigated the potential of an aqueous extract of the root of W. somnifera (W RE ) to modulate cytokines, antioxidants and apoptosis in leukaemic THP-1 cells and peripheral blood mononuclear cells (PBMC's). (
  • Western blotting was used to examine apoptosis-associated protein levels in U-2 OS cells after exposed to CECF. (
  • CECF decreased the percentage of viability, induced DNA damage and DNA condensation, G 0 /G 1 arrest, and apoptosis in U-2 OS cells. (
  • These findings suggest that CECF triggers apoptosis in U-2 OS cells via ROS-modulated caspase-dependent and -independent pathways. (
  • Interestingly, the apoptosis-inducing effect of thiazolides appeared to be cell cycle-dependent and induction of cell cycle arrest substantially inhibited the cell death-inducing activity of these compounds. (
  • hence selective killing of tumor cells by promoting apoptosis pathway is an attractive and effective way for development of anti-cancer agents. (
  • Her team's initial point of entry into the complex signaling network that regulates and executes the various programmed cell death modules (apoptosis, autophagy, and programmed necrosis) is the DAPs (Death Associated Proteins) . (
  • Apoptosis-inducing factor (AIF): Key to the conserved caspase-independent pathways of cell death? (
  • One of these proteins, apoptosis-inducing factor (AIF), is a phylogenetically old flavoprotein which, in healthy cells, is confined to the mitochondrial intermembrane space. (
  • Granule cells from mice in which Bax, a proapoptotic Bcl-2 family member, had been deleted, did not undergo apoptosis in 5 mM potassium, yet did undergo an excitotoxic cell death in response to stimulation with 30 or 100 μM NMDA. (
  • Cell apoptosis was detected via annexin V staining using flow cytometry. (
  • 9 ] showed that 0.5% bupivacaine inflicted temporary functional damage after a single peritendinous injection in the Achilles tendons of rats and caused cell apoptosis at the injection site. (
  • Researchers from Tohoku University in Japan recently published a study 12 in which they tested the effect fatty acids have on programmed cell death, or apoptosis. (
  • During apoptosis the body rids itself of unhealthy cells, which is one mechanism of preventing conditions like cancer. (
  • If DNA damage spreads across too many cells and triggers too much apoptosis it can lead to some of the same chronic diseases that researchers know are associated with eating trans fats. (
  • Streuli, C.H. / Programmed cell death and the mammary gland - The involvement of the Bcl-2 family members in the control of epithelial apoptosis . (
  • Metcalfe, A, Hickman, JA & Streuli, CH 1996, ' Programmed cell death and the mammary gland - The involvement of the Bcl-2 family members in the control of epithelial apoptosis ', Biochemical Society Transactions , vol. 24, no. 3, pp. 347-347. (
  • Apoptosis : An International Journal On Programmed Cell Death is a research journal that publishes research related to Pharmaceutical Science . (
  • The latest Quartile of Apoptosis : an international journal on programmed cell death is Q1 . (
  • How to publish in Apoptosis : An International Journal On Programmed Cell Death? (
  • If your research field is related to Pharmaceutical Science, then visit the official website of Apoptosis : an international journal on programmed cell death and send your manuscript. (
  • This model provides a generic high-level view of the interplays between NFkappaB pro-survival pathway, RIP1-dependent necrosis, and the apoptosis pathway in response to death receptor-mediated signals. (
  • Our wild type and mutant simulations provide novel insights to restore apoptosis in defective cells. (
  • Researchers at the University of Buffalo have developed an imaging technique capable of monitoring the process of apoptosis, or programmed cell death. (
  • The technique allows scientists to view the changes occurring in the cell on a molecular level during apoptosis. (
  • Apoptosis is a process in which cells self-destruct when they are no longer useful. (
  • Ideally, an apoptosis-based therapy would induce self-destruction in diseased cells while sparing healthy cells. (
  • Characterized by different morphologies, apoptosis, autophagic cell death, and necrosis are the three main types of cell death, as they are executed in response to specific stimuli through distinct but sometimes overlapping signaling pathways. (
  • Specifically, apoptosis, or type I cell death, is the process of programmed cell death characterized by cell shrinkage, membrane blebbing, global mRNA decay, and condensation of the chromatin (pyknosis). (
  • Apoptosis is an essential part of various processes, such as normal cell turnover, immune responses, and embryonic development. (
  • Our results demonstrate the selective cytotoxicity of cryptotanshinone in prostate cancer cells PC3 (IC 50 = 15.85 μM) and DU145 (IC 50 = 7.59 μM) as well as the underlying mechanisms of action, in particular the activation of both apoptosis and autophagic cell death. (
  • Furthermore, both PC and ABS emissions induced apoptosis in SAEC with the PC emissions induced four-fold more apoptotic cells than the ABS emission. (
  • Increased dengue virus-infected endothelial cell apoptosis caused by antibodies against nonstructural protein 1. (
  • PANoptosis is a unique inflammatory cell death pathway that integrates components from other cell death pathways. (
  • Using genetic and single-cell RNA transcriptomic analysis in mice, the researchers found that being female confers striking protection against ferroptosis through a particular pathway called nuclear factor erythroid 2-related factor 2, or NRF2. (
  • Here, we test the hypothesis that targeted hyperactivation of the phosphatidylinositol-3-phosphate/AKT (PI3K/AKT)-signaling pathway may be leveraged to trigger CLL cell death. (
  • While direct agonists of BCR-downstream kinases are not available, targeted hyperactivation can be achieved by pharmacological inhibition of negative regulators of the BCR-signaling pathway (e.g., inhibitory phosphatases including SHIP1), resulting in the activation of signaling above a maximum tolerable threshold causing energy stress and cell death. (
  • Upregulation of inhibitory receptors, such as lymphocyte activation gene-3 (LAG-3), may limit the antitumor activity of therapeutic antibodies targeting the programmed cell death protein-1 (PD-1) pathway. (
  • They also examine the involvement of cell death programs in various pathologies and the therapeutic potential of inhibiting key pathway components. (
  • TRAIL also engages the extrinsic apoptotic pathway by binding to the DR4 and DR5 death receptors, which triggers apoptotic signaling ( 3 ). (
  • It has been reported that many tumor cells, including human lung adenocarcinoma A549 cells, are resistant to the apoptotic effects of the TRAIL signaling pathway ( 6 ). (
  • There is enough evidence that most of these agents involved in neural and pancreatic beta cell death exert their toxic effects through the nitric oxide pathway. (
  • Chakraborty, Sayantan (2016): Novel roles of the central cell death pathway and cell corpse engulfment pathways in C. elegans. (
  • Cell Death Pathway array was performed to determine the mechanism of tumor death. (
  • Our results showed that cancer cells (MDA-MB-231) underwent immunogenic cell death via TNF-mediated necrosis signaling pathway after the boiling histotripsy exposure. (
  • Combined, these data verify the p53-independence of cell death caused by inhibitors of the proteasome pathway and support the proposition that the ubiquitin-dependent proteasome pathway may contain molecular targets suitable for antineoplastic drug discovery. (
  • These results allowed us to propose two models, showing the role of LmjMCA in the cell death and also in the autophagy pathway, implicating different protein domains. (
  • To determine the effects of PD-1 pathway blockade on sarcoidosis CD4 + T-cell proliferative capacity. (
  • Flow cytometry was used to measure ex vivo expression of PD-1 and PD-L1 on systemic and bronchoalveolar lavage-derived cells of subjects with sarcoidosis and control subjects, as well as the effects of PD-1 pathway blockade on cellular proliferation after T-cell receptor stimulation. (
  • Analogous to the effects in other chronic lung diseases, these findings demonstrate that the PD-1 pathway is an important contributor to sarcoidosis CD4 + T-cell proliferative capacity and clinical outcome. (
  • As SecA is involved in translocation of bacterial proteins, we predicted that inhibition of the SecA pathway by C3G should decrease H. pylori -induced cell death. (
  • Unlike the UPR in mammalian cells, by now only two pathways have been identified: IRE1α/β pathway and bZIP28 pathway. (
  • The ces (for cell-death specification) genes of the nematode Caenorhabditis elegans control the cell-death fate of individual cell types and are candidates for being the regulators of an evolutionarily conserved general pathway of programmed cell death. (
  • We also show that the HW1-mediated autophagic cell death occurs predominantly via the c-Jun NH 2 -terminal kinase pathway in a caspase-independent manner. (
  • Our results reveal a novel TR2-mediated signaling pathway triggering autophagic cell death and provides a new strategy for the elimination of cancer cells, including TRAIL-resistant tumors, through nonapoptotic cell death. (
  • The cGAS-STING pathway can be activated by radiation induced DNA damage and because of its important role in anti-cancer immunity activation, methods to increase its activation in cancer cells could provide significant therapeutic benefits for patients. (
  • We explored the impact of hafnium oxide nanoparticles (NBTXR3) activated by radiotherapy on cell death, DNA damage, and activation of the cGAS-STING pathway. (
  • However, these inhibitors had only a marginal effect on preventing cell death, suggesting a caspase-independent death pathway downstream of BAX in cerebellar granule cells. (
  • Exosomes are tiny bubbles that act as an advanced communication pathway between cells. (
  • The major signaling pathways that trigger apoptotic cell death are the mitochondrial (the intrinsic) pathway and the death receptor (the extrinsic) pathway. (
  • We speculate that, functioning like a cellular checkpoint, the AMPK Nampt SIRT1 pathway can be activated by decreased nutrient availability to stop the undertaking of energydemanding processes this kind of as cell differentiation for the duration of calorie unfavorable situations and be inactivated, as soon as nutrients turn out to be out there, to permit resumption of physiological development. (
  • The pathologist John Kerr had since 1965 [ 3 ] been calling attention to what he described as "shrinkage necrosis", referring to the collapse of a dying cell, very unlike the osmotic lysis that would be predicted from a cell's having lost control of its ion pumps, taking in water, and bursting [ 4 , 5 ]. (
  • Our results showed that the application of PBM increases cell viability and decreases cell death byapoptosis and necrosis. (
  • Results: Live, but not killed S. aureus or other staphylococcal species, induced release of Th2-promoting cytokines (IL-33 and TSLP) and necrosis in both human and mouse cell lines. (
  • RIP3 , has been defined as they key regulator of programmed necrosis and its expression was elevated in rd10 retinas during cone photoreceptor death and not rod photoreceptor death. (
  • Our findings with ferroptosis provide a unifying concept that sustained increase of cytosolic Ca2+ prior to plasma membrane rupture is a common feature of regulated types of necrosis and position ESCRT-III activation as a general protective mechanism in these lytic cell death pathways. (
  • T cells increased production of proinflammatory cytokines, chief among them tumor necrosis factor alpha, making cancer cells even more vulnerable to oxidative stress . (
  • In fatal cases, autopsies reveal permanent damage to nerve cells, with focal areas of fatty degeneration and necrosis [Stevens et al. (
  • Other pathways of programmed cell death have been discovered. (
  • Cells of metazoans respond to internal and external stressors by activating stress response pathways that aim for re-establishing cellular homoeostasis or, if this cannot be achieved, triggering programmed cell death. (
  • Inhibiting these pathways could reverse the immunosuppressive environment created by tumor-associated macrophages and enable another type of immune cell, cancer-killing T lymphocytes, to attack the tumor. (
  • The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. (
  • Here, we consider the progress that has been made in the last few decades in determining the fates of damaged organelles and damaged cells through discrete, but genetically overlapping, pathways involving the selective autophagy and cell death machinery. (
  • Our findings uncover new players and pathways in this process, opening concrete therapeutic opportunities to selectively eliminate tumor cells in patients. (
  • Control of cell metabolism has key roles in the regulation of cell death pathways. (
  • Changes in glucose metabolism might affect cell death pathways and be crucial in the development and selection of T lymphocytes. (
  • Recent evidence suggests that accumulation of genetic and epigenetic alterations in malignant colonic cells progresses through at least three distinct pathways: chromosomal instability (CIN), microsatellite instability (MSI), and CpG island methylator phenotype (CIMP) [ 6 - 8 ]. (
  • For customers interested in more information about cell death solutions or any other signaling pathways, please visit CD BioSciences at . (
  • Our results demonstrate that CLL cells critically depend on mechanisms to fine-tune PI3K/AKT activity, allowing sustained proliferation and survival but avoid ROS-induced cell death and suggest transient SHIP1-inhibition as an unexpectedly promising concept for CLL therapy. (
  • Signaling derived from the B-cell surface immunoglobulin, the B-cell receptor (BCR), generally promotes the survival and proliferation of B cells. (
  • The results showed that UV LED irradiation (8‑60 J/m2) inhibited the proliferation of HL‑60 cells in a dose‑dependent manner. (
  • Here, we showed that genistein, a major isoflavone compound that exerts its anticancer properties by inhibiting tumor cell proliferation, can induce TRAIL-mediated apoptotic cell death in TRAIL‑resistant human adenocarcinoma A549 cells. (
  • Genistein promotes the inhibition of protein tyrosine kinase by competing with ATP for tyrosine kinase domain binding, resulting in a decrease in cancer cell proliferation due to interruption of the tyrosine kinase cascade stimulated by mitogens ( 12 , 13 ). (
  • Local exposure of 849 MHz and 1763 MHz radiofrequency radiation to mouse heads does not induce cell death or cell proliferation in brain med. (
  • PHLPP (Pleckstrin Homology domain and Leucine rich repeat Protein Phosphatase) dephosphorylates and terminates the activity of several AGC kinases that are important for controlling cell growth, proliferation, and survival (Grzechnik and Newton 2016). (
  • Here we report that NTZ and the bromo-thiazolide RM4819, but not the carboxy-thiazolide RM4825, inhibited proliferation of the colon cancer cell line Caco2 and nontransformed human foreskin fibroblasts (HFF) at or below concentrations the compounds normally exhibit anti-parasitic activity. (
  • Cinnamon extract strongly inhibited tumor cell proliferation in vitro and induced active cell death of tumor cells by up-regulating pro-apoptotic molecules while inhibiting NFκB and AP1 activity and their target genes such as Bcl-2 , BcL-xL and survivin . (
  • In the U.S., with the proliferation of cell phones and the growing needs of cell phone users in recent years, there has been an explosion in cell towers. (
  • They also found that expression of MFF is regulated by Myc, a ubiquitous mediator of cell proliferation that contributes to development of many cancer types. (
  • The researchers found that disruption of the MFF-VDAC1 complex activated multiple mechanisms of mitochondrial cell death, inhibiting tumor cell proliferation and reducing tumor growth in a preclinical model. (
  • Cryptotanshinone, one of the major tanshinones isolated form Danshen, has been reported to inhibit cell proliferation and to induce cell death in various cancer cell lines, including those of colon, cervical, breast, etc. (
  • Zika virus appears to primarily target neural progenitor cells resulting in cell death and disruption of neuronal proliferation, migration and differentiation, which slows brain growth and affects neural cell viability ( 7 - 9 ). (
  • and it alters cell proliferation, cell death, or nutrient supply. (
  • The study results revolve around carefully regulated cell dell death mechanisms that, by killing defective cells or those infected by viruses, are often important cellular defense mechanisms. (
  • The aim of the present study was to examine the effect of UV LED irradiation emitting at 280 nm on cultured HL‑60 human leukemia cells, and to explore the underlying mechanisms. (
  • The mechanisms by which cell death occurs are genetically encoded and carefully controlled. (
  • Chapters are additionally devoted to cell death signaling mechanisms in plants and lower organisms, as well as the evolution of those mechanisms and the influence of pathogens that seek to evade them. (
  • Recent work with crustaceans shows that apoptotic proteins, and presumably mechanisms of cell death regulation, are more diverse in arthropods than appreciated based solely on the excellent work with fruit flies. (
  • Such end points do not fully measure the benefits or mechanisms of the stem cells and their value in preventing heart attack or stroke. (
  • Complete disruption of the cell death machinery can be lethal, but many mutations of the regulatory machinery yield only modest or no phenotypes, indicating substantial redundancy and compensation of regulatory mechanisms. (
  • The exact mechanisms by which S. aureus induces inflammatory responses and cell death in the skin epithelium is unclear. (
  • The aim of this thesis was to elucidate the cellular and molecular mechanisms by which S. aureus induces it's pathogenic effects on keratinocyte and fibroblast cell lines. (
  • Examining how UV light may relate to the production of NO by plants in terms of DNA damage, error-prone repair cell cycles, and the multiple mechanisms of programmed cell death. (
  • It is the basic premise of this proposal that these neuroprotective mechanisms can be exploited to prevent much of the cell death associated with diseases such as glaucoma. (
  • This situation has prompted a search for agents that cause tumor cell death via molecular mechanisms independent of p53. (
  • The data suggested the involvement of two novel extracellular serine proteases, nodulin-like proteins and an Arabidopsis thaliana OPEN STOMATA 1 ( AtOST1 ) homolog in signaling fiber-cell death, as well as mechanisms responsible for hormonal control, nutrient remobilization, regulation of vacuolar integrity and autolysis of the dying fibers. (
  • This new molecular histology of heart development awaits further experiments to clarify the interactive mechanisms that act to ensure the sculpting of the endocardial cushion into valves and septa by determining the size of the cushion cell populations. (
  • Pharmacological blockade of JNK/c-Jun signaling attenuates injury-induced hair cell loss, but with unsolved mechanisms. (
  • Few experimental systems allow the observation of hair cell death mechanisms in vivo, in the intact animal, one of these being the lateral line system in the zebrafish. (
  • In order to further characterize cellular and molecular mechanisms, primary human choroid plexus epithelial cells were exposed to cerebrospinal fluid (CSF) from preterm infants with IVH as well as to Hb-metabolites. (
  • Finding multiple mechanisms of cell death or disease pathology expands our choice of drugs when we think about therapy," Nobuta said. (
  • The team "Cell Death and Childhood Cancers" was initiated in September 2016, around M. Castets, who has a robust expertise in basic research, notably on mechanisms triggering resistance of tumor cells to cell death and J.-Y. Blay, expert in translational and clinical research on sarcoma and rare cancers. (
  • Based on the assumption that children are anything but little adults, our main objective is to elucidate childhood cancers resistance to cell death mechanisms, focusing on their developmental origin context and intratumoral heterogeneity, to move towards more efficient and less toxic innovative therapeutic strategies. (
  • Mitochondria, the organelles that supply energy to our cells, also control multiple cell death mechanisms and play an intricate role in cancer, which is a field of intense research. (
  • In particular, mitochondrial dynamics, a process that orchestrates the size, shape and position of mitochondria within the cell, has been implicated in tumor progression, but, until now, the mechanisms have only been partially elucidated. (
  • This study aims to explore the cytotoxicity of cryptotanshinone on human prostate cancer cell lines PC3 and DU145 as well as the underlying mechanisms of action. (
  • In this study, therefore, we aim to explore the cytotoxicity of cryptotanshinone on human prostate cancer cell lines PC3 and DU145 as well as the underlying mechanisms of action. (
  • These mechanisms, in addition to increased cell death and turnover, are thought to lead to steatosis and carcinogenesis [Palmer and Phillips 2007]. (
  • In the study, published Nov. 9 in Nature , the scientists investigated the healthy turnover of epithelial cells , which are born and die every four to five days, to better understand how the gut maintains a healthy equilibrium. (
  • Dying epithelial cells are shed into the gut lumen, so their active clearance is not necessary and they were thought to have no role in intestinal inflammation. (
  • The investigators sought to understand whether phagocytes can take up dying epithelial cells in the gut and, if so, how these phagocytes respond. (
  • In their experiments, the scientists expressed a green fluorescent protein fused to the diphtheria toxin receptor within intestinal epithelial cells of mice, which made them visible under a microscope and sensitive to diphtheria toxin. (
  • Two key virulence factors of Helicobacter pylori are the secreted virulent proteins of vacuolating toxin A (VacA) and cytotoxin associated protein A (CagA) which lead to damages of gastric epithelial cells. (
  • In vitro characterization of choroid plexus epithelial cells, following exposure to hemorrhagic CSF and to the Hb-metabolites metHb and heme, displayed apoptotic and necrotic cell death and an up-regulation of receptor-related and inflammatory effector molecules similar to that observed in vivo following IVH + PHVD. (
  • The above results are likely associated with the abundant phagocytosis observed at the entry of the lateral oviducts, where numerous cell bodies are massively engulfed by epithelial cells. (
  • Here, we report that the death of ouabain-treated epithelial cells from the Madin-Darby canine kidney (C7-MDCK) and endothelial cells from porcine aortae is suppressed by acidification of medium from pH 7.4 to 7.0, i.e. under conditions when pH(i) was decreased from approximately 7.2 to 6.9. (
  • QAS poisonous effects than the commensal vaginal flora and that QAS significantly attenuate the infectivity of and without affecting the viability of epithelial cells of the vaginal mucosa. (
  • Data are presented as CFU/105 epithelial cells. (
  • Infection of epithelial cells by L2/434/Bu (ATCC VR-902B) was propagated in HeLa cells using standard techniques (19). (
  • Normal human prostate epithelial cells and human prostate cancer cell lines PC3 and DU145 were purchased from the American Type Culture Collection (Manassas, VA, USA). (
  • The scope of this study was to characterize aerosolized emissions from 3D printers and evaluate their toxic effects in human small airway epithelial cells (SAEC). (
  • However, autophagy can also incite cell death due to mitophagy, the loss of mitochondrial membrane potential, caspase cascade activation, and finally lysosomal membrane permeabilization ( 16 ). (
  • during tumorigenesis or oncogenesis processes it functions as a mechanism for tumor suppression ( 21 - 23 ) whereas when a tumor is formed, autophagy provides a cell survival advantage to resist cell death induced by cancer therapy ( 24 ). (
  • In this study, using a Leishmania major MCA-deficient strain, we showed that L. major MCA (LmjMCA) not only had a role similar to caspases in cell death but also in autophagy and this through different domains. (
  • The HW1-induced autophagic cell death was inhibited by an autophagy inhibitor, 3-methyladenine, or by RNA interference knockdown of Beclin-1 and Atg7 . (
  • These data argue for the presence of an autophagy-mediated cell death program in the ovarian follicle cell layer in both species. (
  • We further discuss the ways in which the autophagy machinery may impact the clearance and consequences of dying cells for host physiology. (
  • Autophagy, also known as microautophagy, is a well-defined catabolic process engaged in respond to metabolic crises or damaged cell component removal. (
  • In most cases, autophagy accompanies type II cell death without promoting it. (
  • However, it appears to be involved in cell death in some cases, such as the involution of the salivary gland driven by autophagy-dependent cell death during Drosophila metamorphosis. (
  • Autophagy has been implicated in physiological and pathological processes such as development, cell differentiation, infection and cancer. (
  • Our findings are the first to show that cancer cell death via necroptosis can actually promote tumor growth, as this process results in suppression of the body's immune response against the cancer," said the study's senior investigator, George Miller, associate professor in the Departments of Surgery and Cell Biology, and co-leader of the Cancer Immunology Program at the Perlmutter Cancer Center. (
  • Means to an End is a complex but improbably thrilling read that manages to convey not only the hard work associated with cell biology but also the joy of its eureka moments. (
  • The main aim in this publication is to introduce new theoretical developments and instrumentation for cell biology, to update our understanding of the effects of UV radiation and to evaluate how plants use UV signals to protect against damage and enhance their productivity. (
  • Trends in Cell Biology, 11(12):526-534. (
  • This talk is part of the Cell Biology in Medicine Seminar Series series. (
  • Small molecules that interfere with microtubule dynamics, such as Taxol and the Vinca alkaloids, are widely used in cell biology research and as clinical anticancer drugs. (
  • Therefore, photostatins are both valuable tools for cell biology, and are promising as a new class of precision chemotherapeutics whose toxicity may be spatiotemporally constrained using light. (
  • The team currently employs multiple approaches, including biochemistry and cell biology, proteomics-based strategies , 3D protein structure analysis, and advanced microscopy, to elucidate the functions of the individual DAPs and to map their positions within the cell-death network. (
  • Journal of Cell Biology , 139 (1), 205-217. (
  • He then joined the 2011 Nobel prize Dr Ralph Steinman's Laboratory as a Postdoctoral Fellow under the direction of Dr Nina Bhardwaj at Rockefeller University, New York, NY, USA, from 2000 to 2003, where he studied dendritic cells biology, notably cross-presentation of viral antigens and interactions between virus/myeloid DC/plasmacytoid DC. (
  • The Bcl-2 (Bcl is B-cell lymphocytic-leukaemia proto-oncogene) family comprises two groups of proteins with distinct functional biology in cell-fate signalling. (
  • Anatomical Record A Discovery Molecular, Cell and Evolutionary Biology. (
  • Apoptotic cells can be distinguished from viable cells by phenotypic changes and activity of certain proteins. (
  • Different tissue phagocytes sample apoptotic cells to direct distinct homeostasis programs, Nature (2016). (
  • Consistent with this, we found apoptotic cells in the outer supporting cell region of the cochlea at P1 and P2, indicating that Notch1 is required for outer supporting cell survival during early cochlear maturation. (
  • This study also indicates that the activated phenotype found on apoptotic cells was not a distinctive feature of patients' lymphocytes since it was in similar proportion in apoptotic cells from control lymphocytes. (
  • Flow cytometry was used for measuring the percentage of viable cells, cell-cycle distribution, apoptotic cells in sub-G1 phase, reactive oxygen species (ROS), Ca 2+ levels, and mitochondrial membrane potential (ΔΨ m ). (
  • GliaGen is developing novel technologies to measure cell stress and cell death, while Amnis Corporation offers the ImageStream x system for the high-speed imaging and analysis of apoptotic cells. (
  • Programmed cell death protein-1 (PD-1)-targeted immunotherapy has shown promising results in a variety of malignant tumours. (
  • By studying a mouse model of pancreatic ductal adenocarcinoma (PDAC), researchers from NYU Langone Medical Center and its Laura and Isaac Perlmutter Cancer Center found that the form of orchestrated cell death -- called necroptosis -- in fact induced the production of a small protein CXCL1 to drive the growth of PDAC tumor cells. (
  • A form of orchestrated cell death called necroptosis induces the production of a small protein CXCL1 to drive the growth of pancreatic ductal adenocarcinoma (PDAC) tumor cells. (
  • Dying tumor cells also release another protein, SAP130, that binds to a receptor called named Mincle, on the cell membranes of inflammatory immune cells located within the tumor environment. (
  • The activation of the death receptor recruits Fas-associated death domain protein (FADD) and eventually procaspase-8 to form the death-inducing signaling complex (DISC), leading to the activation of the caspase cascade (caspase-8, -9, -10 and -3) ( 4 , 5 ). (
  • They describe a mechanism by which AML cells regulate a cancer-related protein, mutant IDH2, to increase the buildup of blood cancer cells-a distinguishing characteristic of the disease. (
  • Inflammasomes, are multi-protein complexes that are assembled by cellular sensor proteins that surveilled the cytosol of cells and respond to danger such as infections, cancer or toxic molecules. (
  • It is this cleavage that removes an inhibitory part and thereby converts the rest of the protein into a highly effective cell killer. (
  • Endoplasmic Reticulum (ER) is a vital part for functional protein synthesis in eukaryotic cells. (
  • An oncogenic form of the mammalian PAR-family protein, hepatic leukaemia factor (HLF), is reported to effect programmed cell death in mammalian cells. (
  • Analysis of the death-inducing signaling complex induced by HW1 binding to TR2 exhibits the recruitment of TNF receptor-associated death domain and TNF receptor-associated factor 2, but not Fas-associated death domain, caspase-8, or receptor-interacting protein, which is distinct from that induced by TRAIL. (
  • Lit is activated by a unique sequence in the major head protein of the T4 phage (the Gol sequence) which then cleaves site-specifically the host translation factor EF-Tu, ultimately leading to cell death. (
  • We recently identified a novel and evolutionarily conserved membrane protein, PAC (also known as PACC1 or TMEM206), encoding the proton-activated chloride (Cl − ) channel, whose activity is widely observed in human cell lines. (
  • In "Frontiers in Plant Science" we propose a regulatory circuitry in which RCD1 maintains plant cell vitality by stabilizing the redox-sensitive transcription factor Rap2.4a in activation of genes for chloroplast antioxidant enzymes based on gene expression and protein-protein-interaction studies and discuss rcd1 -phenotypes in context of regulation of the chloroplast antioxidant system. (
  • Necroptosis is an aggressive and proinflammatory mode of cell death that can be prevented by necrostatin-1 administration or receptor-interacting protein kinase (RIP3) deletion. (
  • Transfection of these constructs results in nuclear protein aggregation, filamentous nuclear inclusions, and an increase in cell death. (
  • It is caused by mutations in the proteolipid protein 1 ( PLP1 ) gene that triggers the death of oligodendrocytes that produce protective myelin around nerve axons. (
  • Protein synthesis also decreased rapidly in both wild-type and Bax-deficient granule cells to 50% of control within 12 h after switching to 5 mM potassium. (
  • The death of ouabain-treated cells was independent of inhibition of RNA and protein synthesis with actinomycin D and cycloheximide. (
  • PHILADELPHIA - (Sept. 18, 2019) - Researchers at The Wistar Institute have described the role of mitochondrial fission factor (MFF) in controlling survival of cancer cells, suggesting the protein could represent a promising therapeutic target. (
  • We previously showed that antibodies against DENV nonstructural protein 1 (‎NS1)‎ may cross-react with endothelial cells. (
  • Association between SNPs of Cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), programmed cell death 1 (PD-1)and the susceptibility to chronic Hepatitis C infection in virus C-infected patients. (
  • This form of cell death is dependent on iron and oxidative stress. (
  • According to the results of a recent study, driving up levels of oxidative stress can be fatal to cancer cells . (
  • We also show that hair cells exposed to copper undergo oxidative stress and that antioxidants can protect these cells from the effects of the metal. (
  • The increased abundance of several antioxidant proteins as well as a measured increase in free Fe2+ content of the cells indicates an oxidative stress in this system. (
  • Another clue was a finding that the mutated cells uniquely produced oxidative stress in animal models. (
  • Oxidative stress can damage cell membranes. (
  • J. Gilloteaux, J.M. Jamison, D. Arnold, J.L. Summers: Autoschizis: another cell death for cancer cells induced by oxidative stress. (
  • Here, we demonstrate that growth differentiation factor 15 (GDF15) is associated with retinal ganglion cell death. (
  • This means that all the worms he observed underwent exactly the same process of cell division and differentiation. (
  • He also noted that during the process of cellular differentiation, there is a co-occurring cellular death that is tightly regulated by the organism. (
  • In contrast to vessel elements, which differentiate very rapidly close to the vascular cambium, fiber differentiation is a relatively slow process involving initial expansion of the cells in both the radial and longitudinal dimensions, followed by extensive synthesis of the secondary cell walls. (
  • Inside the case of genotoxic stress mediated cells death, the protective part of Nampt is exerted by way of the mitochondrial SIRT3 and SIRT4 , whereas GR induced Nampt expression mediates its results about the differentiation procedure of skeletal muscle cells by means of the nuclear SIRT1. (
  • [ 18 ] Arylsulfatase A deficiency leads to defective glial and neuronal differentiation from neural progenitor cells. (
  • WISE COUNTY, Va. (WRIC) - The body of Anwar Phillips was discovered on Jan. 4, 2022, in his solitary cell at Virginia's notorious Red Onion State Prison. (
  • New York, USA - June 28, 2022 - To assist life science laboratories advancing productivity of cell death research and freeing up time for more value-added activities, CD BioSciences, a US-based CRO and life science research product supplier, is offering a comprehensive panel of research solutions covering all aspects of cell death study. (
  • Different assays can be used to determine the mechanism of cell death or rule out a mechanism of cell death within a cellular population. (
  • This protection involves the modulation of cell death mechanism and decreased pro-inflammatory cytokine release. (
  • This review focuses on the biochemistry of nitrosative stress, as well as several new forms of cell death, and highlights its role in cell death, which provides important clues for studying the mechanism of cell death-related diseases ( Table 1 ). (
  • Early analyses revealed a reduction in supporting cells in the outer hair cell region between P2-P6, without a comparable increase in outer hair cell number, suggesting a mechanism other than lateral inhibition. (
  • Aberrant cell deaths that produce known phenotypes are typically localized, indicating that the mechanism of activating a programmed death in a specific region, rather than the mechanism of death, is aberrant. (
  • Early, but not late, ferroptotic cells promote the phenotypic maturation of BMDCs and elicit a vaccination-like effect in immune-competent mice but not in Rag-2−/− mice, suggesting that the mechanism of immunogenicity is very tightly regulated by the adaptive immune system and is time dependent. (
  • Our recent investigations with electrophilic prostaglandins enabled us to devise a pharmacophore and mechanism of action hypothesis relevant to this problem: a cross-conjugated α,β-unsaturated dienone with two sterically accessible electrophilic β-carbons is a molecular determinant that confers activity among this class of ubiquitin isopeptidases inhibitors, and that inhibitors of ubiquitin isopeptidases cause cell death in vitro independently of p53. (
  • These data identify the c-Jun stress response as a paracrine mechanism that mediates outer hair cell death. (
  • Although the precise mechanism of pathogenesis of the expanded polyQ tracts is still unknown, these diseases share a number of similar characteristics, including formation of ubiquitinated inclusions, neural dysfunction, and cell type-specific cell death ( Cummings and Zoghbi, 2000 ). (
  • Our data establish adiponectin signaling-mediated increase in S1P secretion as a mechanism via which HFD or PA induced cardiomyocyte lipotoxicity, leading to insulin resistance and cell death, is attenuated. (
  • We strongly believe that during the termination of the above Dipteran oogenesis, an efficient mechanism of absorption of the degenerated follicle cells is selectively activated, in order to prevent the blockage of the ovarioles and thus robustly support the physiological completion of the ovulation process. (
  • In this study, we tested anti-tumor activity and elucidated action mechanism of cinnamon extract using various types of tumor cell lines including lymphoma, melanoma, cervix cancer and colorectal cancer in vitro and in vivo mouse melanoma model. (
  • Programmed cell death is the principal mechanism by which cells are physically eliminated in our body. (
  • Although the apoptotic death of photoreceptor cells in retinal degenerative disorders is well documented, the molecular mechanism is not understood. (
  • In THP-1 cells, W RE decreased pro-inflammatory cytokine levels, which may alleviate cancer cachexia and excessive leukaemic cell growth. (
  • In another words, the dying cells synthesize certain proteins and enzymes to carry out the "suicide" process. (
  • The peroxynitrite anion (ONOO - ) produced during this process can nitrate several biomolecules, such as proteins, lipids, and DNA, to generate 3-nitrotyrosine (3-NT), which further induces cell death. (
  • He then looks at the molecular machinery that links signals that cause cell death to caspases, emphasizing the importance of the BCL-2 family of proteins and the role of cytochrome c released from mitochondria. (
  • Normal IDH proteins are important in cell metabolism and play a role in the production of energy from the breakdown of molecules from food. (
  • The mutant forms of IDH proteins, found in AML cells, take on an extra function of making a cancer-causing molecule called 2-HG. (
  • Using human AML cells, they found that mutant IDH2 was controlled by a master regulator, called FLT3, that can activate and deactivate proteins through a process of modification. (
  • This latest discovery describing how AML cells regulate mutant IDH proteins and the production of 2-HG provides new insights into how mutant IDH-targeting medications work against AML. (
  • The C-terminal domain interacted with proteins, notably proteins involved in stress regulation, such as the MAP kinase LmaMPK7 or programmed cell death like the calpain-like cysteine peptidase. (
  • We found that C3G treatment caused a decrease in activation of the pro-apoptotic proteins caspase-3/-8 in H. pylori -infected cells leading to a decrease in cell death. (
  • To develop new therapies, novel goal molecules should to be recognized and the accessibility of cell floor proteins makes them engaging targets. (
  • SIGNIFICANCE B cell lymphoma-2 (Bcl-2) is the prototypical anti-apoptotic member of the Bcl-2 family that comprises proteins with contrasting effects on cell fate. (
  • Research involves the study of genes and their expression, as well as proteins and other organic substances, and how these co-operate in the living cell. (
  • 2012). Plant cell surface receptors include receptor-likekinases (RLKs) and receptor-like proteins (RLPs), which respondto pathogen-derived apoplastic molecules (Boller & Felix, 2009;Thomma et al. (
  • cell death results from the absence of proteins. (
  • A study led by Duke Health researchers provides some insights: Females, it turns out, have an advantage at the molecular level that protects them from a form of cell death that occurs in injured kidneys. (
  • Researchers revealed new insights into how acute myeloid leukemia (AML) develops and progresses, according to a study published in Molecular Cell on July 20, 2021 . (
  • Compared to the traditional means of restoring circulation - extracorporeal membrane oxygenation (ECMO) - OrganEx "preserved tissue integrity, decreased cell death and restored selected molecular and cellular processes across multiple vital organs," the researchers wrote. (
  • Also, ATP and HMGB1, the best-characterized damage-associated molecular patterns involved in immunogenic cell death, have proven to be passively released along the timeline of ferroptosis and act as immunogenic signal associated with the immunogenicity of early ferroptotic cancer cells. (
  • Despite its key role in the inflammatory outcome of ferroptosis, little is known about the molecular events leading to the disruption of the plasma membrane during this type of cell death. (
  • Dumont, E.A.W.J.. / Molecular imaging of programmed cell death in the heart . (
  • Their nuclei are characterized by condensed chromatin, accompanied with high- but not low-molecular weight DNA fragmentation events exclusively detected in distinct cells of the anterior pole. (
  • In parallel, the group is developing systems level approaches based on RNAi-mediated combinatorial perturbations for identifying new principles delineating the structure/function organization of the entire molecular network underlying cell death. (
  • We characterize the release of "damage associated molecular pattern" by tumor cells killed by these treatments and how it affects the maturation status of dendritic cells. (
  • Over the years, we've been able to get an intimate look into the life of a cell: how it carries out its molecular activities, goes through life transitions, grows old, and finally dies. (
  • Previous studies with fluorescent Zn-DPA molecular probes have shown that they have high selective affinity for dead and dying cells. (
  • The objective of this study was to determine the molecular events leading to the death of photoreceptor cells. (
  • Plant cells undergo particular processes of PCD similar to autophagic cell death. (
  • Taken together, our results revealed that genistein enhanced TRAIL-induced tumor cell death in TRAIL-resistant A549 adenocarcinoma cells by inhibiting autophagic flux. (
  • HW1 treatment as a single agent induces autophagic cell death in a variety of both TRAIL-sensitive and TRAIL-resistant cancer cells, but exhibits much less cytotoxicity on normal cells. (
  • During stage 14, the follicle cells contain autophagic vacuoles, and they do not exhibit caspase activity in all parts of the egg chamber. (
  • As for autophagic cell death (ACD), or type II cell death, it is involved in the autophagic machinery and is characterized by the formation of large intracellular vesicles. (
  • A recent paper also reported the cytotoxicity of cryptotanshinone in multidrug-resistant colon cancer cells SW620 Ad300 and its induction of autophagic cell death in the cells [11] . (
  • Cells can die in a number of different manners, depending on the cellular context and triggering stimulus. (
  • Ferroptosis is a natural type of cell death in which cellular iron plays a major role and is characterized by the oxidative breakdown of cellular membranes. (
  • If anti-choicers are really worried about cellular life, telling people to stop killing their skin cells for those greedy ALS sufferers would be the more direct approach. (
  • Our studies demonstrate that different intracellular concentrations of 2-HG correlate with critical cellular functions that can mean life or death for cancer cells," said Chen. (
  • Once an inflammasome complex is formed, it will rapidly recruit and activate caspase-1, a protease that is essential for the induction of pyroptotic cell death and the subsequent release releases of cellular content and highly-proinflammatory cytokines, like interleukin-1b (IL-1b), that cause fever. (
  • Induction of pyroptotic cell death: Detection of cell stress, toxic molecules or pathogens by cellular sensor results in the assembly of an inflammasome complex signaling platform. (
  • The permeabilisation of the cellular plasma membrane by gasdermin-D pores allows inflammatory molecules and the cytokine IL-1b to spill out of the cell, and eventually, the pores cause the cells to completely burst. (
  • Shikoccin (a diterpene), dibenzylideneacetone, and curcumin fit the pharmacophore hypothesis, inhibit cellular isopeptidases, and cause cell death independently of p53 in isogenic pairs of RKO and HCT 116 cells with differential p53 status. (
  • There must always be a balance between cellular division and cell death to ensure the viability of the species. (
  • A few years after the study of Brenner on C. elegans, John Sulston developed techniques to view the process of cellular division from the fertilized egg of C. elegans to the 959-cell adult worm. (
  • Furthermore, he was able to distinctly identify steps in cellular death and a gene that participates in programmed cell death [4] , nuc-1 gene. (
  • Senescence-induced cell death is a much slower process, involving nuclear degradation, DNA fragmentation and thorough proteolytic degradation of the cellular contents and controlled remobilization of the nutrients [ 9 ]. (
  • Programmed cell death (PCD) is an active cellular suicide that occurs in animals and plants throughout development and in response to both abiotic and biotic stresses. (
  • Cellular uptake of human H-ferritin loaded with 50 or 350 iron ions results in significant cytotoxicity on HeLa cells at submicromolar concentrations. (
  • Using a new technology they developed that delivers a specially designed cell-protective fluid to organs and tissues, the researchers restored blood circulation and other cellular functions in pigs a full hour after their deaths, they report in the Aug. edition of the journal Nature . (
  • The health of metazoan organisms requires an effective response to organellar and cellular damage either by repair of such damage and/or by elimination of the damaged parts of the cells or the damaged cell in its entirety. (
  • Gunnar Schulte's ambition is to understand the cellular dialogue taking place on the cell surface. (
  • Using this analysis, the accumulation of dye in positively-stained cells correlates with the extent of cell membrane damage and thus the amount of cells that are stained with Evan's blue dye under various conditions can be used as an indicator of cellular stress. (
  • Cytokines such as TNF and FASL can trigger death or survival depending on cell lines and cellular conditions. (
  • Our mechanistic studies reveal that increased AKT activity upon inhibition of SHIP1 leads to increased mitochondrial respiration and causes excessive accumulation of reactive oxygen species (ROS), resulting in cell death in CLL with immunogenic features. (
  • In this work, we used the zebrafish lateral line system to monitor the dynamic behavior of mitochondrial and cytoplasmic oxidation occurring within the same dying hair cell following exposure to aminoglycosides. (
  • The increased oxidation observed in both mitochondria and cytoplasm of dying hair cells was highly correlated with mitochondrial calcium uptake. (
  • Application of the mitochondrial uniporter inhibitor Ru360 reduced mitochondrial and cytoplasmic oxidation, suggesting that mitochondrial calcium drives ROS generation during aminoglycoside-induced hair cell death. (
  • Altieri and colleagues showed that, in cancer, MFF interacts with VDAC1, a mitochondrial regulator of cell death, shutting down its function to keep tumor cells alive. (
  • These results suggest that a requirement for survival signals is more general than previously thought and that some normal cell deaths in nonneural tissues may also reflect competition for survival factors. (
  • Together, these results demonstrate that Notch1 is required for supporting cell survival during early maturation and that loss of these cells causes later loss of the hair cells and cochlear dysfunction. (
  • These results reveal an unexpected role for Notch in supporting cell survival during cochlear maturation. (
  • In view of this, the significance of the survival of neural and pancreatic beta cell cannot be over emphasised. (
  • It is also becoming clear that type of cancer cell death determines the antitumor immune response and, therefore, contributes to the efficiency of anti-cancer therapy and long-term survival of patients. (
  • The role of MCAs is subject to debate: roles in cell cycle control, in cell death or even in cell survival have been suggested. (
  • The extent of injury following ischemic damage is a delicate balance between cell death and cell survival signals. (
  • NFκB and AP1 constitutively active in many kinds of cancers and play critical roles in tumor development and progression through modulation of their target genes involved in angiogenesis, metastasis and cell survival [ 19 - 21 ]. (
  • Over the past decade, growing evidence indicates that the tumor microenvironment (TME) contributes with genomic/epigenomic aberrations of malignant cells to enhance cancer cells survival, invasion, and dissemination. (
  • Sickle cell disease is an inherited blood disorder that shortens red blood cell survival, causing anaemia-often called sickle cell anaemia. (
  • Among patients with sickle cell disease (SCD), pediatric survival rates continue to improve. (
  • Western blot analysis of extracts from HeLa, NIH/3T3 and C6 cells untreated, staurosporine-treated (3hrs, 1 μM in vivo) or cytochrome c-treated (1hr, 0.25 mg/ml in vitro), using Caspase-3 Antibody #9662 (upper) or Cleaved Caspase-3 (Asp175) Antibody (lower). (
  • Ultraviolet light-emitting diode irradiation-induced cell death in HL-60 human leukemia cells in vitro. (
  • The programmed cell death (PCD) of xylem has been analyzed in detail in an in vitro system of Zinnia elegans , in which mesophyll cells of Zinnia transdifferentiate into xylem vessels commonly called as tracheary elements in a semi-synchronized manner [ 3 ]. (
  • In vitro fluorescence microscopy of several cancer model cell-lines (MDA-MB-213, Jurkat E6-1) showed that the Zn-DPA liposomes strongly stain dead and dying cancer cells that were treated with the anticancer agent etoposide. (
  • The treatment has been tested on various types of cancer cells in vitro and in vivo with positive results. (
  • Autoschizis: A Mode of Cell Death of Cancer Cells Induced by a Prooxidant Treatment In Vitro and In Vivo. (
  • IMSEAR at SEARO: Sodium butyrate modulates pRb phosphorylation and induces cell death in human vestibular schwannomas in vitro. (
  • The researchers found higher death rates among people with SCD than previous estimates that used other methods. (
  • The researchers then compared these death rates to those of African Americans and to the general population in the corresponding states. (
  • By using multiple diverse sources of data, the researchers were able to gather information about people who may not have been included in previous studies, such as those who received care outside of sickle cell care centers or those who may have had limited or no access to regular medical care. (
  • Many challenges exist for researchers that work to accurately estimate the number of deaths among people with SCD. (
  • Because the researchers who conducted the study described here used multiple sources of information, they were able to gain a more accurate picture of age at death among people with SCD. (
  • A fruit fly model of a rare, neurodegenerative disease is helping researchers trace the series of steps that lead to neuronal cell death. (
  • Researchers have found a way to kill cancerous lymphoma cells using a kind of nanoparticle that has a gold particle at its core, says a new study. (
  • Researchers say that the study has open a new way in defeating cancer cells, which is not inhibiting growth or killing the cells, but essentially letting the cancer cells starve themselves to death. (
  • The book is thus of great use to all biologists interested in how cells function in the context of multicellular organisms and will appeal to everyone from undergraduates encountering the topic for the first time to researchers actively working in the field. (
  • To identify these new molecules, a team of researchers led by Dr. Eikan Mishima and Dr. Marcus Conrad, both from the Institute of Metabolism and Cell Death at Helmholtz Munich, along with collaborators from Tohoku University (Japan), University of Ottawa (Canada) and Technical University of Dresden (Germany), systematically studied a number of naturally occurring vitamins, as well as their derivatives. (
  • In addition, since ferroptosis most likely constitutes one of the oldest types of cell death, the researchers hypothesize that vitamin K might be one of the most ancient types of naturally occurring antioxidants. (
  • Researchers at the University of Chicago Medicine Comprehensive Cancer Center and their collaborators were interested in learning how mutant IDH2 drives the development of AML, and how the leukemia cells are able to regulate the production of 2-HG to promote spread and avoid cell death. (
  • Researchers have found that decay of tissues after death can be halted and cell functions restored based on early experiments in pigs that may eventually help increase the number of transplantable human organs. (
  • Adilza Condessa Dode, PhD, one of the engineering researchers as well as the coordinator of the Brazilian study, addresses those who are concerned about cell phone tower radiation and explains the Brazil study does not stand alone. (
  • This discovery suggests that, "the rescue is caused by the effective decrease of the extracellular iron concentration rather than making more iron available to cells," the researchers note. (
  • Hundereds of international researchers will cooperate to map millions of cells in all tissues of thebody. (
  • In experiments performed in mice, researchers report they have identified the cascade of cell death events leading to the physical and intellectual degeneration associated with Parkinson's diseas. (
  • Researchers have estimated that every year, there are 1.3 to 4.0 million cases, and 21 000 to 143 000 deaths worldwide due to cholera. (
  • Dead cells are observed in many developing animal tissues, but the causes of these normal cell deaths are mostly unknown. (
  • Because cells, called phagocytes, can clear dying cells so quickly in the body, it had been difficult to study this process in tissues. (
  • Surprisingly, we identified that vitamin K, including phylloquinone (vitamin K1) and menaquinone-4 (vitamin K2), is able to efficiently rescue cells and tissues from undergoing ferroptosis" Dr. Eikan Mishima, first author of the study explained. (
  • Your cells die, at that point microscopic organisms, creatures, and indeed the body itself digests your organs and tissues. (
  • We used this dataset for in silico transcript profiling of a particular process in the woody tissues of the Populus stem: the programmed death of xylem fibers. (
  • One EST library in POPULUSDB originates from woody tissues of the Populus stem where xylem fibers undergo cell death. (
  • Results suggest that ethylene is perceived in all maize root tissues and cortical-cell-specific PCD is controlled downstream of ethylene perception. (
  • Pyroptosis is a highly inflammatory form of programmed cell death that occurs most frequently upon infection with intracellular pathogens and is likely to form part of the antimicrobial response in myeloid cells. (
  • The purpose of this study was to evaluate the effect of photobiomodulation (PBM) on C2C12 muscle cells exposed to B. jararaca, B. jararacussu, and B. moojeni venoms on events involved in cell death and the release of inflammatory mediators. (
  • Perturbations that enhance or suppress cell death may lead to cancer, neurodegeneration, and inflammatory diseases. (
  • The next phase of Blander's research will be to investigate how the inflammatory conditions of IBD alter cell death and the homeostatic immunosuppressive functions of intestinal phagocytes , in both mouse models and different groups of IBD patients undergoing anti-TNF therapy at the Jill Roberts Center for Inflammatory Bowel Disease at New York-Presbyterian and Weill Cornell Medicine. (
  • In PBMC's and THP-1 cells, W RE proved to effectively modulate antioxidant activity, inflammatory cytokines and cell death. (
  • To elucidate the effect of PHLPP2 removal on inflammatory gene expression, signaling, and cell death levels under conditions that mimic ischemic injury, I performed Western blotting, mRNA analysis, and an ELISA-based cell death assay. (
  • Spinal cord injury initiates a complex series of inflammatory and immune responses including the influx of monocytes, macrophages, T-cells, NK cells and so on, into the injured area. (
  • Cytologic examination of bronchioalveolar lavage (BAL) samples yielded few inflammatory cells. (
  • Macrophage polarization induced by immunogenic cell death was examined using qPCR array. (
  • We demonstrate that histotripsy causes the mechanical destruction of cancer cells and promotes immunogenic cell death, ultimately leading to an anticancer immune response. (
  • In 2009, he joined Dr Marc Gregoire's Laboratory, INSERMU892, Nantes, to study immune response against pleural mesothelioma and innovative strategies to induce Immunogenic cell death of this cancer. (
  • Unlike conventional chemotherapeutics, SCNPs cause immunogenic cell death or ICD. (
  • The inability to clear dying cells has been linked to inflammation and autoimmunity. (
  • We know there is excessive cell death, inflammation and microbial imbalance in IBD, so the prediction is that the immunosuppressive program in phagocytes, associated with natural cell death in the gut epithelium, would be disrupted," Blander said. (
  • For select patients, notably those with high levels of inflammation, a study using stem cells injected into the heart could offer promise-but the study fell short in a key measure important to payers. (
  • The study examined the use of mesenchymal precursor cells (MPCs), which were injected into the heart to target inflammation and treat the worst cases of chronic HF-on top of what can be achieved with guideline-directed medication. (
  • In a composite of time to first event among patients with elevated inflammation were combined, results markedly favored with elevated inflammation, who saw a 45% reduced risk of time to first-event for cardiac death or non-fatal heart attack or stroke (HR 0.551, 95% CI: 0.345-0.876, P = .012). (
  • Severe acute pancreatitis is characterized by acinar cell death and inflammation. (
  • Alzheimer's disease is the most common type of neurodegenerative disorder oriented dementia which is regulated by chronic inflammation in brain cells. (
  • A further study demonstrated the pathogenic role of anti-NS1 antibodies on endothelial dysfunction by inducing cell death and inflammation. (
  • Cell viability was evaluated using the WST-8 assay. (
  • In the cell viability assay, lidocaine decreased cell viability in a dose-dependent manner, and NTP did not affect cell viability. (
  • Three analogous and reduced the viability of the gonococci that were capable of infecting HeLa cells. (
  • To assay for bacterial invasion and measure the viability of the gonococci that were capable of Ampiroxicam infecting host cells, cell monolayers were washed with PBS, followed by the addition of 100 l of PBS supplemented with 0.5 mM EDTA to each well. (
  • In this method, Evan's blue, an azo dye, is used to assay for cell viability. (
  • Effects of violacein on the cell viability of CHO-K1, MRC-5 and HeLa cells, as determined by the Trypan blue dye exclusion method after exposure to 0.75-6 μM violacein for 24 ( a ) and ( b ) 48 h. (
  • Cell viability was measured by MTT assay. (
  • It occurs as a result of repeated stimulation of specific T-cell receptors (TCR) and it helps to maintain the periphery immune tolerance. (
  • This effect likely occurs because pre-B ALL cells are in an early developmental B-cell stage, where B cells are subject to central tolerance checkpoints for removal of autoreactive clones 15 . (
  • Programmed cell death has been found in many multicellular organisms and occurs as a part of normal development as well as in pathological processes associated with some diseases. (
  • Neural and pancreatic beta cell death occurs in a variety of ways. (
  • Considerable sculpting of the embryo occurs by cell deaths during organogenesis, and appropriate cell numbers, especially in the CNS and in the immune system, are generated by massive overproduction of cells and selection of a few, with death of the rest. (
  • Programmed cell death also occurs in plants in response to external factors, such as avirulent pathogens, giving rise to the so-called hypersensitive response (HR) and in response to shortening daylength - manifested in the senescence of leaves. (
  • AMR occurs when bacteria, viruses, fungi and parasites change over time and no longer respond to medicines making infections harder to treat and increasing the risk of disease spread, severe illness and death. (
  • They defined RIP kinase as a mediator of necrotic cell death in cones. (
  • Our results show that a combination of necrotic cell death, accompanied by apoptotic features such as rapid DNA fragmentation, lead to the loss of these cells. (
  • and cell shrinkage. (
  • HR cell death is usually fast and it shares certain features with the apoptotic death of animal cells, such as nuclear shrinkage and fragmentation of DNA into oligonucleosomal multiples of 180-bp fragments [ 8 ]. (
  • Like mammalian cells, Leishmania parasites also show typical features of apoptotic death, like cell shrinkage, nuclear condensation and DNA damage in response to heat stress, serum deprivation and a range of antileishmanial drugs. (
  • Activation-induced cell death (AICD) is a programmed cell death caused by the interaction of Fas receptor (Fas, CD95)and Fas ligand (FasL, CD95 ligand). (
  • Background: To evaluate the changes of immune environment of distant tumors after combined microwave ablation (MWA) and anti- programmed death receptor - 1 (anti-PD-1) therapy, and assess the changes of systemic immune response. (
  • Genistein is also known as an estrogen receptor agonist that can antagonize the multiplication of breast cancer cells due to estradiol exposure ( 14 ). (
  • This is a multi-center, open-label, first-in-human Phase 1 study evaluating the anti-programmed death receptor 1 (anti-PD-1) antibody dostarlimab (also known as TSR-042) n participants with advanced solid tumors who have limited available treatment options. (
  • or 500 mg, 50 mg/mL) is a humanized monoclonal antibody that binds with high affinity to PD-1 resulting in inhibition of binding to programmed death receptor ligands 1 and 2 (PD-L1 and PD-L2). (
  • The receptor tyrosine kinase (RTK) encoding RET was previously identified as a putative downstream target gene to FUS-DDIT3 and here we show that cultured MLS cells expressed phosphorylated RET together with its ligand Persephin. (
  • Human cancer cell lines which vary in their expression levels of Tf receptor (TfR/CD71) and PAI-2 target, receptor bound urokinase (uPA) selectively internalized the conjugates. (
  • H9c2 cardiomyocytes were treated ±0.1 mM PA, the adiponectin receptor agonist AdipoRon, or the antioxidant MnTBAP then assays to analyze reactive oxygen species (ROS) production and cell death were conducted. (
  • Gain and loss of function studies suggested S1P secretion and autocrine receptor activation mediated the effect of AdipoRon to attenuate PA-induced ROS production and cell death. (
  • Surprisingly, a strong hypersensitive response (HR) cell death was observed when soybean MAPK KINASE KINASE1 ( GmMEKK1 ), a homolog of Arabidopsis ( Arabidopsis thaliana ) MEKK1 , was silenced. (
  • To have an insight of the fate decision under ER stress in Arabidopsis, we present our data using different experimental systems, from single cell protoplast system to plant leaf tissue system. (
  • We have previously identified transcriptomic changes associated with heat- and senescence-induced PCD in an Arabidopsis cell suspension culture [Plant J. 30 (2002) 431]. (
  • The three of them discussed these shrunken cells and, comparing notes and new data, realized how common this type of death could be, frequently appearing in tumors, mild intoxications, and elsewhere. (
  • Dr. Gang Zhou, author of the study, expressed hope that these findings will help improve immunotherapy treatments by making it easier for T cells to target tumors. (
  • A subsequent application is to use the liposomes to deliver anticancer drugs to tumors and initiate cell death processes that amplify the liposome targeting at later time points in the therapy. (
  • Results of the present study indicated that Na-Bu treatment modulated pRb phosphorylation status and caused apoptotic cell death in VS tumors. (
  • CXCL1 is known to attract specialized immunosuppressive cells, tumor-associated macrophages, which reduce the ability of the human immune system to recognize and destroy cancer cells. (
  • However, when we began to study the same process in mice, we were surprised to see just the opposite effect, and this was mainly due to the immune response of the cells surrounding the tumor. (
  • The process enables selection of fittest cells amongst the parasites within the sandfly vector and within the mammalian cells for necessary control of parasite numbers and for the evasion of immune responses. (
  • Intrinsic Innate Immune Responses Control Viral Growth and Protect against Neuronal Death in an Ex Vivo Model of West Nile Virus-Induced Central Nervous System Disease. (
  • Triggering tumor cells elimination, notably via immune system stimulation. (
  • Our laboratory is studying two new therapeutic strategies to treat this cancer, which are based on the induction of an immunogenic tumor cell death which may induce an anti-tumor immune response. (
  • Amongpreviously reported NLR helpers, NRC1 (NB-LRR proteinrequired for hypersensitive-response (HR)-associated cell death 1)stands out for having been reported as a signaling hub required forthe cell death mediated by both cell surface immune receptors suchas Cf-4, Cf-9, Ve1 and LeEix2, as well as intracellular immunereceptors, namely Pto, Rx and Mi-1.2 (Gabriels et al. (
  • Many factors, produced or de novo synthesized by immune, stromal, or malignant cells, acting in a paracrine and autocrine fashion, remodel TME and the adaptive immune response culminating in metastasis. (
  • c) acquisition by cancer cells of aberrant immune-phenotypic traits (NT5E/CD73, CD68, and CD163) that enhance the interactions among TME components through the production of immune-suppressive mediators. (
  • In this review we summarize results and suggest new hypotheses that favour the growing impact of tumor-infiltrating immune cells on tumour progression, metastasis, and therapy resistance. (
  • It is well established that the metastatic spread is promoted by communications between tumour and immune cells via the secretion of cytokines, growth factors, and proteases that remodel the tumour microenvironment (TME) [ 12 , 13 ]. (
  • Exposure to aminoglycoside antibiotics can lead to the generation of toxic levels of reactive oxygen species (ROS) within mechanosensory hair cells of the inner ear that have been implicated in hearing and balance disorders. (
  • Reactive oxygen species (ROS) such as peroxide and superoxide are natural byproducts of the metabolism of oxygen, and they play a role in certain cell functions. (
  • We use a combination of membrane and nuclear live stains, ultrastructural analysis and measurement of reactive oxygen species to characterize the events leading to the death of hair cells under these conditions. (
  • These ideas were not ignored, but they hovered quietly, primarily in the thinking of developmental biologists and others aware that cell death was often predictable. (
  • This volume is therefore an essential reference for cell and developmental biologists, cancer biologists, and all who wish to explore recent progress in our understanding of cell death programs. (
  • In the present study, we describe the features of programmed cell death of ovarian follicle cells, occurring during the late developmental stages of oogenesis in the olive fruit fly, Bactrocera oleae and the medfly, Ceratitis capitata. (
  • Recent studies suggest AIF to be a major factor determining caspase-independent neuronal death, emphasizing the central role of mitochondria in the control of physiological and pathological cell demise. (
  • In multicellular organisms, cell death is required for normal development, homeostasis, and the elimination of infected or injured cells. (
  • In multicellular organisms, cell death is the process by which cells cease to function. (
  • They injected into the intestinal walls of these mice a carefully titrated dose of toxin to induce cell death. (
  • Recent studies have shown that nitrosative stress plays an important role in the pathophysiological processes of cell death. (
  • Green (St Jude Children s Research Hospital) provides a comprehensive look at the current understanding of the multilayered processes by which cells in the body die. (
  • Algor mortis and rigor mortis are two processes that occur in the body after death and are used as a way of estimating the time of death when a body is discovered. (
  • Depletion of Microglia in an Ex Vivo Brain Slice Culture Model of West Nile Virus Infection Leads to Increased Viral Titers and Cell Death. (
  • A rat thymus atrophy model was used to access the in vivo cell death targeting capability of Zn-DPA liposomes. (
  • In vivo studies show that SCNPs not only kill cancer cells, but also boost an anticancer immunity. (
  • Additionally, what we still have to prove is that nitrosative stress and not other stresses related to oxygen metabolism disorders affects cell death. (
  • Dr. Marcus Conrad, Director, Institute of Metabolism and Cell Death at Helmholtz Munich Dr. Eikan Mishima, Senior Scientist, Institute of Metabolism and Cell Death at Helmholtz Munich. (
  • In a study published in Cell Metabolism , a research team at Augusta University examined the effects of adaptive T cell therapy on the metabolism of cancer cells. (
  • An international team of investigators found that abnormal iron metabolism and hypersensitivity to free extracellular iron play an important role in oligodendrocyte death. (
  • Lymphocyte selection by starvation: glucose metabolism and cell death. (
  • As Tidball and Albrecht later observed, an entire organ could disappear in 20 days with only 3 or 4 dying cells being visible in any given tissue section. (
  • In our initial studies, inhibiting necroptosis in PDAC cells increased their ability to grow in tissue culture. (
  • An aggregation of cells performing similar functions is called a tissue. (
  • Programmed cell death is a regulatory process to maintain the appropriate number and age of cells present within a tissue. (
  • Yet circulation was restored and organs in the deceased pigs that received OrganEx treatment appeared functional at the level of cells and tissue. (
  • In summary, liposomes coated with multiple copies of Zn-DPA targeting groups are effective cell death imaging agents for fluorescence microscopy and they can target dead and dying tissue in living animals. (
  • Tissue and Cell, 36: 197-209. (
  • It is essential for maintaining tissue homeostasis and eliminating potentially harmful cells. (
  • Localization of gra-b in TUNEL positive neurons indicates that gra-b might play a crucial role in neuronal death and contributes to the pathophysiology of spinal cord injury. (
  • 4156 - Triple blockade of EGFR, MEK and PD-L1 as effective antitumor treatment in PD-L1 overexpressing, MEK inhibitor resistant colon cancer cells. (
  • Furthermore, we show that a catalytic-site proteasome inhibitor causes cell death independently of p53. (
  • Up-regulation of inhibitor receptors, such as programmed death-1 (PD-1) and its ligand, PD-L1, are important inhibitors of T-cell function. (
  • Treatment with RET specific kinase inhibitor Vandetanib failed to reduce RET phosphorylation and inhibit cell growth, suggesting that other RTKs may phosphorylate RET. (
  • Treatment of cultured MLS cells with HSP90 inhibitor 17-DMAG, caused loss of RET and ERBB3 phosphorylation and lead to rapid cell death. (
  • Cell death stage dictates the immunogenicity of ferroptotic cancer cells," in Virtual IMMUNOLOGY2021 , 2021, vol. 206, no. (
  • These results place BAX downstream of metabolic changes, changes in mRNA levels, and increased phosphorylation of c-Jun, yet upstream of the activation of caspases and indicate that BAX is required for apoptotic, but not excitotoxic, cell death. (
  • In wild-type cells, Boc-Asp-FMK and ZVAD-FMK, general inhibitors of caspases, blocked cleavage of DEVD-AMC and blocked the increase in TdT-mediated dUTP nick end labeling (TUNEL) positivity. (
  • Light stress activated caspases, calpain 2, and cathepsin D independently and led to the demise of the cell. (
  • During development, Notch signaling plays an important role in the decision to become either a hair cell or supporting cell, by mediating lateral inhibition. (
  • Recently, we observed that ouabain kills epithelial and endothelial cells via its interaction with Na(+), K(+) -ATPase, but independently of inhibition of Na(+), K(+) -ATPase-mediated ion fluxes and inversion of the [Na(+)](i)/[K(+)](i) ratio. (
  • The rescue of ouabain-treated C7-MDCK cells was also detected under selective intracellular acidification caused by inhibition of Na(+)/H(+) exchanger. (
  • They also suggest that the protective action of acidification is mediated by de novo expression of genes involved in inhibition of the cell death machinery. (
  • This study estimated death rates among people with sickle cell disease (SCD) by matching up data from studies that monitor all people with SCD in a population with state death records. (
  • Read more about the sickle cell disease mortality study here external icon . (
  • Sickle Cell Disease is a group of genetic (inherited) red blood cell disorders. (
  • In someone who has SCD, the red blood cells become hard and sticky, and they look like a C-shaped farm tool called a "sickle. (
  • The sickle cells die early, which causes a constant shortage of red blood cells. (
  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been documented to cause vasoocclusive crisis and acute chest syndrome in patients with sickle cell anemia ( 1 ). (
  • Lomé - African health ministers today launched a campaign to ramp up awareness, bolster prevention and care to curb the toll of sickle cell disease, one of the most common illnesses in the region but which receives inadequate attention. (
  • More than 66% of the 120 million people affected worldwide by sickle cell disease live in Africa. (
  • Poor blood oxygen levels and blood vessel blockages in people with sickle cell disease can cause extreme pain in the back, chest, hands and feet as well as severe bacterial infections. (
  • In the African region, 38 403 deaths from sickle cell disease were recorded in 2019, a 26% increase from 2000. (
  • The burden of sickle cell stems from low investment in the efforts to combat the disease. (
  • Many public health facilities across the region lack the services for prevention, early detection and care for sickle cell disease. (
  • The campaign, launched at a side event on enhancing advocacy on sickle cell disease during the Seventy-second World Health Organization (WHO) Regional Committee for Africa-the region's flagship health meeting, aims to shore up political will and engagement as well as financial resources for sickle cell disease prevention and control across the region. (
  • Most African countries do not have the necessary resources to provide comprehensive care for people with sickle cell disease despite the availability of proven cost-effective interventions for prevention, early diagnosis and management of this condition," said Dr Matshidiso Moeti, WHO Regional Director for Africa. (
  • Additionally, data collection for sickle cell disease is not included in most national population-wide surveys. (
  • Although most patients with rare diseases like sickle cell disease (SCD) are treated in the primary care setting, primary care physicians may find it challenging to keep abreast of medication improvements and complications associated with treatment for rare and complex diseases. (
  • Many people with sickle cell disease (SCD) are healthier and living longer thanks in part to research led and supported by the National Institutes of Health (NIH). (
  • If we could cure sickle cell disease in a safe and effective way, such as a pill that can reverse the disease, that would be a home run. (
  • In order to have SCD, a person must inherit the sickle cell trait from their birth mother, father, or both parents. (
  • Many people don't realize the severity of this disease,' says John Tisdale, M.D., senior investigator at NIH's National Heart, Lung, and Blood Institute, who leads NIH sickle cell disease research along with Griffin Rodgers, M.D., director of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). (
  • Though counterintuitive, our data show that genetic hyperactivation of PI3K/AKT-signaling or blocking the activity of the inhibitory phosphatase SH2-containing-inositol-5′-phosphatase-1 (SHIP1) induces acute cell death in CLL cells. (
  • AML is a cancer of the blood cells that can occur when immature white blood cells, cells that normally fight infection, acquire certain genetic mutations that cause them to multiply rapidly and build up the bone marrow and blood. (
  • The timing, identity, and genetic control of specific cells that die have been well documented in Caenorhabditis , but in other embryos the stochastic nature of the deaths limit our ability to do more than identify the regions in which cells will die. (
  • It is controlled by one or more genetic programs that kill the targeted cell. (
  • We demonstrated that genetic deletion of Pac abolished the proton-activated Cl − currents in mouse neurons and also attenuated the acid-induced neuronal cell death and brain damage after ischemic stroke. (
  • She is now researching the general genetic causes of ageing and has shown, amongst other things, that our stem cells gather more mutations during our lives than previously known. (
  • ABSTRACT Cell death is prominent in gametogenesis and shapes and sculpts embryos. (
  • PROJECT SUMMARY/ABSTRACT Glaucoma is a disease characterized by visual field loss as a result of the death of retinal ganglion cells. (
  • abstract = "The signaling cascade resulting in the death of several types of cells treated with ouabain or other cardiotonic steroids (CTS) remains poorly understood. (
  • Immunofluorescent analysis of HeLa cells using α-Tubulin (DM1A) Mouse mAb #3873 (red) and Phospho-Histone H3 (Ser10) (D2C8) XP ® Rabbit mAb #3377 (green). (
  • Confocal immunofluorescent analysis of HeLa cells, untreated (left) or treated with Staurosporine (1 μM) #9953 and Z-VAD (50 μM) for 3 hours (right), using Cytochrome c (6H2.B4) Mouse mAb (green). (
  • HeLa cells (3x10 5 cell/ml) were treated with various concentrations of CCCP for 15 minutes prior to labeling with 200 nM TMRE. (
  • To test the effect of the QAS on infection, HeLa cells seeded the day before on 24-well plates were equilibrated in HBSS and incubated at 37C with for 1 h at an MOI of 5, in the presence or absence of each of the QAS. (
  • The ability of Zn-DPA liposomes to target a chemical model of the PS cell death biomarker was assessed using a fluorescence quenching assay. (
  • An assay was developed wherein 661W cells, a cone photoreceptor cell line, were stressed with light and percentage of surviving cells was determined. (
  • The degree of cell death was established using the MTT assay. (
  • A blood film for the patient showed normochromic normocytic erythrocytes and a few hemighost cells ( Figure , panel A). A 2-stage G6DP assay confirmed G6DP deficiency (0.8 IU/g hemoglobin). (
  • Furthermore, the cone photoreceptor cell death was rescued by RIP3 deficiency and by pharmacological treatment with RIPkinase inhibitors. (
  • We searched for new inhibitors of apoptotic cell death by testing existing collections of P element insertion lines for their ability to enhance a small-eye phenotype associated with eye-specific expression of the Drosophila cell death activator Reaper. (
  • To specifically determine the mechanistic role of S1P, gain and loss of function studies were conducted with adding S1P to cells or the inhibitors THI and SKI-II, respectively. (
  • These strategies are (1) the use of epigenetic drugs such as hypomethylating drugs and/or histone deacetylase inhibitors, and (2) the use of oncolytic virus, such as the vaccine attenuated strain of Measles virus, which kills specifically tumor cells. (
  • and Chemical Screening to screen inhibitors or activators of certain types of cell death. (
  • The hope was that a single injection of healthy stem cells from a donor would reduce the number of trips to the hospital and the number of major cardiovascular (CV) events, such as heart attacks or strokes. (
  • The stem cell treatment did reduce non-fatal heart attack and strokes by 65%, and reduced CV death. (
  • Our findings indicate stem cell therapy may be considered for use in addition to standard guideline therapies. (
  • For reduction of risk of non-fatal heart attack or non-fatal stroke, results favored the stem cell treatment, with HR 0.346 (95% CI: 0.180-0.664, P = .001). (
  • Do stem cells grow better in space? (
  • I must confess that this cartoon about stem cells is my favorite of the week. (
  • As you scientists know, stem cells can grow into anything in any animal. (
  • You can take a stem cell from the eyeball of an earthworm and put it into a human embryo in the foot department and it will become a foot. (
  • Targeting EYA2 tyrosine phosphatase activity in glioblastoma stem cells induces mitotic catastrophe. (
  • From these skin cells, investigators generated induced pluripotent stem cell lines. (
  • However, deleterious effects of these agents have been reported [ 9 - 12 ], especially damaging effects on chondrocytes, fibroblasts, tenocytes, and human mesenchymal stem cells [ 1 , 13 - 15 ]. (
  • Now we can take the patient's own bone marrow, use an engineered virus that carries genes to the bone marrow, and give repaired bone marrow stem cells back to the patient so that healthy bone marrow cells can grow,' Dr. Tisdale says. (
  • Methods: Human keratinocytes (HEKa), and mouse embryonic fibroblasts (MEF) from the NC/Nga dermatitis prone mouse strain were used to investigate the induction of Th2-promoting cytokines (IL-33 and TSLP) and cell death by S. aureus. (
  • The main aims of this thesis were 1) to provide evidence that ZOU regulates endosperm cell death and 2) to test whether ZOU function in controlling endosperm cell death could be separated from that in embryonic epidermal cuticle development. (
  • To achieve this goal, 1) TUNEL assays were performed in the seeds to confirm the zou endosperm cell death phenotype, 2) ALE1 expression in the ESR in zou mutants was rescued using the ZOU-independent AtSUC5 promoter to investigate whether one or both of zou phenotypes were complemented, 3) Candidate ZOU target genes were validated and characterized to determine their functions in endosperm cell death and/or embryonic epidermal cuticle development. (
  • In conclusion, ZOU has independent roles in endosperm cell death and embryonic epidermal cuticle development. (
  • Macrophages, one kind of phagocyte, expressed genes that help process the increased lipid and cholesterol load they acquired from dying cells . (
  • Skin cells are functional parts of human organisms. (
  • He thought that if he wanted to observe organ development and cell death, he cannot use unicellular models like yeast and bacteria since it is very difficult to study organ development and the interplay between different cells in such organisms. (
  • Photostatins modulate microtubule dynamics with a subsecond response time and control mitosis in living organisms with single-cell spatial precision. (
  • however, studies over the past years have shown that single celled organisms such as Leishmania can also undergo programmed cell death. (
  • It is the most common mode of cell death in cancer cells exposed to ionizing radiation and many other anti-cancer treatments. (
  • However, when the particle attaches itself to the cancer cells, it blocks the cholesterol from entering the cell and actually removes all the fat from the cell, thus letting the cancer cell starve to death. (
  • Although 2-HG can drive the development of cancer, at high concentrations it becomes toxic, killing cancer cells. (
  • Ferroptosis, an iron-dependent form of cell death leading to lipid peroxidation in cells, is currently actively studied but whether ferroptotic cancer cells are immunogenic is unknown. (
  • However, many cancer cells with apoptotic defects are resistant to treatment with TRAIL alone, limiting its potential as an anticancer therapeutic. (
  • But while high levels of ROS can kill normal cells and damage DNA, energy-hungry cancer cells consume greater quantities of ROS. (
  • Cancer cells must turn off this internal system in order to proliferate. (
  • The metastatic process is a multistep event that entails cancer cells to escape from the primary tumour, survive in the circulation, seed at distant sites, and grow [ 14 , 15 ]. (
  • Consistent with this idea, driver gene mutations ( APC , TP53 , SMAD4 , PIK3CA , and KRAS ) along with genomic and epigenomic instability determine tumour initiation, while the interaction of cancer cells with microenvironmental stimuli provided by nontransformed cells is needed to evolve towards a metastatic cancer [ 15 - 19 ]. (
  • The anticancer potential of tanshinones, bioactive constitutes in Danshen, have also been reported previously, in particular in colon cancer cells and mouse xenograft models [6, 7] . (
  • et al also demonstrated the cytotoxicity of cryptotanshinone and dihydrotanshinone in various colon cancer cells, in particular in those cells with multidrug resistance [9, 10] . (
  • However, the anticancer potential of cryptotanshinone on prostate cancer cells has not been well-studied yet. (
  • The study shows that NaCl nanoparticle s (SCNPs) but not salts are highly toxic to cancer cells. (
  • When dissolved inside cancer cells, SCNPs cause a surge of osmolarity and rapid cell lysis. (
  • ferroptosis, an iron-dependent form of cell death and Wallerian degeneration. (
  • Souma and colleagues conducted studies in mice focusing on a form of cell death called ferroptosis, which was only recently discovered. (
  • In males, however, the sex hormone testosterone reduces the activity of NRF2, thus promoting ferroptosis and undermining cell resiliency in kidney injury. (
  • Further experiments showed that chemically activating NRF2 protected male kidney cells from ferroptosis, demonstrating that NRF2 could be a potential therapeutic target to prevent failed renal repair after acute kidney injury. (
  • cells dying by ferroptosis "+" vitamin K efficiently prevents ferroptosis. (
  • In conclusion, these results indicate that induction of ferroptosis in cancer might be another option to overcome cell death resistance and enhance the efficacy of anti-cancer therapy. (
  • Here we show that a sustained increase in cytosolic Ca2+ is a hallmark of ferroptosis that precedes complete bursting of the cell. (
  • Importantly, Ca2+ fluxes during ferroptosis induce the activation of the ESCRT-III-dependent membrane repair machinery, which counterbalances the kinetics of cell death and modulates the immunological signature of ferroptosis. (
  • Almost 20 years ago a new form of lytic cell death - called pyroptosis - was identified that contrasts starkly with apoptotic cell death. (
  • During pyroptosis, cells enlarge and balloons within minutes, until it explodes. (
  • Thus, our results show that very modest intracellular acidification is sufficient to inhibit the Na(+) (i)/K(+) (i)-independent death signal triggered in epithelial and endothelial cells by CTS. (
  • Upon constitutively strong autoantigen binding, B cells undergo an active negative selection process that eliminates or inactivates autoreactive B-cell clones 3 . (
  • The fertilized egg will then undergo mitosis which will cause a rapid exponential increase in the number of cells in the developing embryo. (
  • Dissociated cerebellar granule cells maintained in medium containing 25 mM potassium undergo an apoptotic death when switched to medium with 5 mM potassium. (
  • Your assistance in this effort will help prevent silicosis-related death and disease, a national goal for health promotion and disease prevention stated in Healthy People 2000 [PHS 1990]. (
  • Specifically, the study tried to ascertain which genes are expressed by phagocytes after the uptake of dead cells . (
  • Through a series of experiments, they found that several of the genes modulated up or down in phagocytes bearing dead cells overlapped with the same genes that have been associated with susceptibility to IBD. (
  • Dendritic cells, another type of phagocyte, activated genes responsible for instructing the development of regulatory CD4 T cells, a class of suppressive white blood cells . (
  • Because the same genes that confer susceptibility to IBD were modulated in response to apoptotic cell sampling, the research indicates that a disruption of the phagocytes' immunosuppressive response would have consequences for homeostasis - or stable conditions - in the gut. (
  • Cell-death genes are expressed in (
  • Genome-wide expression analysis revealed a constitutive induction of salicylic acid-related (SA) pathogen defence and cell death genes in over-expression lines. (