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.
... dendritic cells and natural killer cells. TWEAK can induce apoptosis via multiple pathways of cell death in a cell type- ... "Dual role for TWEAK in angiogenic regulation". Journal of Cell Science. 115 (Pt 2): 267-74. PMID 11839778. Kaplan MJ, Lewis EE ... and Fas ligand mediate monocyte death induced by autologous lupus T cells". Journal of Immunology. 169 (10): 6020-9. doi: ... "Multiple pathways of TWEAK-induced cell death". Journal of Immunology. 168 (2): 734-43. doi:10.4049/jimmunol.168.2.734. PMID ...
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At the same time, CHOP-induced apoptosis can also trigger cell death by inhibiting the expression of cell cycle regulatory ... The regulation of CHOP expression could be a potential approach to affecting cancer cells through the induction of apoptosis. ... Death receptor-mediated apoptosis occurs via activation of death ligands (Fas, TNF, and TRAIL) and death receptors. Upon ... "ER stress-induced cell death mechanisms". Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. 1833 (12): 3460-3470. ...
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... and HIV-1 gp120 induced neuronal cell death". Neurotoxicology. 19 (4-5): 683-8. PMID 9745929. Leslie CC (2004). "Regulation of ... Cell Biol. 82 (1): 1-17. doi:10.1139/o03-080. PMID 15052324. Mavoungou E, Georges-Courbot MC, Poaty-Mavoungou V, et al. (1997 ... types in human airway epithelial cells induced by tumor necrosis factor-alpha and IFN-gamma". J. Interferon Cytokine Res. 22 (9 ...
Li Y, Wang H, Lu H, Hua S (2016). "Regulation of Memory T Cells by Interleukin-23". International Archives of Allergy and ... Cell Death & Disease. 10 (4): 315. doi:10.1038/s41419-019-1540-2. PMC 6453898. PMID 30962426. ... Innate lymphoid cells and also gamma delta T cells also produce IL-23. B cells produces IL-23 through BCR signaling. Secretion ... Similar effects as IL-23 has on Th17 cells were described on type 3 innate lymphoid cells which actively secrete Th17 cytokines ...
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... and HIV-1 gp120 induced neuronal cell death". Neurotoxicology. 19 (4-5): 683-8. PMID 9745929. Feng Y, Walsh CA (June 2001). " ... "Protein-protein interactions, cytoskeletal regulation and neuronal migration". Nature Reviews. Neuroscience. 2 (6): 408-16. doi ... and that which is synthesized de novo by plaque inflammatory cells (macrophages, T cells, mast cells)." It is used as a marker ... It is an enzyme produced by inflammatory cells and hydrolyzes oxidized phospholipids in LDL. Lp-PLA2 is platelet-activating ...
This cell death is very rapid Greene ER, Huang S, Serhan CN, Panigrahy D (November 2011). "Regulation of inflammation in cancer ... prostate cancer cell population harbors self-renewing long-term tumor-propagating cells that resist castration". Cell Stem Cell ... LNCaP cells express AR, but PC-3 and DU-145 cells express very little or no AR. The proliferation of LNCaP cells is androgen- ... In particular, arachidonate 5-lipoxygenase inhibitors produce massive, rapid programmed cell death in prostate cancer cells. ...
July 2008). "Itch: a HECT-type E3 ligase regulating immunity, skin and cancer". Cell Death and Differentiation. 15 (7): 1103-12 ... Aki D, Zhang W, Liu YC (July 2015). "The E3 ligase Itch in immune regulation and beyond". Immunological Reviews. 266 (1): 6-26 ... ITCH serves as a paradigm for our understanding of the regulation of the ubiquitylation machinery by direct protein ... Itchy mice develop a severe immunological phenotype after birth that includes hyperplasia of lymphoid and hematopoietic cells, ...
Ghosh Roy S, Sadigh B, Datan E, Lockshin RA, Zakeri Z (May 2014). "Regulation of cell survival and death during Flavivirus ... "Cell death and virus infection - a short review". 20 Years of Cell Death. 1 (1): 292-325. doi:10.13140/RG.2.2.35359.97447. ... virus replication and protection from cell death require ER stress (PERK) pathway activation". Cell Death & Disease. 7 (e2127 ... "Flavivirus NS4A-induced autophagy protects cells against death and enhances virus replication". The Journal of Biological ...
"Regulation of cell death protease caspase-9 by phosphorylation". Science. 282 (5392): 1318-21. doi:10.1126/science.282.5392. ... CAR T cells). CAR T cells are genetically modified T cells that exhibit cytotoxicity to tumor cells. Evidence shows that CAR T ... This, in turn, induces expression of caspase-9, which triggers cell death of the CAR T cells. Through alternative splicing, ... Mace PD, Riedl SJ (December 2010). "Molecular cell death platforms and assemblies". Current Opinion in Cell Biology. 22 (6): ...
FOXO1 plays a role in the protection of cells from oxidative stress. It seems to promote cell death when oxidative stress is ... resulting in apoptosis of the beta cells. FOXO1 activation plays a role in cell cycle progression regulation. The transcription ... Further, it was revealed that DNA damage-induced cell death in p53-deficient and p53-proficient cells was reduced when human ... It suppresses survival of tumor cells by inducing apoptosis in prostate cancer cells and glioma cells by upregulating the ...
Chestnut BA, Chang Q, Price A, Lesuisse C, Wong M, Martin LJ (November 2011). "Epigenetic regulation of motor neuron cell death ... The surviving cells reaffirmed that the loss of DNMT1 led to hypomethylation in the neural cell genome. These cells also ... Furthermore, over-expression of this de novo methyl transferase is also implicated in cell death of motor-neuron analogs. A ... Studies have shown that accumulation of manganese leads to dopaminergic cell death and consequently plays a role in the onset ...
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This cell death is very rapid. *^ a b c Greene ER, Huang S, Serhan CN, Panigrahy D (November 2011). "Regulation of inflammation ... rapid programmed cell death in prostate cancer cells.[186][187][188]. Cancer models. Scientists have established a few prostate ... lo Prostate Cancer Cell Population Harbors Self-Renewing Long-Term Tumor-Propagating Cells that Resist Castration". Cell Stem ... LNCaP cells express androgen receptor (AR), but PC-3 and DU-145 cells express very little or no AR. AR, an androgen-activated ...
Cell Death and Differentiation. 17 (4): 689-98. doi:10.1038/cdd.2009.174. PMID 19911008. Lua T, Yang M, Huang D, Wei H, Ozer GH ... complex role in cell regulation]". Pathologie-Biologie. 50 (3): 204-11. doi:10.1016/s0369-8114(02)00289-4. PMID 11980335. Garg ... Cell-type-specific phosphorylation is also observed for RELA. Multiple-site phosphorylation is common in endothelial cells, and ... RELA is expressed alongside p50 in various cell types, including epithelial/endothelial cells and neuronal tissues. RELA is one ...
Rudin CM, Thompson CB (1997). "Apoptosis and disease: regulation and clinical relevance of programmed cell death". Annual ... Every cell division and cell death in the development of C. elegans from embryo to adult has been studied and documented to ... Hengartner MO, Ellis RE, Horvitz HR (April 1992). "Caenorhabditis elegans gene ced-9 protects cells from programmed cell death ... When the cell receives an apoptotic signal via a receptor commonly referred to as a "death receptor", the protein EGL-1 is ...
... anandamide and the regulation of mammalian cell apoptosis". Cell Death & Differentiation. 10 (9): 946-955. doi:10.1038/sj.cdd. ... Essential fatty acids play an important role in the life and death of cardiac cells. Additionally, essential fatty acids are ... Arachidonic acid is the major precursor of prostaglandins, leukotrienes that play a vital role in cell signaling, and an ... Landmark K, Alm CS (November 2006). "[Alpha-linolenic acid, cardiovascular disease and sudden death]". Tidsskrift for den ...
Shen J, Tower J (December 2009). "Programmed cell death and apoptosis in aging and life span regulation". Discovery Medicine. 8 ... Mutations of the cell pathway can either promote cell death or disallow cell death creating a huge amount of disease in the ... Genetic and biochemical abnormalities within a cell normally trigger programmed cell death to rid the body of irregular cell ... Riedl SJ, Salvesen GS (May 2007). "The apoptosome: signalling platform of cell death". Nature Reviews. Molecular Cell Biology. ...
"Cell Death and Diseases of the Nervous System". Cell Death and Diseases of the Nervous System. ISBN 0896034135. "Cell Death and ... "Transcriptional regulation of survival and death in neurons". His studies have helped identify strategies for limiting neuronal ... "Cell Death and Diseases of the Nervous System, edited by Vassilis E. Koliatsos and Rajiv R. Ratan". Retrieved 12 ... He co-edited the 1999 book Cell Death and Diseases of the Nervous System and wrote two chapters in it. It was reviewed by Acta ...
positive regulation of programmed cell death. • negative regulation of apoptotic process. • response to glucocorticoid. • ... positive regulation of B cell proliferation. • negative regulation of cell growth. • cell cycle arrest. • response to ... positive regulation of cell death. • response to organic cyclic compound. • negative regulation of cyclin-dependent protein ... regulation of mitotic cell cycle. • intestinal epithelial cell maturation. • cellular response to ionizing radiation. • cell ...
Cell Death & Disease. 9 (11): 1-10. doi:10.1038/s41419-018-1129-1. Ge, Tongtong; Fan, Jie; Yang, Wei; Cui, Ranji; Li, Bingjin ( ... July 1995). "Effects of the obese gene product on body weight regulation in ob/ob mice". Science. 269 (5223): 540-3. doi: ... Cell Death & Disease. 9 (11): 1-10. doi:10.1038/s41419-018-1129-1. ISSN 2041-4889. Gavello, Daniela; Carbone, Emilio; Carabelli ... June 2010). "A new missense mutation in the leptin gene causes mild obesity and hypogonadism without affecting T cell ...
2002). "Inflammatory cytokine regulation of TRAIL-mediated apoptosis in thyroid epithelial cells". Cell Death Differ. 9 (3): ... of dendritic cells leads to up-regulation of cellular FLICE-inhibitory protein and concomitant down-regulation of death ligand- ... 2003). "TNF-related apoptosis-inducing ligand death pathway-mediated human beta-cell destruction". Diabetologia. 45 (12): 1678- ... 2000). "Mechanisms of resistance of normal cells to TRAIL induced apoptosis vary between different cell types". FEBS Lett. 482 ...
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... s in cell cycle proliferation and cell death Ornithine Decarboxylase: Expression and regulation in rat brain and in ... in the regulation of polyamine analogue-induced growth inhibition and cell death in human breast cancer cells". Cancer Biology ... In addition, they are directly involved in regulation of programmed cell death. Polyamines promote homologous recombination (HR ... Moschou, PN; Roubelakis-Angelakis, KA (Nov 11, 2013). "Polyamines and programmed cell death". Journal of Experimental Botany. ...
Ito S, Greiss S, Gartner A, Derry WB (Feb 2010). "Cell-nonautonomous regulation of C. elegans germ cell death by kri-1". ... "KRIT-1/CCM1 is a Rap1 effector that regulates endothelial cell cell junctions". The Journal of Cell Biology. 179 (2): 247-254. ... KRIT1 has been shown to interact with multiple signaling pathways including; ITGB1BP1., reactive oxygen species, cell death, ... CCM2 or CCM3 in affected endothelial cells". Human Molecular Genetics. 18 (5): 911-8. doi:10.1093/hmg/ddn420. PMC 2640205. PMID ...
Kumar, S (2006). "Caspase function in programmed cell death". Cell Death and Differentiation. 14 (1): 32-43. doi:10.1038/sj.cdd ... Riedl, Stefan J.; Shi, Yigong (Nov 2004). "Molecular mechanisms of caspase regulation during apoptosis". Nature Reviews ... Caspases have other identified roles in programmed cell death such as pyroptosis and necroptosis. These forms of cell death are ... 1993). "The C. elegans cell death gene ced-3 encodes a protein similar to mammalian interleukin-1 beta-converting enzyme". Cell ...
Goff SP (August 2003). "Death by deamination: a novel host restriction system for HIV-1". Cell. 114 (3): 281-3. doi:10.1016/ ... and subsequent proteolysis and degradation by the proteasome are important mechanisms in the regulation of the cell cycle, cell ... For instance, in breast cancer cells, a high expression level of the PSMB7 protein suggests a shorter survival than in cells ... Zong C, Gomes AV, Drews O, Li X, Young GW, Berhane B, Qiao X, French SW, Bardag-Gorce F, Ping P (August 2006). "Regulation of ...
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, ... microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression ... Haflidadóttir BS, Bergsteinsdóttir K, Praetorius C, Steingrímsson E (2010). "miR-148 regulates Mitf in melanoma cells". PLOS ... "Differential microRNA regulation of HLA-C expression and its association with HIV control". Nature. 472 (7344): 495-8. Bibcode: ...
Sun T, Han X (2019). "Death versus dedifferentiation: The molecular bases of beta cell mass reduction in type 2 diabetes". ... and inappropriate regulation of metabolism by the central nervous system.[10] However, not all people with insulin resistance ... a type 2 diabetic will have lost about half of their beta cells.[52] Fatty acids in the beta cells activate FOXO1, resulting in ... Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance.[13] Insulin ...
It also contains pacemaker cells and nonpacemaker cells that initiate spontaneous breathing. Research is being conducted on the ... The complex regulation of respiratory rhythm involves the integration of multiple signaling molecules and the activation of ... it has been used as a model to study pathological conditions such as apnea of prematurity and sudden infant death syndrome. The ... It is one of the four cell groups of the Ventral Respiratory Group (VRG). It is hypothesized that the pre-Bötzinger complex is ...
... estate recovery regulations also vary by state. (Federal law gives options as to whether non-long-term-care-related ... T-cell count drops below 200).[76] The Medicaid eligibility policy contrasts with the Journal of the American Medical ... sickle cell anemia; sepsis; congestive heart failure; chronic obstructive pulmonary disease; and complications of devices, ... or in certain patients commencing at an even higher T-cell count. Due to the high costs associated with HIV medications, many ...
The skin consists of a thin outer epidermis with mucous cells and sensory cells, and a connective tissue dermis consisting ... This causes death by respiratory failure leading to cerebral anoxia. No antidote is known, but if breathing can be kept going ... "The Animals (Scientific Procedures) Act 1986 Amendment Regulations 2012". The National Archives. Retrieved 18 February 2015.. ... Other colour-changing cells are reflective iridophores and white leucophores.[93] This colour-changing ability is also used to ...
Cell polarity regulationEdit. In C. crescentus, cell polarity is readily apparent by the assembly of polar organelles and by ... "Aging and Death in an Organism That Reproduces by Morphologically Symmetric Division". PLOS Biology. 3 (2): e45. doi:10.1371/ ... Cell cycle regulation includes feedback signals that pace progression of the cell cycle engine to match progress of events at ... The central feature of the cell cycle regulation is a cyclical genetic circuit-a cell cycle engine-that is centered around the ...
"Loss of Smad3-Mediated Negative Regulation of Runx2 Activity Leads to an Alteration in Cell Fate Determination". Molecular Cell ... General gene knock out of the TGF-β resulted in death. Conditional inactivation of TGF-βr2 of osteochondroprogenitor cells in ... Osteochondroprogenitor cells are progenitor cells that arise from mesenchymal stem cells (MSC) in the bone marrow. They have ... Sox9 blocked osteochondroprogenitor cells were found to express osteoblast marker genes, reprogramming the cells into the ...
Pays, E. (2005). "Regulation of antigen gene expression in Trypanosoma brucei". Trends Parasitol. 21 (11): 517-20. doi:10.1016/ ... the number of cell types or morphology all proposed as possible metrics.[2][3][4] ... Daniel, Chammiran; Behm, Mikaela; Öhman, Marie (2015). "The role of Alu elements in the cis-regulation of RNA processing". ... "Transpositional shuffling and quality control in male germ cells to enhance evolution of complex organisms". Annals of the New ...
"Androgen receptor in human skeletal muscle and cultured muscle satellite cells: up-regulation by androgen treatment". The ... Whereas DHT was equally potent as testosterone at preventing prostate cell death after castration.[18] ... The mesoderm-derived epithelial cells of the sex cords in developing testes become the Sertoli cells, which will function to ... These are Leydig cells. Soon after they differentiate, Leydig cells begin to produce androgens. ...
"sickle cell disease". Genetics Home Reference. Retrieved 2016-11-11.. *^ MD, Kenneth R. Bridges. "How Does Sickle Cell Cause ... of known causes of death in diagnosed patients relating to cardiovascular complications and congestive cardiac failure. Other ... Regulation of gene expression. *Gene regulatory network. *Developmental-genetic toolkit. *Evolutionary developmental biology ... Sickle cell anemia is a genetic disease that causes deformed red blood cells with a rigid, crescent shape instead of the normal ...
Demonstration model of a direct-methanol fuel cell. The actual fuel cell stack is the layered cube shape in the center of the ... Design is limited by a number of factors, including funding, government regulations and safety standards. These constraints ... The 1984 Bhopal disaster in India resulted in almost 4,000 deaths.[citation needed] These incidents, along with other incidents ... The 1974 Flixborough disaster in the United Kingdom resulted in 28 deaths, as well as damage to a chemical plant and three ...
Grummt I. (1999). "Regulation of mammalian ribosomal gene transcription by RNA polymerase I.". Prog Nucleic Acid Res Mol Biol. ... So the two classes of enzyme have arisen independently twice in the early evolution of cells. One line led to the modern DNA ... Structure of eukaryotic RNA polymerase II (light blue) in complex with α-amanitin (red), a strong poison found in death cap ...
For organisms between 10 and 50 microns, such as certain types of phytoplankton, current regulations allow less than 10 cells ... human deaths related to domoic acid poisoning have been prevented because of stringent monitoring programs that arose after a ... only one cell released into the environment could exponentially grow into many thousands of cells over a short amount of time. ... Even though ballast water regulations are in place to protect against potentially invasive species, there exists a loophole for ...
In aged and chemotherapy treated females, oocytes and follicles are depleted by apoptosis (programmed cell death) leading to ... regulation of double-strand break repair via homologous recombination. • DNA metabolic process. • telomere organization. • ... Esophageal squamous cell cancer. Over-expression. 47%. Immunohistochemistry. [24]. Renal cell carcinoma. Under-expression. 100% ... "Association of BRCA1 with Rad51 in mitotic and meiotic cells". Cell. 88 (2): 265-75. doi:10.1016/s0092-8674(00)81847-4. PMID ...
Ultimately, the Danes lost control of Wessex in 1042 on the death of both of Canute's sons. Edward the Confessor retook Wessex ... The Herepath has a characteristic form which is familiar on the Quantocks: a regulation 20 m wide track between avenues of ... Nearby on Lydiard Fields in Lydiard Tregoze is Johnson Matthey Fuel Cells, which in 2002 was the world's first production site ... Farming prospered until it was severely hit by the Black Death which arrived in Dorset in 1348 and quickly spread through ...
"London attack: Death toll rises after body found in Thames". BBC News. 7 June 2017. Retrieved 7 June 2017.. ... she called for tighter internet regulations to "deprive the extremists of their safe spaces online", saying that technology ... Brussels ISIL terror cell. *Insurgency in the North Caucasus. *Islamic State of Iraq and the Levant ... On 7 May 2019, an inquest into the deaths of the victims opened at the Old Bailey in London. Chief coroner Mark Lucraft QC and ...
肥胖症是最常見的可预防性致死因素(英语:Preventable causes of death)之一[37][38][39]。歐美的大規模研究指出身體質量指數(BMI)介於20到25公斤/平方公尺的非吸菸者[36][40]以及BMI介於24-27公斤/平 ... When EMA and FDA decisions conflict: differences in patients or in regulation?. BMJ (Clinical research ed.). 2013-08-21, 347: ... Cell (Review). 2004, 116 (2): 337-50. PMID 14744442. doi:10.1016/S0092-8674(03)01081-
... the sole cell cycle-regulated factor required for regulation of histone mRNA processing, at the end of S phase". Molecular and ... in apoptosis as yeast carrying mutations of this residue are resistant to hydrogen peroxide-induced apoptotic cell death.. ... SLBP levels are controlled by cell-cycle proteins, causing SLBP to accumulate as cells enter S phase and degrade as cells leave ... "Cell. 148 (4): 664-78. doi:10.1016/j.cell.2011.12.029. PMC 3281992. PMID 22325148.. ...
Cell Death Differ. 14 (1): 192-5. doi:10.1038/sj.cdd.4402008. PMID 16841087. Fu J, Yoon HG, Qin J, Wong J (2007). "Regulation ... Cell. 19 (4): 523-34. doi:10.1016/j.molcel.2005.06.027. PMID 16109376. Cottone G, Baldi A, Palescandolo E, Manente L, Penta R, ... Cell. Biol. 23 (14): 4859-69. doi:10.1128/MCB.23.14.4859-4869.2003. PMC 162212 . PMID 12832472. Beausoleil SA, Jedrychowski M, ... Cell. Biol. 27 (13): 4641-51. doi:10.1128/MCB.00857-06. PMC 1951478 . PMID 17452463. FactorBook CCNT2. ...
His work in 2005 on the regulation of adhesion, migration and polarity of the cell cytoskeleton was awarded the Louis Jeantet ... DNA from a rhabdomyosarcoma cell line and a fibrosarcoma cell line transformed a NIH/3T3 mouse fibroblast cell line. After ... 2015 deaths. Hidden categories: *All articles with dead external links. *Articles with dead external links from October 2016 ... cells. Downregulation of RhoA in the HBE cell lines using siRNAs showed a lack of apical junction formation in contrast with ...
"The SREBP pathway: regulation of cholesterol metabolism by proteolysis of a membrane-bound transcription factor". Cell 89: 331 ... a meta-analysis of individual data from 61 prospective studies with 55,000 vascular deaths". Lancet 370 (9602): 1829-39. doi: ... Espenshade PJ, Hughes AL (2007). "Regulation of sterol synthesis in eukaryotes". Annu. Rev. Genet. 41: 401-27. doi:10.1146/ ... Cholesterol is primarily synthesized from acetyl CoA through the HMG-CoA reductase pathway in many cells and tissues. About 20- ...
Value of detailed chromosome studies on large numbers of cells in CML". American Journal of Hematology. 3 (2): 121-6. doi: ... lethal condition resulting in sudden infant death syndrome (SIDS),[9] infantile onset of a hepatic Reye-like syndrome, and late ...
Cell movement - Chemotaxis, contraction, cilia and flagella.. *Cell signaling - Regulation of cell behavior by signals from ... and cell death. The cell cycle is divided into four distinct phases, G1, S, G2, and M. The G phases - which is the cell growth ... When the cell has completed its growth process, and if it is found to be damaged or altered it undergoes cell death, either by ... Prokaryotic cells are much smaller than eukaryotic cells, making prokaryotic cells the smallest form of life.[11] Cytologists ...
The regulations concerning such activities do not apply when the ability to work or the health of a person would be negatively ... Some scientists have indicated that a fast will cause white blood cells to break down during the fasting, resulting in new ones ... who had contracted leprosy and was on the verge of death. Chenrezig taught her the method of Nyung Ne[27] in which one keeps ... Pope Pius XII had initially relaxed some of the regulations concerning fasting in 1956. In 1966, Pope Paul VI in his apostolic ...
"for their discoveries concerning 'genetic regulation of organ development and programmed cell death'"[۷۷] ... "for their discovery of جی پروتئینs and the role of these proteins in ورارسانی پیام in cells"[۷۳] ... "for their discoveries concerning the mechanism and regulation of the کلسترول and اسید چرب دگرگشت"[۵۴] ... "for their discoveries concerning the interaction between tumour viruses and the genetic material of the cell"[۶۱] ...
Prolonged hypoxia induces neuronal cell death via apoptosis, resulting in a hypoxic brain injury.[1][2] ... Nov 2001). "Hypoxia induces apoptosis via two independent pathways in Jurkat cells: differential regulation by glucose". ... Cell Physiology. 281 (5): C1596-603. doi:10.1152/ajpcell.2001.281.5.c1596. PMID 11600423.. ... Brain cells are very sensitive to reduced oxygen levels. Once deprived of oxygen they will begin to die off within five minutes ...
"Margarine Regulations". Archived from the original on 2007-10-11.. *^ "Enriched White Bread in Canada". The Canadian Celiac ... Before the 20th century, babies born with congenital lactase deficiency often did not survive,[2] but death rates decreased ... "Transcriptional heterogeneity in the lactase gene within cell-type is linked to the epigenome". Scientific Reports. 7 (1): ... of Regulation (EC) No 1924/2006". EFSA Journal. 8 (10). 2010. doi:10.2903/j.efsa.2010.1763.. ...
Decreased expression of MHC class I and up-regulation of MIC-A can happen when cells are infected by a virus or become ... They are usually first responders to microbial infection; their activity and death in large numbers form pus. They are commonly ... T cells: *CD4+ helper T cells: T cells displaying co-receptor CD4 are known as CD4+ T cells. These cells have T-cell receptors ... B cells: releases antibodies and assists activation of T cells. *T cells: *CD4+ Th (T helper) cells: activate and regulate T ...
... it caused 3.2 million deaths, more than 90% in the developing world,[3] up from 2.4 million deaths in 1990.[7][19] The number ... The inflammatory cells involved include neutrophil granulocytes and macrophages, two types of white blood cells. Those who ... A number of developed countries have successfully improved outdoor air quality through regulations. This has resulted in ... and became the fourth leading cause of death.[2] In 2012 it became the third leading cause as the number of deaths rose again ...
heterotypic cell-cell adhesion. • positive regulation of transforming growth factor beta production. • cell-cell adhesion. • ... negative regulation of interleukin-6 secretion. • negative regulation of neuron death. • negative regulation of matrix ... heterophilic cell-cell adhesion via plasma membrane cell adhesion molecules. • cell recognition. • homophilic cell adhesion via ... negative regulation of macrophage activation. • regulation of immune response. • negative regulation of leukocyte activation. • ...
... there is a risk of death. In 1995, the Los Angeles Times reported at least 61 deaths associated with police use of pepper spray ... Control of Weapons Regulations 2011 (Vic) *^ "Arms (Restricted Weapons and Specially Dangerous Airguns) Order 1984". ... The Scoville rating of these sprays are 500,000 (sabre MK9 HVS unit) and 2,000,000 (Sabre, cell buster fog delivery). This was ... "Regulations of the People's Republic of China on Use of Police Implements and Arms by the People's Police". www.lawinfochina. ...
... Min Liang,1,2 Hannah R. Cornell,1 Nasim Zargar Baboldashti,1,3 ... A. Rukenstein, R. E. Rydel, and L. A. Greene, "Multiple agents rescue PC12 cells from serum-free cell death by translation- and ... Serum starvation (1% FCS) slightly increased TUNEL positive cells. However, hypoxia (0.1% O2) significantly induced cell death ... Percentage of apoptotic cells versus total cells (mean ± SE, ; versus 10% FCS alone; versus 1% FCS alone; ns not significant ...
... and are exploring the potential medical benefits that might arise from inhibition of death in certain disease states. ... The Jeffery Molkentin Lab is investigating the molecular mechanisms that underlie cell death, ... Regulation of Cell Death Through the Mitochondria We are investigating the molecular mechanisms that underlie cell death, and ... or necrotic cell death. Thus, inhibition of nodal cell death pathways could have a significant implication in combating ...
Cell Death & Disease. Fig. 4: The m6A regulation of chemokine in immune evasion.. From: Emerging role of RNA modification N6- ... and plasmacytoid dendritic cells (pDCs), and suppress-tumor immunity by chemokines involved in immune cell including CD8 T cell ... The m6A could affect the chemokine functions including pro-tumor effects of chemokines involved in Immune cell such as ... granulocytic and monocytic myeloid derived suppressor cells (MDSCs), Treg cells, Th22 cells, ...
The Gene Ontology (GO) project is a collaborative effort to address the need for consistent descriptions of gene products across databases. You can use this browser to view terms, definitions, and term relationships in a hierarchical display. Links to summary annotated gene data at MGI are provided in Term Detail reports.
Apoptosis is one type of programmed cell death. Increasingly, non-apoptotic cell death is recognized as being genetically ... Global survey of cell death mechanisms reveals metabolic regulation of ferroptosis.. Shimada K1, Skouta R1, Kaplan A1, Yang WS1 ... mut: cells tumor-transformed due to HRASG12V overexpression, wt: isogenic cells without HRASG12V. b. Lipid ROS generation. Flow ... Cells were grown under DMSO or ATOC (α-tocopherol)s existence. shRNA screens in b,c were performed once in four cell lines. ...
Dnmt-mediated cell death seems to be another program for cell death. The specific gene targets of apoptosis-related DNA ... Epigenetic Regulation of Motor Neuron Cell Death through DNA Methylation. Barry A. Chestnut, Qing Chang, Ann Price, Catherine ... Epigenetic Regulation of Motor Neuron Cell Death through DNA Methylation. Barry A. Chestnut, Qing Chang, Ann Price, Catherine ... Epigenetic Regulation of Motor Neuron Cell Death through DNA Methylation. Barry A. Chestnut, Qing Chang, Ann Price, Catherine ...
... an effector known to inhibit cell death via pyroptosis, we have identified OspD2 and IpaH1.4 as cell death inhibitors. In ... Synthetic bottom-up approach reveals the complex interplay of Shigella effectors in regulation of epithelial cell death. ... Synthetic bottom-up approach reveals the complex interplay of Shigella effectors in regulation of epithelial cell death ... Synthetic bottom-up approach reveals the complex interplay of Shigella effectors in regulation of epithelial cell death ...
Down-regulation of copper/zinc superoxide dismutase causes apoptotic death in PC12 neuronal cells. C M Troy and M L Shelanski ... Down-regulation of copper/zinc superoxide dismutase causes apoptotic death in PC12 neuronal cells ... Down-regulation of copper/zinc superoxide dismutase causes apoptotic death in PC12 neuronal cells ... Down-regulation of copper/zinc superoxide dismutase causes apoptotic death in PC12 neuronal cells ...
Learn more about the Regulation Of Programmed Cell Death Pathway from related diseases, pathways, genes and PTMs with the Novus ... Regulation Of Programmed Cell Death Pathway Bioinformatics. Programmed cell death is a process that can either be regulatory or ... The Regulation Of Programmed Cell Death Pathway has been linked to: *Programmed Cell Death ... The negative regulation of cell death is necessary to ensure that too many cells are not destroyed, for if they are serious ...
Regulation of Cell Death Protease Caspase-9 by Phosphorylation. By Michael H. Cardone, Natalie Roy, Henning R. Stennicke, Guy S ... Regulation of Cell Death Protease Caspase-9 by Phosphorylation. By Michael H. Cardone, Natalie Roy, Henning R. Stennicke, Guy S ... Regulation of Cell Death Protease Caspase-9 by Phosphorylation Message Subject. (Your Name) has forwarded a page to you from ... transfected 267 cells as compared to control 267 cells (4). Treatment of Ras(V12)-expressing cells with the PI3K inhibitor ...
Regulation of an ATG7-beclin 1 Program of Autophagic Cell Death by Caspase-8 ... Regulation of an ATG7-beclin 1 Program of Autophagic Cell Death by Caspase-8 ... Regulation of an ATG7-beclin 1 Program of Autophagic Cell Death by Caspase-8 ... Regulation of an ATG7-beclin 1 Program of Autophagic Cell Death by Caspase-8 ...
... activates both innate and adaptive arms of the immune system during apoptotic cancer cell death. With respect to cancer ... activates both innate and adaptive arms of the immune system during apoptotic cancer cell death. With respect to cancer ... immunotherapy, the process of ICD elicits enhanced adjuvanticity and antigenicity from dying cancer cells, and consequently, ... immunotherapy, the process of ICD elicits enhanced adjuvanticity and antigenicity from dying cancer cells, and consequently, ...
Autophagic cell death (programmed cell death type II) and apoptosis (programmed cell death type I) were activated together in ... Arsenic trioxide induces not only apoptosis but also autophagic cell death in leukemia cell lines via up-regulation of Beclin-1 ... In this study, we investigated the in vitro effects of As2O3 on cell growth inhibition and cell death in human T-lymphocytic ... Although recent data shows that arsenic trioxide (As2O3) is capable of inducing cell death via cell cycle arrest and apoptosis ...
Lymphoid expression and regulation of A20, an inhibitor of programmed cell death.. M Tewari, F W Wolf, M F Seldin, K S OShea, ... Lymphoid expression and regulation of A20, an inhibitor of programmed cell death. ... Lymphoid expression and regulation of A20, an inhibitor of programmed cell death. ... Lymphoid expression and regulation of A20, an inhibitor of programmed cell death. ...
Glial Cell Line-Derived Neurotrophic Factor and Developing Mammalian Motoneurons: Regulation of Programmed Cell Death Among ... Glial Cell Line-Derived Neurotrophic Factor and Developing Mammalian Motoneurons: Regulation of Programmed Cell Death Among ... Glial Cell Line-Derived Neurotrophic Factor and Developing Mammalian Motoneurons: Regulation of Programmed Cell Death Among ... Glial Cell Line-Derived Neurotrophic Factor and Developing Mammalian Motoneurons: Regulation of Programmed Cell Death Among ...
... and plays an important role in cell survival, differentiation, and apoptosis. To investigate its role in cell fate ... NGF treatment augmented the cell death induced by TrkA overexpression. This TrkA-induced cell death was blocked by the tyrosine ... TrkA-mediated cell death was shown by the annexin-V binding assay to be, at least in part, apoptotic in both SK-N-MC and U2OS ... Interestingly, TrkA overexpression induced substantial cell death even in the absence of NGF, by stimulating ERK ...
Ischemic insults induce necroptotic cell death in hippocampal neurons through the up-regulation of endogenous RIP3. ... Ischemic insults induce necroptotic cell death in hippocampal neurons through the up-regulation of endogenous RIP3 ... Ischemic insults induce necroptotic cell death in hippocampal neurons through the up-regulation of endogenous RIP3. ...
We conclude that acquisition of the task triggered the rescue of newborn neurons by a targeted regulation of cell death. ... indicating that BrdU-positive cells were spared to the detriment of non-labeled cells. In addition, a fine analysis of cell ... indicating that BrdU-positive cells were spared to the detriment of non-labeled cells. In addition, a fine analysis of cell ... The overall level of cell death did not change across training and was similar in conditioned and pseudo-conditioned groups, ...
The following article reviews previous studies on cell death regulation in IEC and a potential role of necroptosis for gut ... Cell death in the intestinal epithelium has to be tightly regulated and irregularities might cause pathologies. Excessive cell ... Moreover, an apoptosis-independent mode of programmed cell death, termed necroptosis, has been identified and described in the ... Intestinal epithelial cells (IEC) are organised as a single cell layer which covers the intestine. Their primary task is to ...
Tsujimoto, Y. and Shimizu, S. VDAC regulation by the Bcl-2 family of proteins. Cell Death Diff. 7: 1174-1181,2000CrossRefGoogle ... Tsujimoto Y. (2002) Regulation of Cell Death by the Bcl-2 Family of Proteins. In: Nagatsu T., Nabeshima T., McCarty R., ... The Bcl-2 family of proteins is a major cell death regulator and is implicated in determining the survival or death of neurons ... Tsujimoto, Y Prevention of neuronal cell death by Bcl-2. Results Probi. Cell Differ. 24: 137-55, 1998Google Scholar ...
Workshop The biochemistry and regulation of programe cell death. Zoom *Title Carlos Martínez, Abelardo López Rivas, John A. ...
In the present study, we investigated the time course of ganglion cell apoptosis following intraorbital crushing of the optic ... Retrograde degeneration of retinal ganglion cells as a consequence of optic nerve lesion has been shown to fulfil the criteria ... Thus, retinal ganglion cell death might be prevented by ablation of Bax protein in these cells, or by up-regulation of Bax- ... Up-regulation of Bax protein in degenerating retinal ganglion cells precedes apoptotic cell death after optic nerve lesion in ...
... ... Cell Death and Disease On the subject. Cell and Molecular Biology Search outside of DiVA. GoogleGoogle Scholar. ... In the present study, we investigated the potential role of XIAP in regulation of cell death and inflammation during acute ... regulation of cell death from necrosis to apoptosis may have practicably therapeutic value. X-linked inhibitor of apoptosis ...
T Cell Function Mediated through Programmed Cell Death-1 and Programmed Cell Death-1 Ligand Interaction. Young-June Kim, Su- ... T cells (cells in circles) and DCs (cells in boxes), which are distinguished from dead cells (cells with low FSC and high SSC ... CD8+ T cells become exhausted, inducing cell surface protein programmed cell death-1 (PD-1) as chronic virus diseases or tumors ... T cell-like cells in M-DC/IL-10/IFN-γ cells led us to speculate that loss of the CD8+ T cells as noted in Fig. 4A might result ...
... cell death regulatory factors thus significantly influencing cell death susceptibility in both P53 wild-type and mutant cell ... to define the exact time point in spheroid growth when central cell death occurs and to identify the modes of cell death ... The pathogenesis and regulation of cell death in glioblastoma : experimental studies using glioma spheroid cultures ... U373 cells transfected with wild-type P53 died 3 days post transfection. Cell death susceptibility was not altered in either ...
"Regulation of cell death in flower petals, Plant Molecular Biology" on DeepDyve, the largest online rental service for ... Regulation of cell death in flower petals. Regulation of cell death in flower petals Rubinstein, Bernard 2004-10-16 00:00:00 ... Regulation of cell death in flower petals. Rubinstein, Bernard Add Journal to My Library Plant Molecular Biology , Volume 44 (3 ... The involvement of cysteine proteases and protease inhibitor genes in the regulation of programmed cell death in plants ...
... which increased p38 MAPK activation but did not induce appreciable cell death, decreased the RPE cell death induced by a higher ... Regulation Of Retinal Pigment Epithelial Cell Death Induced By Oxidative Stress You will receive an email whenever this article ... Purpose: : To investigate the regulation of RPE cell death induced by oxidative stress. Specifically, the role of p38 Mitogen- ... C. Hutnik, H. Liu, A. Mao, T. Peng; Regulation Of Retinal Pigment Epithelial Cell Death Induced By Oxidative Stress . Invest. ...
... and time-dependent cell death in Ara-C-resistant cells compared to Ara-C-sensitive cell lines. The extent of cell death and ... Taken together, our data show that HCQ-induced apoptotic cell death in Ara-C-resistant AML cells through autophagy regulation. ... Also, apoptotic cell death and caspase activation in U937/AR cells were increased by HCQ, provided evidence that HCQ-induced ... Induction of cytosine arabinoside-resistant human myeloid leukemia cell death through autophagy regulation by ...
HIF-1-dependent Regulation of Hypoxic Induction of the Cell Death Factors BNIP3 and NIX in Human Tumors. Heidi M. Sowter, Peter ... a physiological stress that can activate cell death pathways and, thus, result in the selection of cells resistant to death ... HIF-1-dependent Regulation of Hypoxic Induction of the Cell Death Factors BNIP3 and NIX in Human Tumors ... HIF-1-dependent Regulation of Hypoxic Induction of the Cell Death Factors BNIP3 and NIX in Human Tumors ...
Fgfr inhibition promoted cell death in the distal mesenchyme (Fig. 2B). In S9-S10 limbs, Fgfr inhibition increased cell death ... RA increased the ongoing cell death and also induced cell death at the tip of the digits (Fig. 5B; also see Fig. S2 in the ... although induction of cell death was more evident between 6 and 8 hours of treatment. RA induced cell death in the entire ... as RA activated cell death in regions in which Bmp7 expression was not induced and noggin did not reduce RA-induced cell death ...
  • In skeletal muscle, progressive loss of myofibers associated with muscular dystrophy is also regulated by specific molecular pathways that mediate apoptotic and / or necrotic cell death. (
  • Thus, inhibition of nodal cell death pathways could have a significant implication in combating diseases of striated muscle. (
  • The positive regulation of programmed cell death is mediated by several proteins including RPR, HID, GRIM, and the YihE protein kinase that all work to initiate pathways that lead to the activation of the cell-destroying caspases. (
  • Understanding the pathways by which endogenous cell death occurs in tumours may be of considerable value when identifying potential therapies. (
  • Ara-C-sensitive (U937, AML-2) and Ara-C-resistant (U937/AR, AML-2/AR) human AML cell lines were used to evaluate HCQ-regulated cytotoxicity, autophagy, and apoptosis as well as effects on cell death-related signaling pathways. (
  • Solid tumors contain regions of hypoxia, a physiological stress that can activate cell death pathways and, thus, result in the selection of cells resistant to death signals and anticancer therapy. (
  • Candidate signaling pathways against acquired resistance to tamoxifen are implicated including various signaling networks that control of cell proliferation or survival [ 5 - 7 ]. (
  • The IRCMB series maintains the highest standard by publishing timely topics authored by prominent cell and molecular biologists, with this release covering Developmental and seasonal regulation of neural cell death in birds, Post-translational modifications in cell death regulation, The role of cell death in tissue regeneration and fibrosis, Crosstalk between the apoptosis and autophagy signaling pathways, IP3 receptor signal integration in cell death and survival decisions, and more. (
  • Incubation of human prostate cancer cells and lymphocytes from leukemia patients with 213 Bi-immunoconjugates has been reported to activate apoptotic pathways ( 11 , 12 ), whereas treatment of gastric cancer cells expressing d9-E-cadherin with 213 Bi-d9MAb triggered nonapoptotic pathways ( 10 ). (
  • A number of biochemical events constitute different GCH-activated death-triggering pathways and transcription activity regulation, either upstream and/or downstream in the pathways, is essential to apoptosis. (
  • This review will focus on the principal hormones and nutrients, as well as downstream signalling pathways regulating beta-cell mass in the adult. (
  • The results suggest that EE extract induced caspase-independent cell death via down-regulation of ERK and Akt pathways in B16 cells. (
  • The mitochondria represent an integration and amplification hub for various death pathways including that mediated by granzyme B (GB), a granule enzyme expressed by cytotoxic lymphocytes. (
  • The mitochondria represent an integration and amplification hub for various death pathways including that of GB. (
  • How is activation of mitochondria-based pathways for the signaling of apoptotic and necrotic cell death avoided under conditions of hypoxia, anoxia, diapause, estivation and anhydrobiosis? (
  • Functional trade-offs in environmental tolerance may have occurred in parallel with the evolution of diversified pathways for the signaling of cell death in eukaryotic organisms. (
  • Mitochondria are fundamental for eukaryotic cells as they participate in critical catabolic and anabolic pathways. (
  • In response to genotoxic insults, cells activate DNA damage checkpoint pathways that stimu-late DNA repair, lead to a transient cell cycle arrest, and/or elicit programmed cell death (apoptosis) of affected cells. (
  • In the event of amino acid starvation, the cell activates two main protective pathways: Amino Acid starvation Response (AAR), to inhibit global translation, and autophagy, to recover the essential substrates f. (
  • Tumor necrosis factor is a proinflammatory cytokine, which can target its two cognate receptors and initiate the activation of NF-κB, caspase, and the JNK pathways, leading to immune cell gene regulation, apoptosis, and/or their immune cell activation. (
  • Collectively, the results of this study indicated that chrysin induced programmed cell death by activating the ER stress response and inactivating the PI3K signaling pathways in human endometriotic cells. (
  • TWEAK can induce apoptosis via multiple pathways of cell death in a cell type-specific manner. (
  • The negative regulation of apoptosis is done by the blocking of the Fas receptor or introduction of a caspase-3 inhibitor. (
  • Programmed cell death-1 (PD-1) is implicated as a major cell surface inhibitory receptor capable of regulating virus-specific CD8 + and CD4 + T cell exhaustion in mice, and in primates and humans during chronic virus infection ( 4 - 7 ). (
  • Such sensitization is achieved through transcriptional up-regulation of death receptor 4 (DR4), a death receptor of TRAIL. (
  • This ligand binding initiates receptor conformational changes and formation of a death-inducing signaling complex by further recruiting an adaptor molecule Fas-associated death domain and caspase-8/10, which consequently results in the autoactivation of caspase-8/10 to trigger the caspase cascade and eventually leads to apoptosis. (
  • We have reported previously that Andro is capable of using the death receptor-mediated apoptotic pathway to induce apoptosis in human cancer cells ( 15 ). (
  • According to recent clinical studies, tumour growth can be effectively reduced and survival can be improved by blocking the programmed death receptor-1 (PD-1)/programmed death-ligand 1 (PD‑L1) pathway. (
  • In recent studies, the programmed-death receptor-1 (PD-1 and CD279)/programmed-death ligand 1 (PD-L1, B7-H1 and CD274) pathway has been indicated to be critical for regulating T-cell responses and maintaining immune suppression ( 1 - 4 ). (
  • Apoptosis and cell death by R(+)-MA were not affected by antagonists of cannabinoid receptors (CB 1 , CB 2 ) and vanilloid receptor 1. (
  • Recent studies from our laboratory have shown that cannabinoids induce the expression of the cyclooxygenase (COX)-2 enzyme in human neuroglioma cells via a cannabinoid- and vanilloid receptor-independent pathway involving increased synthesis of ceramide (Ramer et al. (
  • This hypothesis relies on the finding that during the initiation of immune response, acquisition of co-inhibitory receptors such as programmed cell death-1 (PD-1) is determined by the pattern of antigen exposure in conjunction with Toll-like receptor (TLR)-dependent stimulation, critically affecting the magnitude and profile of secondary immunity. (
  • These present observations suggested that PFG-1 antigen is a novel cell death receptor which is different from the apoptosis-mediating receptors(Fas or TNF receptor), and that PFG-3 antigen may act as a decoy receptor and inhibit apoptotic signal induced by lgM antibodies. (
  • Ezrin belongs to the ERM (ezrin-radixin-moesin) protein family and has been demonstrated to regulate early steps of Fas receptor signalling in lymphoid cells, but its contribution to TRAIL-induced cell death regulation in adherent cancer cells remains unknown. (
  • Using ezrin phosphorylation or actin-binding mutants, we provide evidence that negative regulation of death receptor-induced apoptosis by ezrin occurs in a cytoskeleton-and DISC-independent manner, in colon cancer cells. (
  • In apoptotic pathway, nimbolide activated c-Jun N-terminal kinase (JNK) phosphorylation, BH3 interacting-domain death agonist (Bid) and up-regulated the death receptor 5 (DR5) level. (
  • Previous studies have demonstrated that resistance of hRPE to TNF-a induced cell death is associated with an increased ratio of a survival factor, c-FLIP (a primary inhibitor of the death receptor signaling pathway) to the pro-apoptotic protein caspase-8. (
  • They trigger target cell death either through the death receptor pathway or through the cytotoxic granule pathway, which relies on perforin-dependent delivery of granzyme serine proteases into the cytosol of the target cell [ 7 - 19 ]. (
  • PTH-independent regulation of blood calcium concentration by the calcium-sensing receptor. (
  • We next investigated the receptor responsible for VEGI-induced endothelial cell apoptosis. (
  • DR3 is a receptor for VEGI and thus we first focused on confirming if DR3 is the receptor responsible for VEGI-mediated endothelial cell death. (
  • Fas (CD95/Apo-1) is a cell surface death receptor belonging to the tumor necrosis factor receptor super family. (
  • Mice with Fas-defective lymphoproliferation and with FasL-defective generalized lymphoproliferative disease (gld) mutations develop autoimmune disease and lymphoadenopathy, indicating that the death receptor Fas is a functional molecule in eliminating either autoreactive peripheral T lymphocytes and B lymphocytes or tumor cells. (
  • abstract = "Glucocorticoids (GCs) and topoisomerase II inhibitors are used to treat acute lymphoblastic leukaemia (ALL) as they induce death in lymphoid cells through the glucocorticoid receptor (GR) and p53 respectively. (
  • as a result, this technique only allows a short time frame in which seeding of TRM cells can occur and cannot be used to transfer of monoclonal T cell receptor transgenic (TCR-tg) T cells may not accurately reflect the same trafficking and localization boost existing AC220 (Quizartinib) TRM populations (Shin and Iwasaki, 2012). (
  • The NO-induced increase in NMDA channel activity as well as NMDA receptor-mediated cell death provide firm evidence that NO modulates the NMDA channel in a manner consistent with both a physiological role under normoxic conditions and a pathophysiological role under hypoxic conditions. (
  • In TNF-treated cells, TNFR1, TNFR-associated death domain protein (TRADD), Fas-associated death domain protein, and receptor-interacting protein kinase proteins form the signaling complex via modular interaction within their C-terminal death domains. (
  • Phospho-S215LKD and phospho-S296LAE motifs are also critical to TRADD for recruiting Fas-associated death domain protein and receptor-interacting protein kinase. (
  • TNF-bound TNFR1 recruits TNFR-associated death domain protein (TRADD), an adaptor protein that serves as the platform for additional recruitment of receptor-interacting protein kinase (RIP) and Fas-associated death domain protein (FADD), initiating both NF-κB activation and apoptosis induction ( 1 - 3 ). (
  • Several reports have demonstrated that caspase-8, and its substrate BID, are frequently activated in response to certain apoptotic stimuli in a death receptor-independent manner. (
  • As2O3 significantly inhibited the proliferation of Molt-4 and Mutz-1 cells in dose- and time-dependent manner. (
  • Moreover, TrkA overexpression inhibited long-term proliferation of both the neuronal SK-N-MC cells and the non-neuronal U2OS cells, suggesting a potential role of TrkA as a tumor suppressor. (
  • PD-1 is also induced on tumor-infiltrating T cells, and blockade of PD-1 increases tumor-specific T cell proliferation and function, suggesting that PD-1 signaling may result in human tumor-specific T cell exhaustion ( 9 , 10 ). (
  • Regions of proliferation, death and differentiation were first assessed using a variety of immunohistochemical and microscopical techniques. (
  • SAHA inhibited the proliferation of TAMR/MCF-7 cells in a dose-dependent manner. (
  • For that purpose, gene expression of 213 Bi-treated tumor cells was quantified using a real time quantitative-PCR low-density array covering 380 genes in combination with analysis of cell proliferation and the mode of cell death. (
  • The aim of this study was to investigate key biological processes such as the mode of cell death, cell survival, and proliferation with regard to gene expression after incubation of HSC45-M2 gastric cancer cells with 213 Bi-d9MAb conjugates. (
  • All together, the results of these and other studies suggest that there is no universal mechanisms by which plant-derived, synthetic, and endogenous cannabinoids affect cell viability and proliferation of glioma cells. (
  • Tumor necrosis factor (TNF-), an inflammatory cytokine that plays an important role in the control of cell proliferation, differentiation, and apoptosis, has previously been used in anti-cancer therapy. (
  • Our findings overall indicate that nimbolide may enhance TNF--mediated cellular proliferation inhibition through increasing cell apoptosis of HT-29 cells by up-reglation of DR5 expression via the JNK pathway. (
  • Thus, the identification of the molecular regulators of beta-cell mass and a better understanding of the processes of beta-cell differentiation and proliferation may provide further insight for the development of new therapeutic targets for diabetes. (
  • Cell turnover of BCECs by the balance of cell proliferation and cell death is critical for maintaining the integrity of BBB. (
  • Evidence from this new study indicates that phenoxodiol inhibits proliferation of many cancer cell lines and some primary immune cells. (
  • Phenoxodiol selectively limits plasma membrane electron transport in cancer cells, by binding to a cancer specific surface plasma membrane electron transport element on cancer cells thereby inhibiting their proliferation, whereas the compound has no such effect on normal healthy cells. (
  • The results showed that chrysin suppressed the proliferation of endometriosis and induced programmed cell death through changing the cell cycle proportion and increasing the cytosolic calcium level and generation of reactive oxygen species. (
  • This cytokine is also found to promote proliferation and migration of endothelial cells, and thus acts as a regulator of angiogenesis. (
  • We are investigating the molecular mechanisms that underlie cell death, and are exploring the potential medical benefits that might arise from inhibition of death in certain disease states. (
  • Global survey of cell death mechanisms reveals metabolic regulation of ferroptosis. (
  • However, the full extent and diversity of alternative cell death mechanisms remain uncharted. (
  • Here we surveyed the landscape of pharmacologically accessible cell death mechanisms. (
  • The discovery of missense mutations leading to reduced enzymatic activity in the copper/zinc superoxide dismutase (SOD1) in human familial amyotrophic lateral sclerosis has heightened interest in the role of free radicals in neurodegenerations but left the mechanisms by which they may cause neuronal death unexplained. (
  • Although recent data shows that arsenic trioxide (As2O3) is capable of inducing cell death via cell cycle arrest and apoptosis both in acute promyelocytic leukemia (APL) and in non-APL cells, the mechanisms of As2O3-mediated cell death are not fully understood. (
  • CD8 + T cells become exhausted, inducing cell surface protein programmed cell death-1 (PD-1) as chronic virus diseases or tumors progress, but underlying mechanisms of this are unclear. (
  • The efficacy of the floral system as well as the research tools now available make it likely that important information will soon be added to our knowledge of the molecular mechanisms involved in petal cell death. (
  • In search of the molecular mechanisms responsible for DR4 up-regulation, we found that the tumor suppressor p53 plays an essential role in DR4 transcriptional activation. (
  • Therefore, the mechanisms underlying the unknown regulation of PD-L1 expression in the HNSCC microenvironment remain to be elucidated. (
  • Elucidation of the molecular mechanisms triggered by α-emitters in tumor cells could help to improve strategies of α-emitter radioimmunotherapy. (
  • In particular, between a number of GCH-induced genes, GITR and GILZ can inhibit apoptosis through interaction with mechanisms involved in T-cell survival regulation including the NF-kappaB transcription activity and the expression of the Fas/FasL system. (
  • Finally, this model implies that new and optimized immunization approaches for cancer and certain viral infections must induce highly efficacious T cells, refractory to a broad range of immune-inhibiting mechanisms, rather than solely or primarily focusing on the generation of large pools of vaccine-specific lymphocytes. (
  • However, regulation mechanisms of ovarian cell apoptosis are not well understood. (
  • l produced unique monoclonal antibodies to reveal the molecular mechanisms regulating follicular granulosa cell apoptosis in porcine ovaries. (
  • As most chemotherapeutics were discovered by empirical screens, the molecular mechanisms of how they kill cells are poorly understood. (
  • Unraveling the mechanisms by which organisms in extreme environments avoid cell death may suggest possible interventions during disease states and biostabilization of mammalian cells. (
  • This proposal is designed to understand the molecular mechanisms underlying the anti-tumor effect of proteasome inhibitors, and to determine whether certain molecular changes in cancer cells such as elevated expression of LC3 or SCCA1 can confer tumor cell sensitive to proteotoxic agents in vivo. (
  • In conclusion, this study will identify mechanisms for regulation of apoptosis by ceramide that are critical for normal brain development and/or the etiology of subsequent, pathological disorders in adulthood. (
  • The molecular mechanisms of VEGI activity on endothelial cells remain undefined. (
  • We therefore provide several mechanisms to control VEGI-mediated endothelial cell death, one being the activation of NF-κB to suppress the apoptotic potential of VEGI and the needed presence of DR3 for VEGI to initiate apoptosis, a role that is possibly independent of ligand binding. (
  • Mechanisms underlying ALL cell death and the contribution of the bone marrow microenvironment to drug response/resistance remain unclear. (
  • However, the protective effects and mechanisms of HSP22 in hippocampal neuronal cells under oxidative stress remain unknown. (
  • However, multiple obstacles are faced in islet transplants, including cellular rejection akin to the mechanisms involved in autoimmune destruction of β-cells, and also primary nonfunction, a phenomena related to lack of nutrients, hypoxia, and nonspecific inflammatory mediators ( 10 - 12 ). (
  • Determining the molecular basis of β-cell susceptibility to apoptosis would increase our understanding of the mechanisms underscoring β-cell loss, as well as reveal potential gene therapy candidates for the creation of "death-defying" islets ( 13 ), capable of resisting immune and nonimmune insults. (
  • This suggests that post-transcriptional mechanisms control the translation of PUMA mRNA in heat-shocked cells. (
  • This study is expected to have an important impact in the fields of RNA editing, signal transduction, and diseases that involve cell death mechanisms and therefore contribute to improve human health. (
  • Autophagy and ER stress are involved in maintaining some well-orchestrated mechanisms aimed at either restoring cellular homeostasis or performing cell death. (
  • This new research supports previous findings by Professor James Morre, Ph.D. at Purdue University, which showed that phenoxodiol interacts with the tumor-specific protein, tNOX, to selectively block cancerous cells from dividing by switching off a variety of pro-survival signaling mechanisms within the cancer cell, causing it to die. (
  • Under these tools, the well scientific multivariate book Mechanisms of Lymphocyte Activation and Immune Regulation VI: Cell Cycle and Programmed not were to contact to a including group. (
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  • We are currently focusing most of our efforts on elucidating the mitochondrial (intrinsic) cell death pathway, with a specific emphasis on the process of mitochondrial permeability pore formation. (
  • The negative regulation of autophagy is maintained with the continuous activation of the mTOR pathway, which is done so by sensing proper cellular levels of growth factors, amino acids, oxygen, and energy. (
  • We have 3089 products for the study of the Regulation Of Programmed Cell Death Pathway that can be applied to Western Blot, Flow Cytometry, Chromatin Immunoprecipitation, Immunocytochemistry/Immunofluorescence, Immunohistochemistry, Chromatin Immunoprecipitation (ChIP) from our catalog of antibodies and ELISA kits. (
  • Blockade of the PD-1 signaling pathway in chronically infected mice rescues function of exhausted T cells ( 8 , 9 ). (
  • The presence of these regulatory factors, sub-lethal stress and a high apoptotic index suggests the p53 pathway may be involved in the cell death response around these areas. (
  • In order to investigate cell death regulatory factors in vitro, particularly those relating to the p53 pathway, the glioma spheroid system was utilised. (
  • Inhibition of the mitogen-activated protein kinase (Mapk) pathway prevents the survival effect of Fgf8 on interdigital cells and the accompanying Erk1/2 phosphorylation and induction of Mkp3 expression. (
  • These findings provides additional evidence that TNF-a modulates hRPE survival/death by affecting c-FLIP expression via signaling cross talk with the PI3 kinase pathway and that c-FLIP may be a critical determinant in governing hRPE fate in response to TNF-a exposure. (
  • The results also showed caspase-independent activity and the down-regulation of ERK and Akt signaling pathway. (
  • GB activates the proapoptotic B cell CLL/lymphoma 2 (Bcl-2) family member BH3-interacting domain death agonist (BID) to switch on the intrinsic mitochondrial death pathway, leading to Bcl-2-associated X protein (Bax)/Bcl-2 homologous antagonist/killer- (Bak-) dependent mitochondrial outer membrane permeabilization (MOMP), the dissipation of mitochondrial transmembrane potential (ΔΨm), and the production of reactive oxygen species (ROS). (
  • Studies of ROS biogenesis have revealed that GB must enter the mitochondria for ROS production, making the mitochondrial entry of cytotoxic proteases (MECP) an unexpected critical step in the granzyme death pathway. (
  • In this review, we provide a brief overview of the canonical mitochondrial death pathway in order to put into perspective this new insight into the GB action on the mitochondria to trigger ROS-dependent cell death. (
  • GA cleaves its substrates after lysine or arginine residues to trigger a caspase-independent, B cell CLL/lymphoma 2- (Bcl2-) insensitive, and mitochondrial outer membrane permeabilization- (MOMP-) independent cell death pathway with the morphological feature of apoptosis [ 23 - 27 ]. (
  • Similarly, to initiator caspases, GB activates the proapoptotic Bcl-2 member BID to switch on the intrinsic mitochondrial death pathway [ 34 - 37 ]. (
  • The BCL-2 family of proteins governs whether a cell continues to live or instead commits to death through the mitochondrial apoptotic pathway. (
  • In the present study, we demonstrated that transduced Tat-HSP22 attenuates oxidative stress-induced hippocampal neuronal cell death through the mitochondrial signaling pathway and plays a crucial role in inhibiting neuronal cell death, suggesting that Tat-HSP22 protein may be used to prevent oxidative stress-related brain diseases including ischemia. (
  • Citation Query A conserved checkpoint pathway mediates DNA damage-induced apoptotsis and cell cycle arrest in C. (
  • Our preliminary data has shown that ADAR1 directly interacts with the NF-kB pathway and up-regulates NF-kB activities through IKK protein complex in mammalian cells. (
  • Phenoxodiol induces the destruction of cancer cells by disrupting a stress pathway in the outer cell membrane, causing down regulation of the FLICE-inhibitory protein, FLIP, and resulting in caspase-dependent and independent degradation of the X-linked inhibitor of cell death, XIAP. (
  • In addition, chrysin activated endoplasmic reticulum (ER) stress by stimulating the unfolded protein response proteins, especially the 78-kDa glucose-regulated protein-PRKR-like ER kinase (PERK)-eukaryotic translation initiation factor 2α (eIF2α) pathway in both endometriotic cell lines. (
  • Remarkably, by limiting the translocation of a single effector, VirA, OspD2 controls the timing of epithelial cell death via calpain-mediated necrosis. (
  • Eguchi, Y, Shimizu, S. and Tsujimoto, Y: Intracellular ATP levels determine cell death fate by apoptosis or necrosis. (
  • Cell death, including apoptosis and necrosis are critical pathology of AP, since the severity of pancreatitis correlates directly with necrosis and inversely with apoptosis Therefore, regulation of cell death from necrosis to apoptosis may have practicably therapeutic value. (
  • XIAP deletion on cell apoptosis, necrosis and inflammatory response were examined. (
  • Deletion of XIAP resulted in the reduction of amylase activity, decrease of NF-kappa B activation and less release of TNF-alpha and IL-6, together with increased caspases activities and RIP1 degradation, leading to enhanced apoptosis and reduced necrosis in pancreatic acinar cells and ameliorated the severity of acute pancreatitis. (
  • Our results indicate that deletion of XIAP switches cell death away from necrosis to apoptosis and decreases the inflammatory response, effectively attenuating the severity of AP/SAP. (
  • In glioblastoma, two main types of cell death are observed, apoptosis and necrosis. (
  • Glioma spheroids are known reproduce some of the regional heterogeneity found in vivo and they form areas of necrosis as the spheroids become larger and the central core of cells becomes metabolically compromised. (
  • Onset of central cell death was seen to occur over week 3 and these spheroids were examined using electron microscopy to establish the primary mode of cell death (apoptosis or necrosis). (
  • The primary cell death morphology observed was necrosis, followed by increases in perinecrotic apoptotic index. (
  • In conclusion, in large 3-dimensional glioma spheroid cultures, necrosis is the primary cell death event, followed by increases in perinecrotic apoptotic index. (
  • Bcl2/adenovirus EIB 19kD-interacting protein 3 (BNIP3) is a cell death factor that is a member of the Bcl-2 proapoptotic family recently shown to induce necrosis rather than apoptosis. (
  • Vascular Endothelial Growth Inhibitor (VEGI) is an endothelial cell autocrine factor and a member of the tumor necrosis family of ligands. (
  • We report that inhibition of gene transcription sensitized β-cells to tumor necrosis factor (TNF)-α-induced apoptosis, indicating the presence of a regulated antiapoptotic response. (
  • Apoptosis or necrosis: what type of cell death am I looking at? (
  • Tubular cell necrosis may involve disruption of respiration complexes, loss of mitochondrial membrane potential, and mitochondrial permeability transition, while apoptosis is precipitated by mitochondrial outer membrane permeabilization and consequent release of apoptogenic factors such as cytochrome c . (
  • Finally, leukemia cells treated with 4 microM As2O3 showed a considerable up-regulation of Beclin-1 (a Bcl-2-interacting protein) expression, which was independent of transcription of mRNA and required protein synthesis. (
  • In addition, Molt-4 cells treated with As2O3 exhibited the down-regulation of Bax protein expression, suggesting that Bax may be involved in accumulating of Beclin-1 and triggering autophagic cell death in As2O3-treated leukemia cells. (
  • In addition, we examined expression patterns of the anti-apoptotic proteins Bcl-2 and Bcl-X and the cell death-promoting protein Bax in retinae after crushing the optic nerve. (
  • In contrast, Bax protein, which was expressed in most ganglion cells at moderate baseline levels, was sharply increased as early as 30 min after crush, reached peak levels after 3 days, and remained up-regulated for at least 1 week thereafter. (
  • Thus, retinal ganglion cell death might be prevented by ablation of Bax protein in these cells, or by up-regulation of Bax-antagonists such as Bcl-2 or Bcl-X. (
  • Signal transduction may involve G-proteins, calcium activity changes and the regulation of protein phosphorylation and dephosphorylation. (
  • Specifically, the role of p38 Mitogen-Activated Protein Kinase (MAPK) in oxidative stress-induced RPE cell death was examined. (
  • The extent of cell death and features of HCQ-induced autophagic markers including increase in microtubule-associated protein light chain 3 (LC3) I conversion to LC3-II, beclin-1, ATG5, as well as green fluorescent protein-LC3 positive puncta and autophagosome were remarkably greater in U937/AR cells. (
  • Knock down of p62/SQSTM1 using siRNA were prevented the HCQ-induced LC3-II protein level as well as significantly reduced the HCQ-induced cell death in U937/AR cells. (
  • Using cDNA arrays and serial analysis of gene expression, we found that hypoxia induces up-regulation of BNIP3 and its homologue, Nip3-like protein X. Analysis of human carcinoma cell lines showed that they are hypoxically regulated in many tumor types, as well as in endothelial cells and macrophages. (
  • Regulation was hypoxia inducible factor-1-dependent, and hypoxia inducible factor-1 expression was suppressed by von Hippel-Lindau protein in normoxic cells. (
  • It was first identified approximately 20 years ago, and since that time extensive investigations into both mkp-1 mRNA and protein regulation and function in different cells, tissues, and organs have been conducted. (
  • In this study, PD-L1 protein extracted from the cell membrane was found to be downregulated in OSC-20 cells compared with OSC-19 cells, despite a higher PD-L1 expression in the total cell lysate of the OSC-20 compared with the OSC-19 cells. (
  • Our expanded product line includes products for apoptosis, cell cycle, gene regulation, nitric oxide and protein phosphorylation. (
  • ARPE-19 cells in which c-FLIP RNA and protein was eliminated by RNA interference showed similar morphological changes in response to TNF-a. (
  • We have found that CsA- and FK5O6-treated cells did not exhibit transcription of FasL mRNA after activation and were lacking functional FasL protein on their surface as determined by staining and the ability to induce apoptosis in Fas+ target cells. (
  • These findings prompt us to hypothesize that there exists a previously uncharacterized cell death mechanism that involves protein aggregate formation and intracellular activation of caspase-8. (
  • Our main hypothesis is that simultaneous upregulation of endogenous ceramide and ceramide-associated proteins (CAPs) results in formation of a pro-apoptotic protein complex (PAC) that triggers apoptosis in mitotic neuronal stem cells by suppression of anti-apoptotic, cell survival signaling. (
  • Heat shock protein 22 (HSP22) is known to protect cells against oxidative stress. (
  • Protein transduction domains (PTDs) facilitate the delivery of molecules including proteins into cells or tissues. (
  • Our data demonstrate that Tat-HSP22 protein significantly inhibits oxidative stress-induced hippocampal HT-22 cell death and mitochondrial dysfunction, suggesting Tat-HSP22 protein may allow for the development of a therapeutic protein for neuronal diseases including ischemia. (
  • Recent reports have claimed that activation of protein kinase C (PKC)-β is sufficient for both differentiation and apoptosis in promyeloid HL60 cells. (
  • ADAR1 (Adenosine Deaminase Acting on RNA -1) is an essential protein required for cell survival and embryonic development. (
  • Knockout of the gene encoding for this protein in mice gives rise to rapid and wide-spread cell death resulting in embryo death. (
  • The central hypothesis is that ADAR1 modulates NF-kB mediated gene expression through a protein-protein interaction that contributes to regulation of the balance between cell death and cell survival. (
  • The protein binding domain of ADAR1 will be determined through expressions of mutated and truncated ADAR1 in mammalian cells and detect their capabilities to bind IKK2 and regulate NF-kB target gene transcriptions. (
  • The positively or negatively functioning protein fragments will also be tested whether they rescue the cell death phenotype of ADAR1 deficiency. (
  • This protein domain may lead to a discovery of a peptide which will be used to treat diseases due to unbalance NF-kB signaling and cell death. (
  • In previous research, we found that lamprey immune protein (LIP) possessed cytocidal activity against tumor cells, but the mechanism of the selective recognition and killing of tumor cells by LIP was not ident. (
  • The drug appears to work by targeting a certain tumor-specific protein, which triggers a series of events that selectively induce cancer cell death. (
  • Dynamin-related protein 1 (Drp1), a critical mitochondrial fission protein, translocated to mitochondria early during tubular cell injury, and both siRNA knockdown of Drp1 and expression of a dominant-negative Drp1 attenuated mitochondrial fragmentation, cytochrome c release, caspase activation, and apoptosis. (
  • The BH3 interacting-domain death agonist, or BID, gene is a pro-apoptotic member of the Bcl-2 protein family. (
  • Cell survival in both untreated and nerve growth factor (NGF)-treated PC12 cells was inhibited by down-regulation of SOD1, with NGF-treated cells dying at lower levels of inhibition than untreated cells. (
  • The TrkA tyrosine kinase is activated by autophosphorylation in response to NGF, and plays an important role in cell survival, differentiation, and apoptosis. (
  • The Bcl-2 family of proteins is a major cell death regulator and is implicated in determining the survival or death of neurons under physiological as well as pathological conditions. (
  • Regulation of T-cell survival is a physiological process involved in determining the immune response development, and also the expansion of T-cell tumours. (
  • The absence of apoptotic indices in GSK-3β-induced cell death in insulin-deprived HCN cells corroborates the notion that HCN cell death following insulin withdrawal represents the genuine model of ACD in apoptosis-intact mammalian cells and identifies GSK-3β as a key negative effector of NSC survival downstream of insulin signaling. (
  • Thus, the BH3 mimetics are a new class of cancer drugs that specifically target a mechanism of cancer cell survival to selectively kill cancer cells. (
  • Survival presumably requires that unwanted initiation of cell death, in any of its various forms, is blunted or precluded. (
  • The focus of this commentary is to consider the role of the mitochondrion in cell death processes, to highlight fundamental similarities and differences in the regulation of cell death that exist across phylogenetically diverse groups, and to evaluate recent information that indicates `putting the brakes' on apoptosis is a critical event for cell survival during energy-limited states. (
  • It has long been known that Ca2+ signals govern a host of vital cell functions and so are necessary for cell survival. (
  • In Specific Aim 3, we will test the hypothesis that elevation of ceramide and down-regulation of cell survival signaling is synchronized by the cell cycle and growth factors. (
  • FACS analysis and caspase 8 assays demonstrated that CM promoted cell pro-survival trend. (
  • Shi, J & Wei, L 2007, ' Rho kinase in the regulation of cell death and survival ', Archivum Immunologiae et Therapiae Experimentalis , vol. 55, no. 2, pp. 61-75. (
  • The critical role of ADAR1 in cell survival indicates a potent role for ADAR1 in regulation of the balance between cell survival and cell death under physiologic conditions, and suggests that dysregulation of ADAR1 could lead to pathology. (
  • Our research has shown that permeability transition, as regulated by cyclophilin D in the inner mitochondrial matrix, serves a nodal function in controlling cell death in response to oxidative injury and calcium overload. (
  • Interestingly, granzyme A (GA), GB, and caspase 3 can all directly target the mitochondrial respiratory chain complex I for ROS-dependent cell death. (
  • In addition, Tat-HSP22 markedly inhibited H 2 O 2 -induced mitochondrial membrane potential, cytochrome c release, cleaved caspase-3, and Bax expression levels, while Bcl-2 expression levels were increased in HT-22 cells. (
  • The mechanism of mitochondrial damage, a key contributor to renal tubular cell death during acute kidney injury, remains largely unknown. (
  • Following either ATP depletion or cisplatin treatment of rat renal tubular cells, mitochondrial fragmentation was observed prior to cytochrome c release and apoptosis. (
  • Further in vivo analysis revealed that mitochondrial fragmentation also occurred in proximal tubular cells in mice during renal ischemia/reperfusion and cisplatin-induced nephrotoxicity. (
  • This study demonstrates a rapid regulation of mitochondrial dynamics during acute kidney injury and identifies mitochondrial fragmentation as what we believe to be a novel mechanism contributing to mitochondrial damage and apoptosis in vivo in mouse models of disease. (
  • Despite these findings, the mechanism underlying mitochondrial damage during tubular cell apoptosis remains elusive. (
  • For example, inhibition of cell death in the heart could potentially rescue an individual from death or serious disease following myocardial infarction injury. (
  • These results suggest that the induction of cell death by inhibition of SOD1 is due to free radical induction of apoptosis and that growth factor therapy for free-radical-mediated disease may require antioxidants in order to be effective. (
  • Mutant pro-Casp9(Ser196Ala) was resistant to Akt-mediated phosphorylation and inhibition in vitro and in cells, resulting in Akt-resistant induction of apoptosis. (
  • In this study, we investigated the in vitro effects of As2O3 on cell growth inhibition and cell death in human T-lymphocytic leukemia and myelodysplastic syndrome (MDS) cell lines. (
  • The in vivo pancreatitis model was induced by the administration of cerulein with or without lipopolysaccharide (LPS) or by the administration of L-arginine in wild-type or XIAP-deficient mice, and ex vivo model was induced by the administration of cerulein+LPS in AR42J cell line following XIAP inhibition. (
  • The critical role of XIAP in cell death and inflammation suggests that inhibition of XIAP represents a potential therapeutic strategy for the treatment of acute pancreatitis. (
  • Both inhibition of p38 MAPK with a selective inhibitor SB203580 and knockdown of p38 MAPK with siRNA enhanced t-BOOH induced RPE cell death. (
  • Similarly, GCH-mediated inhibition of apoptosis also requires gene transcription regulation. (
  • These observations indicate that this GCH-activated dual effect, induction and/or inhibition of T-cell death, requires transcription regulation. (
  • Suppression of R(+)-MA-induced prostaglandin (PG) E 2 synthesis with the selective COX-2 inhibitor celecoxib (0.01-1 μM) or inhibition of COX-2 expression by COX-2-silencing small-interfering RNA was accompanied by inhibition of R(+)-MA-mediated DNA fragmentation and cell death. (
  • In contrast, no inhibition of the elevated Fas mRNA expression was observed in cells activated in the presence of CsA or FK506. (
  • We provide evidence for the role of miR-24-2 and miR-29a as mediators of this repression and that strategies directed at the inhibition of these miRNAs could be effective in sensitizing cells to heat-induced apoptosis. (
  • Graphical Abstract INTRODUCTION Cellular immunity is largely mediated by CD4+ and CD8+ T cells and requires direct recognition of non-self peptides presented on major histocompatibility complexes (MHCs). (
  • Abstract: Background: We investigated the role of the programmed cell death 4 (PDCD4) tumor suppressor gene in specimens of transitional cell carcinoma and of healthy individuals. (
  • A farnesyl transferase inhibitor (FTI) reversed the resistance of Ras cytosolic extracts to cyto c ( Fig. 1 E), which suggests that the phenomenon is not due to secondary genetic changes in these cells. (
  • Furthermore, 3-methyladenine (an autophagy inhibitor) significantly reduced autophagic cell death and sequentially induced apoptosis. (
  • Lymphoid expression and regulation of A20, an inhibitor of programmed cell death. (
  • We investigated the effects of the autophagy inhibitor hydroxychloroquine (HCQ) on cell death of cytosine arabinoside (Ara-C)-resistant human acute myeloid leukemia (AML) cells. (
  • Pretreatment with an antioxidant ( N -acetylcysteine) or a c-Jun NH 2 -terminal kinase inhibitor (SP600125) effectively prevented Andro-induced p53 activation and DR4 up-regulation and eventually blocked the Andro-induced sensitization on TRAIL-induced apoptosis. (
  • The expression of PD-L1 was significantly restored by a specific inhibitor of MMP-13 (CL82198), which suggested the involvement of MMP-13 in the shedding/cleavage of PD-L1 in the OSC-20 cells. (
  • Cells were also protected from apoptotic cell death by other COX-2 inhibitors (NS-398 {[ N -[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide]} and diclofenac) and by the ceramide synthase inhibitor fumonisin B 1 , which interferes with COX-2 expression by R(+)-MA. (
  • We also reported that an endogenous serine/cysteine protease inhibitor SerpinB3 (also termed squamous cell carcinoma antigen 1, SCCA1) may function as a molecular signature for predicting efficacy with proteotoxicity-based anti-cancer therapy. (
  • VEGI is able to specifically inhibit endothelial cell growth and is an efficient inhibitor of angiogenesis. (
  • High molecular weight proteins reacting with the RIPK1 antibody increased in the presence of CM and were reduced upon incubation with the BIRC3 inhibitor AT406 in C7 cells suggesting that they represent ubiquitinated forms of RIPK1. (
  • Notably, both tubular cell apoptosis and acute kidney injury were attenuated by mdivi-1, a newly identified pharmacological inhibitor of Drp1. (
  • This reaction is part of a complex mechanism for gene regulation. (
  • Emphasis is given to lipid oxidation products serving as messengers with functions in gene regulation. (
  • Up-regulation of K(ir)2.1 by ER stress facilitates cell death of brain capillary endothelial cells. (
  • Kito H, Yamazaki D, Ohya S, Yamamura H, Asai K, Imaizumi Y. Up-regulation of K(ir)2.1 by ER stress facilitates cell death of brain capillary endothelial cells. (
  • Brain capillary endothelial cells (BCECs) form blood brain barrier (BBB) to maintain brain homeostasis. (
  • We determined VEGI had diminished apoptotic activity in endothelial cells that are depleted of DR3 by siRNA. (
  • However, it was determined that the apoptotic stimuli, LPS and TNFα, were also unable to mediate cell death in DR3-depleted endothelial cells. (
  • This symposium will discuss the importance of cellular senescence and immune signaling in IPF as well as the roles of endothelial cells and alveolar epithelial cells, which are emerging as key drivers of disease. (
  • We propose that phagocytosis by IFN-γ-stimulated M-DC/IL-10 cells, which may be DCs or, alternatively, a unique subset of macrophages, may be a mechanism by which IFN-γ-producing CD8 + T cells are tolerized after type 1 immune responses to chronic virus or tumor, and that IFN-γ links effector CD8 + T cells to their phagocytic clearance. (
  • Here we determined that downregulation of Fgf8 expression in the ectoderm overlying the interdigital areas is the event that triggers ICD, whereas RA is the persistent cell death-inducing molecule that acts on the distal mesenchyme by a mechanism involving the induction of Bax expression. (
  • Thus, ICD is determined by the antagonistic regulation of cell death by Fgf8 and RA and occurs through a progressive, rather than massive, cell death mechanism. (
  • The principal mechanism leading to retinal ganglion cell damage during glaucoma is not well understood, however, putative culprits have been proposed including excitotoxicity, neurotrophin deprivation, mechanical compression, ischemia, reactive astrocytes and oxidative stress. (
  • Recent findings have suggested that granulosa cell apoptosis is the mechanism underlying ovarian follicular atresia. (
  • This study aims to investigate the mechanism of EE extract on cell death induction in melanoma cells. (
  • Aside from its role in normal cell biology, β-cell apoptosis has been implicated in the pathophysiology of type 1 diabetes, both at its initiation phase and as the final effector mechanism ( 5 , 6 ). (
  • Here, Hobbs and Nolz describe a mechanism to rapidly expand the number of antigen-specific TRM CD8+ T cells in the skin, using topical application of antigenic peptide to boost localized protective immunity. (
  • This mechanism of TRM growth significantly improved protecting immunity in the skin, suggesting its potential power as a cells- and Ag-specific vaccine improving strategy. (
  • The objective in this application is to identify the mechanism of ADAR1 in the regulation of NF-kB signaling. (
  • Findings from the study, to be presented at the New Zealand Society of Oncology meeting to be held May 9-11, help explain the mechanism by which phenoxodiol induces cancer cell death. (
  • Hypoxia caused sustained upregulation of several proapoptotic proteins known to mediate hypoxia-induced apoptosis, such as Bnip3 and Nix, but others were unchanged although they were reportedly hypoxia-sensitive in other cell types. (
  • The virulence of numerous bacterial pathogens is dependent on nanomachines that inject tens of proteins (effectors) into host cells. (
  • Over the course of an infection, many Gram-negative bacterial pathogens use complex nanomachines to directly inject tens to hundreds of proteins (effectors) into the cytosol of infected host cells. (
  • Tsujimoto, Y. and Shimizu, S. VDAC regulation by the Bcl-2 family of proteins. (
  • Bcl-2 and Bcl-X proteins were expressed in ganglion cells at low levels. (
  • and finally, (iv) to ascertain whether modulation of the P53 status of the cells has an effect on the development of cell death and the expression of p53-related proteins within glioma spheroid cultures. (
  • Selective targeting of tumor cells with radionuclides is achieved via antibodies recognizing cell surface proteins that are overexpressed or exclusively expressed by tumor cells ( 1 ). (
  • The Bcl-2 family of proteins contains both anti and pro-apoptotic members that have been shown to regulate neuronal cell death during development and in many models of acute and chronic neurodegeneration. (
  • named PFG-3 and PFG-1 antigens, respectively) of granulosa cells of healthy follicles and PFG-4 recognized the same two membrane proteins. (
  • Anti-apoptotic BCL-2 family proteins antagonize death signaling by forming heterodimers with pro-death proteins. (
  • Under certain conditions, antagonism of anti-apoptotic BCL-2 family proteins can unleash pro-death molecules in cancer cells. (
  • The cells obtain mutations in key cellular proteins that allow the developing cancer to grow, although breaking certain cellular rules, such as genomic instability, oncogene activation, loss of adhesion, along with breach of cell cycle checkpoints. (
  • Moreover, both cell cycle arrest and pachytene apoptosis responses depend on conserved DNA damage check-point proteins. (
  • I will discuss what we these studies have taught us about allosteric regulation of GPCR structure by G proteins and ligands. (
  • Therefore, SXXE/D motifs found in the cytoplasmic domains of many TNFR family members and their adaptor proteins may serve to function as a specific interaction module for the α-helical death domain signal transduction. (
  • The C terminals of TNFR1, TRADD, FADD, and RIP all carry a discrete region termed the "death domain," which is composed of six continuous α-helical bundles and responsible for homotypic interactions among these four proteins. (
  • Conversely, proteins participating in redox homeostasis and apoptotic cell clearance had a lower abundance in Meishan than in Large White fetuses. (
  • These results underline the importance of not only fetal age but also maternal intrauterine environment in the regulation of several proteins in subcutaneous adipose tissue. (
  • TRAIL is a promising anticancer agent for its ability to selectively induce apoptosis in tumor cells but not in normal cells ( 1 , 2 ). (
  • Tumor cells are efficiently killed after incubation with α-emitter immunoconjugates targeting tumor-specific antigens. (
  • Therefore, application of α-emitter immunoconjugates is a promising therapeutic option for treatment of carcinomas that are characterized by dissemination of single tumor cells in the peritoneum like ovarian cancer or gastric cancer. (
  • In diffuse-type gastric cancer, 10% of patients express mutant d9-E-cadherin on the surface of tumor cells that is targeted by the monoclonal antibody d9MAb. (
  • The use of α-emitter immunoconjugates is promising in the therapy of minimal residual disease as well as in the elimination of disseminated single tumor cells ( 3 ). (
  • 213 Bi-d9MAb conjugates have been used to selectively target and to eliminate tumor cells expressing d9-E-cadherin both in vitro and in vivo ( 7 - 10 ). (
  • PD-L1 promotes differentiation and maintains function of induced regulatory T cells (Tregs) by enhancing Foxp3 expression in Tregs ( 18 ). (
  • At concentrations of Doppa below 50 nM, only PKC-βl was activated by 2 min and apoptosis was induced, but there was no differentiation of cells towards monocytes. (
  • Thus, initial activation of PKC-βl is insufficient for differentiation of U937 cells, but may lead to the induction of apoptosis. (
  • Lord, Janet M. / Doppa induces cell death but not differentiation of U937 cells : Evidence for the involvement of PKC-βl in the regulation of apoptosis . (
  • G) Fluorescence strength profiles assessed at three different period factors (1, 2 and 5 times of differentiation) for cells pursuing transects as proven clearly uncovered the difference between nuclear and cytoplasmic fluorescence. (
  • Although the factors governing the differentiation of TRM cells are not completely understood, recruitment of effector T cells into peripheral tissues can be sufficient to generate a TRM population (Casey et al. (
  • Fig. 4: The m6A regulation of chemokine in immune evasion. (
  • The m6A could affect the chemokine functions including pro-tumor effects of chemokines involved in Immune cell such as granulocytic and monocytic myeloid derived suppressor cells (MDSCs), Treg cells, Th22 cells, and plasmacytoid dendritic cells (pDCs), and suppress-tumor immunity by chemokines involved in immune cell including CD8 T cell and Th1 cell. (
  • These screens identified previously missed Shigella effectors that inhibit induced epithelial cell death, an important arm of the host innate immune system triggered in response to invading pathogens. (
  • Immunogenic cell death (ICD) activates both innate and adaptive arms of the immune system during apoptotic cancer cell death. (
  • Cancer ICD requires the presentation of various "hallmarks" of immunomodulation, which include the cell-surface translocation of calreticulin, production of type I interferons, and release of high-mobility group box-1 and ATP, which through their compatible actions induce an immune response against cancer cells. (
  • Epigenetic modifiers have a direct effect on cell viability and appear to fundamentally change the immunogenic properties of cancer cells, by actively subverting tumor microenvironment-associated immunoevasion and aiding in the development of an antitumor immune response. (
  • when PD-1 ligates with tumour-associated PD-L1, the apoptosis or downregulation of effector cytotoxic T lymphocytes is induced, thereby resulting in an escape from T-cell-mediated immune surveillance ( 11 ). (
  • This hypothesis, based upon the acquisition and co-regulation of pivotal inhibitory receptors by CD8 + T cells, offers a rationale for gene-based immunization as an effective priming strategy and, in addition, outlines a new dimension to immune homeostasis during immune reaction to pathogens. (
  • Cancer cells attain the capacity to evade the body's own immune response and to grow in a stressful environment where both oxygen and nutrients are limited. (
  • The activation of microglia, resident immune cells of the central nervous system, and inflammation-mediated neurotoxicity are typical features of neurodegenerative diseases, for example, Alzheimer's and Parkinson's diseases. (
  • Depletion of tryptophan and the accumulation of tryptophan metabolites mediated by the immunosuppressive enzyme indoleamine 2,3-dioxygenase 1 (IDO1), trigger immune cells to undergo apoptosis. (
  • Viability of four engineered BJ cell lines treated with ( a ) CIL56 or ( e ) FIN56 for 48 hrs. (
  • Effects of ferroptosis inhibitors on viability of HT-1080 cells co-treated with ( c ) CIL56 or ( f ) FIN56 for 48 hrs. (
  • Cell viability was assessed by both the MTT assay and the trypan blue assay. (
  • The present study investigated a possible relationship between the recently shown induction of cyclooxygenase (COX)-2 expression by the endocannabinoid analog R (+)methanandamide [R(+)-MA] and its effect on the viability of H4 human neuroglioma cells. (
  • Cell viability of ARPE-19 cells was determined by XTT assay. (
  • The treatment of EE extract resulted in a dose- and time-dependent reduction in cell viability in B16 cells. (
  • The induction of programmed cell death is currently being studied as a treatment for several diseases including cancer, and recent publications show cannabinoids to be factors that induce cell death in cancerous cells, while leaving normal cells alone. (
  • Moreover, resistance to cyto c-mediated activation of caspases was not an artifact of over-expressing oncogenic Ras, because extracts from DLD-1 colon cancer cells, which contain an endogenous activated Ki-Ras gene, displayed similar resistance to cyto c. (
  • With respect to cancer immunotherapy, the process of ICD elicits enhanced adjuvanticity and antigenicity from dying cancer cells and consequently, promotes the development of clinically desired antitumor immunity. (
  • Antitumor T cells can detect and eliminate cancer cells in a highly precise, antigen-specific fashion. (
  • Appropriately activated antitumor T cells can target cancer cells at both local and metastatic sites and, most importantly, can kill existing as well as possibly relapsing cancerous cells. (
  • Therapeutic interventions promoting antitumor T cell immunity are at the forefront of next-generation cancer therapeutic strategies and as such are highly desired in clinics. (
  • Promoting antitumor T cell responses in cancer-bearing hosts is challenging ( 4 ). (
  • Myeloid-derived suppressor cells (MDSCs), described as CD11b + GR-1 + cells in mice, suppress T cells in various cancer models ( 22 - 25 ). (
  • Human cell lines were obtained from the Imperial Cancer Research Fund cell service and grown in DMEM, RPMI 1640, or Hams F-12 supplemented with 10% FCS (Globepharm), l -glutamine (2 μ m ), penicillin (50 IU/ml), and streptomycin sulfate (50 μg/ml). (
  • SAHA-mediated autophagic cell death is a promising new strategy to treatment of tamoxifen-resistant human breast cancer. (
  • Breast cancer is the most frequently diagnosed cancer in woman and one of the leading causes of cancer death in worldwide [ 1 ]. (
  • Because of its competitive antagonism, tamoxifen is binding to the ER and hence blocking breast cancer cell growth [ 4 ]. (
  • Here, we showed that pretreatment with Andro significantly enhances TRAIL-induced apoptosis in various human cancer cell lines, including those TRAIL-resistant cells. (
  • However, the anticancer application of TRAIL is unfortunately shadowed by the fact that some types of cancer cells are resistant to TRAIL-induced cell death ( 4 , 5 ). (
  • In the present study, we show that Andro sensitizes TRAIL-induced apoptosis in TRAIL-resistant human cancer cells. (
  • Coupling of the α-emitter 213 Bi to d9MAb provides an efficient tool to eliminate HSC45-M2 gastric cancer cells expressing d9-E-cadherin in vitro and in vivo . (
  • Although much research has been conducted on PD1, global miRNA regulation of PD1 in a cancer model has not been investigated. (
  • Ezrin is a positive regulator of apoptosis in T-lymphoma cell line Jurkat, but a negative regulator in colon cancer cells. (
  • Combination of Nimbolide and TNF--Increases Human Colon Adenocarcinoma Cell Death through JNK-mediated DR5 Up- regulation', Asian Pacific Journal of Cancer Prevention , 17(5), pp. 2637-2641. (
  • Cancer cells show deviant behavior that induces apoptotic signaling. (
  • To survive, cancer cells typically acquire changes enabling evasion of death signals. (
  • A truly cancer-selective therapy must target a molecule or property that is selectively present in cancer cells to avoid toxicity to normal cells. (
  • Cancer cells have a unique requirement to overcome death signaling engendered by these behaviors. (
  • 6 Metabolomics and Cell Biology Platforms, Gustave Roussy Comprehensive Cancer Institute, 94805 Villejuif, France. (
  • Therefore, SCCA1 on one hand may confer resistance to chemotherapy by protecting cells against lysosomal injury, on the other hand, it may sensitize cancer cells to proteotoxicity. (
  • The cancer can progressively lose its sensitivity to chemotherapy until cancer cells become unresponsive causing resistance, a major barrier to successful cancer treatment. (
  • In laboratory studies and Phase II clinical trials, phenoxodiol showed promise in restoring drug sensitivity to resistant cancer cells. (
  • By inhibiting plasma membrane electron transport selectively in cancer cells, phenoxodiol subjects these cells to stress that leads to cell death. (
  • Arsenic trioxide induces not only apoptosis but also autophagic cell death in leukemia cell lines via up-regulation of Beclin-1. (
  • Autophagic cell death (programmed cell death type II) and apoptosis (programmed cell death type I) were activated together in leukemia cell lines after exposed to As2O3. (
  • Cytotoxicity, apoptosis and autophagic cell death induced by SAHA were studied. (
  • Interestingly, expression of the autophagic cell death markers, LC3-II and beclin-1, was significantly increased in TAMR/MCF-7 cells treated with SAHA. (
  • Autophagic cell death induced by SAHA was confirmed by acridine orange staining and transmission electron microscopy (TEM) in TAMR/MCF-7 cells. (
  • These results suggest that SAHA can induce caspase-independent autophagic cell death rather than apoptotic cell death in TAMR/MCF-7 cells. (
  • Some animals like embryos of the brine shrimp, Artemia franciscana , exhibit profound metabolic depression and survive anoxia at room temperature for years ( Clegg, 1997 ) with no evidence of apoptotic or necrotic cell death. (
  • However, more recently it has become clear that cellular Ca2+ overload, or perturbation of intracellular Ca2+ compartmentalization, can cause cytotoxicity and trigger either apoptotic or necrotic cell death. (
  • TRAIL induces apoptosis through recognizing and binding to its cognate death receptors, DR4 and DR5 (also named as TRAIL-R1 and TRAIL-R2), on the cell surface ( 2 , 3 ). (
  • Immunoinhibitory cell receptors that can induce a state of T cell exhaustion upon exposure to tumor antigen include Programmed Cell Death-1 (PD1). (
  • Using whole cell and single- channel patch-clamp techniques, we have shown that (Z)-1-[N(3-ammoniopropyl)- N-(n-propyl)amino]-NO (PAPA-NO) and diethylamine NO, commonly termed NONOates, potentiate the glutamate-mediated response of recombinant rat NMDA receptors(NR1/NR2A) expressed in HEK-293 cells. (
  • We conclude that acquisition of the task triggered the rescue of newborn neurons by a targeted regulation of cell death. (
  • These adult born neurons originate from stem cells proliferating in the subventricular zone of the lateral ventricles, giving birth to neuroblasts which then migrate to the OB. (
  • Loss of vision in glaucoma results from the death of retinal ganglion cells, the neurons that send visual information from the retina to the brain. (
  • PAPA-NO also enhanced cell death in primary cultures of rodent cortical neurons deprived of oxygen and glucose. (
  • In an examination of 56 caspase-independent lethal compounds, modulatory profiling showed that 10 compounds induced three different types of regulated non-apoptotic cell death. (
  • GB cleaves its substrates after aspartic acid residues to induce cell death either in a caspase-dependent or caspase-independent manner [ 22 , 28 - 31 ]. (
  • The following article reviews previous studies on cell death regulation in IEC and a potential role of necroptosis for gut homeostasis. (
  • Since RPE cells play a key role in the homeostasis of the retina, this finding may have significant implications of retinal ganglion cell and photoreceptor health. (
  • Preface - Life through death: Key role of cellular suicide for colonial and organismal homeostasis Johan K.E. Spetz and Lorenzo Galluzzi 1. (
  • Pancreatic beta-cells, which secrete the hormone insulin, are the key arbiters of glucose homeostasis. (
  • Furthermore, the truncated form (p18) of Bax accumulated in the TrkA-induced cells, suggesting that TrkA induces mitochondria-mediated apoptosis. (
  • In this short review, we discuss the differential implication of mitochondria in the major forms of regulated cell death. (
  • This study shows that genes regulating cell death can be hypoxically induced and are overexpressed in clinical tumors. (
  • We screened for genes induced by hypoxia in a breast carcinoma cell line (T47D) using gene expression arrays and detected an up-regulation of BNIP3. (
  • and down-regulation of SPP1, CDC25 phosphatases , and of genes involved in chromosome segregation. (
  • These results consolidate significant cross-talk between NO and H2O2, provide new insight into the early transcriptional response of plants to increased NO and H2O2 levels, and identify target genes of the combined action of NO and H2O2 during the induction of plant cell death. (
  • We are extending these and other key observations in an attempt to better characterize the molecular underpinnings of cell death in mammalian tissues. (
  • The cell lines were transfected with wild-type and dominant negative P53 transcripts to investigate the effect of increasing and decreasing levels of endogenous p53 on cell death susceptibility within 3-dimensional spheroid cultures. (
  • Further, the large populace of effector and memory space cells resulting from the patterns of the relatively rare, polyclonal endogenous Ag-specific CD8+ T cell repertoire (Badovinac et al. (
  • 2007). Here, we display that topical software of antigenic peptide to pores and skin harboring endogenous TRM CD8+ T cells causes swelling and locally expands the Ag-specific (but not bystander) TRM populace by recruiting fresh TRM precursors from your blood circulation. (
  • Overexpression of BNIP3 and its homologue NIX (10 , 11 , 12) in Rat-1 fibroblasts and MCF-7 breast carcinoma cells induces cell death within 12 h. (
  • Galluzzi is best known for major experimental and conceptual contributions to the fields of cell death, autophagy, tumor metabolism and tumor immunology. (
  • We hypothesized that miRNAs exist that can silence PD1 in vitro and revert symptoms of T cell exhaustion. (
  • Our own studies with in vitro differentiated embryonic stem (ES) cells have shown that induction of apoptosis by ceramide is concurrent with up-regulation of PAR-4. (
  • Antihuman Fas mAb HFE7A, which cross-reacts with Fas of various mammals, ranging from humans to mice, can induce apoptosis in vitro both in human and mouse Fas-expressing T-cell lines. (
  • We have previously reported that hippocampal neural stem (HCN) cells derived from the adult rat brain undergo autopahgic cell death (ACD) following insulin withdrawal without hallmarks of apoptosis despite their normal apoptotic capabilities. (
  • Further, we showed that Tat-HSP22 transduced into animal brain and inhibited cleaved-caspase-3 expression levels as well as significantly inhibited hippocampal neuronal cell death in the CA1 region of animals in the ischemic animal model. (
  • BNIP3 and NIX are expressed ubiquitously in most human tissues as assessed by Northern blotting (12) , although it is not known which cell types express BNIP3 and NIX or if their pattern of expression differs in malignant tissue. (
  • Immunochemical reactions against these antibodies were only detected in follicular granulosa cells but not any other ovarian tissues or other organs. (
  • After that, 400 m Parasagittal Cerebellar pieces had been cut utilizing a McIlwain tissues chopper, sectioned off into specific pieces and positioned 4 per put on collagen-coated cell lifestyle inserts (Millicell, Merck Millipore, Burlington, MA, USA) in moderate. (
  • In Brief Tissue-resident memory (TRM) T cells provide a first line of host defense against pathogen invasion at environmental barrier tissues. (
  • Because many intracellular infections occur within non-lymphoid tissues, memory T cells must either be already positioned at the site of pathogen entry or be able to rapidly localize to inflamed tissues following re-infection. (
  • In theory, expanding the number of memory T cells in the circulation would lead to increased surveillance of peripheral tissues and responsiveness to secondary challenge. (
  • Cytosolic extracts from Ras(V12)-expressing cells are refractory to cyto c-induced caspase activation. (
  • This is largely because cancers employ numerous evasion strategies that are non-conducive toward T cell activation and function. (
  • Activation leads to a down-regulation of A20 expression in both mature thymocytes and peripheral T cells. (
  • Apoptotic cell death in TrkA-overexpressing cells: kinetic regulation of ERK phosphorylation and caspase-7 activation. (
  • Interestingly, TrkA overexpression induced substantial cell death even in the absence of NGF, by stimulating ERK phosphorylation and caspase-7 activation leading to PARP cleavage. (
  • Additionally, preconditioning with a low dose of t-BOOH, which increased p38 MAPK activation but did not induce appreciable cell death, decreased the RPE cell death induced by a higher dose of t-BOOH. (
  • Activation of p38 MAPK protects human RPE cells against oxidative-induced injury. (
  • Also, apoptotic cell death and caspase activation in U937/AR cells were increased by HCQ, provided evidence that HCQ-induced autophagy blockade. (
  • In agreement with the critical decline in Fgf8 expression for the activation of ICD, distal interdigital cells acquire a proximal position as interdigit regression occurs. (
  • Although SAHA induced G2/M phase arrest of cell cycle, apoptotic cell death was very low, which is correlated with the slight change in the activation of caspases and PARP cleavage. (
  • Such sensitization effect is achieved through p53-dependent transcriptional up-regulation of DR4, a process mediated by several sequential events including reactive oxygen species (ROS) production, c-Jun NH 2 -terminal kinase (JNK) activation, p53 phosphorylation, and stabilization. (
  • In the combination group, nimbolide markedly sensitized TNF--induced JNK, Bid, caspase-3 activation and the up-regulation of DR5. (
  • We have previously reported that activation of murine T cell hybridomas leads to expression of Fas (CD95) and its ligand (FasL) which subsequently interact, even on the same cell, leading to apoptotic cell death. (
  • Since the immunosuppressive drugs cyclosporin A (CsA) and FK506 block activation-induced apoptosis in T cell hybridomas, we examined whether such compounds affect cell death by interfering with expression of Fas, FasL or both, or whether they block Fas signal transduction. (
  • We therefore conclude that CsA and FK506 block activation-induced apoptosis in T cell hybridomas predominantly by interfering with activation signals leading to FasL expression and, further, that the regulation of the expression of Fas and FasL on activated T cells is differentially controlled. (
  • Both pharmacological and genetic inactivation of GSK-3β significantly decreased ACD, while activation of GSK-3β increased autophagic flux and caused more cell death without inducing apoptosis following insulin withdrawal. (
  • SCCA1 is believed to limit cellular damage resulting from unscheduled activation of lysosomal protease that is detrimental to the cell, hence may contribute to tumorigenesis and chemo-resistance. (
  • Regulation of caspase-3 processing by cIAP2 controls the switch between pro-inflammatory activation and cell death in microglia. (
  • A central question emerging from this finding is what prevents caspase-3 during the microglia activation from killing those cells? (
  • We demonstrate that counteracting the repressive effect of cIAP2 on caspase-3 activation, using small interfering RNA targeting cIAP2 or a SMAC mimetic such as the BV6 compound, reduced the pro-inflammatory activation of microglia cells and promoted their death. (
  • Though later changes in islet gene expression after cytokine activation have been mapped in a number of studies ( 14 , 15 ), we focused only on the immediate early response, as it is this response that determines cell fate after inflammatory insult ( 16 - 19 ). (
  • S381DHE motif of TNFR1-death domain as well as S215LKD and S296LAE motifs of TRADD-death domain) are phosphorylated, and this is required for stable TNFR1-TRADD complex formation and subsequent activation of NF-κB. (
  • processes such as metamorphosis, neural development and epithelial cell turnover would be disrupted. (
  • Its caspases display regulation by nucleotides that is consistent with `applying the brakes' to cell death during energy limitation. (
  • IL-10 increased PD-1 ligand expression on M-DC, and IL-10-stimulated M-DCs (M-DC/IL-10) induced expression of PD-1 on, and apoptosis of, CD8 + T cells and phagocytosed CD8 + T cells. (
  • Cell Death Regulation in Health and Disease - Part C, Volume 353 in the International Review of Cell and Molecular Biology series, reviews and details current advances in cell and molecular biology. (
  • In this book, the authors discuss the biology, regulation and clinical significance of VEGF. (
  • Biology (Sci) : The physical and chemical properties of the cell and its components in relation to their structure and function. (
  • Any one of the courses listed below is appropriate for fulfilling the Master's program prerequisites for 'a university-level course in general physiology, cell biology, or molecular biology' for non-life science students wishing to study in the department. (
  • Biology (Sci): This course introduces the student to our modern understanding of cells and how they work. (
  • Taken together, our data show that HCQ-induced apoptotic cell death in Ara-C-resistant AML cells through autophagy regulation. (
  • Cytokine induction of A20 mRNA in primary islets and insulinoma cells was rapid and observed within 1 h, consistent with A20 being an immediate early response gene in β-cells. (
  • For a cancerous cell to develop, it must obtain the ability to surmount essential checkpoints that would normally send a deregulated cell to its demise. (
  • One of the promising approaches for the treatment or prevention of neurodegenerative diseases, including Parkinson's disease, is to investigate the molecular basis of neurodegeneration or neuronal death and elucidate possible therapeutic molecular targets. (
  • Poly (ADP-ribose) (PAR)-dependent cell death in neurodegenerative diseases Hyejin Park, Tae-In Kam, Ted M. Dawson and Valina L. Dawson 2. (
  • Neural stem cells (NSCs) hold great potential for the treatment of neurodegenerative diseases. (
  • The kinase Akt and p21-Ras, an Akt activator, induced phosphorylation of pro-caspase-9 (pro-Casp9) in cells. (
  • Over-expression of a dominant active mutant of MKK6 (MKK6E), a kinase upstream of p38 MAPK, increased phosphorylation of p38 MAPK and attenuated t-BOOH-induced RPE cell death. (
  • In addition, CM selectively affected GR phosphorylation in a site and cell-specific manner. (
  • IκB kinase β plays a critical role in TNFR1 phosphorylation of S381, which leads to subsequent T cell migration and accumulation. (
  • MDSCs recruited by tumors contribute to tolerance of antitumor CD8 + T cell responses to evade antitumor immunity ( 22 - 25 ). (
  • MDSCs are abundant in local tumor environments, especially those enriched with M-CSF, which affect the suppressive capacity of MDSCs to tumor Ag-specific T cell immunity and possibly trigger PD-L1 expression ( 9 , 21 ). (
  • Expanded TRM CD8+ T cells significantly increase anti-viral protection, suggesting that this approach Angpt1 could be used to rapidly boost tissue-specific cellular immunity. (
  • Autophagy is the degradation of organelles inside the cell by lysosomal machinery, and can help with regulating cellular energy levels. (
  • The present results suggest that the up-regulation of K(ir)2.1 is, at least in part, responsible for cell death/cell turnover of BCECs induced by a variety of cellular stresses, particularly ER stress, under pathological conditions. (
  • This review, based on recent molecular, cellular, and animal studies, focuses on the current understanding of ROCK signaling in the regulation of apoptosis and highlights new findings from recently generated ROCK-deficient mice. (
  • Ryu, S, Bazer, FW, Lim, W & Song, G 2018, ' Chrysin leads to cell death in endometriosis by regulation of endoplasmic reticulum stress and cytosolic calcium level ', Journal of Cellular Physiology . (
  • In contrast to almost all type III effectors, OspD2 does not target a host cell process, but rather regulates the activity of the Shigella type III secretion apparatus limiting the cytosolic delivery (translocation) of effectors during an infection. (
  • The utility of this system was revealed by the finding that upon treatment with genotoxic agents, premeiotic C. elegans germ cells transiently halt cell cycle progression, whereas meiotic prophase germ cells in the late pachytene stage readily undergo apoptosis. (
  • We previously showed that M-CSF is important for developing tolerogenic dendritic cells (DCs) from human CD14 + monocytes. (
  • Among the anticancer drugs conventionally used in the treatment of patients with HNSCC, paclitaxel increased MMP-13 expression in R/M HNSCC cells (HOC313 cells) co-cultured without/with dendritic cells (DCs). (
  • Leukocytes are the main source of TWEAK including human resting and activated monocytes, dendritic cells and natural killer cells. (
  • Tobacco (Nicotiana tabacum) leaves exposed to moderate high light dramatically potentiated NO-mediated cell death in catalase-deficient (CAT1AS) but not in wild-type plants, providing genetic evidence for a partnership between NO and H2O2 during the induction of programmed cell death. (
  • In this article, we identify M-CSF-derived DCs (M-DCs) after stimulation with IL-10 as myeloid-derived suppressor cells with additional tolerogenic activities to CD8 + T cells. (
  • PD-1/PD-L interactions regulate peripheral self-reactive CD8 + T cell tolerance on encounter with DCs bearing self-antigen ( 16 , 17 ). (
  • Therefore, Bmp members could regulate cell death directly in the mesenchyme (e.g. (
  • Here, we speculate on how S1P and disruption of S1P breakdown may regulate cell death and autophagy. (
  • The negative regulation of cell death is necessary to ensure that too many cells are not destroyed, for if they are serious diseases and disorders could arise such as those associated with neurodegeneration. (
  • John J. Shacka and Kevin A. Roth, " Regulation of Neuronal Cell Death and Neurodegeneration by Members of the Bcl-2 Family: Therapeutic Implications", Current Drug Targets - CNS & Neurological Disorders (2005) 4: 25. (
  • In mice bearing the TAMR/MCF-7 cell xenografts, SAHA significantly reduced the tumor growth and weight, without apparent side effects. (
  • In combination with TNF-, nimbolide significantly enhanced-induced cell death. (
  • The deep resting membrane potential increased the resting intracellular Ca(2+) concentration due to Ca(2+) influx through non-selective cation channels and thereby partly but significantly regulated cell death in t-BBEC117. (
  • We found that Tat-HSP22 transduced into HT-22 cells and that H 2 O 2 -induced cell death, oxidative stress, and DNA damage were significantly reduced by Tat-HSP22. (
  • Retrograde degeneration of retinal ganglion cells as a consequence of optic nerve lesion has been shown to fulfil the criteria of apoptosis. (
  • Double labelling for Bax and TUNEL in retinal sections, however, did not reveal colocalization of the two signals in individual retinal ganglion cells, consistent with the idea that increases in Bax precede apoptosis after optic nerve lesion. (