The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
CELL LINE derived from the ovary of the Chinese hamster, Cricetulus griseus (CRICETULUS). The species is a favorite for cytogenetic studies because of its small chromosome number. The cell line has provided model systems for the study of genetic alterations in cultured mammalian cells.
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.
Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
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.
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.
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)
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.
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.
Endogenous and exogenous compounds and that either inhibit CASPASES or prevent their activation.
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 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.
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 genus of the family Muridae consisting of eleven species. C. migratorius, the grey or Armenian hamster, and C. griseus, the Chinese hamster, are the two species used in biomedical research.
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.
Irreversible cessation of all bodily functions, manifested by absence of spontaneous breathing and total loss of cardiovascular and cerebral functions.
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.
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.
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.
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 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.
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 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.
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.
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.
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.
A cell line derived from cultured tumor cells.
Established cell cultures that have the potential to propagate indefinitely.
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.
Inhibitors of SERINE ENDOPEPTIDASES and sulfhydryl group-containing enzymes. They act as alkylating agents and are known to interfere in the translation process.
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.
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.
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.
Exogenous and endogenous compounds which inhibit CYSTEINE ENDOPEPTIDASES.
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 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.
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.
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.
A member of the Bcl-2 protein family that reversibly binds MEMBRANES. It is a pro-apoptotic protein that is activated by caspase cleavage.
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.
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.
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.
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 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.
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.
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.
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)
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)
Elements of limited time intervals, contributing to particular results or situations.
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.
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.
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.
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.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
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.
Glycosides from DIGITALIS lanata leaf. Lanatoside C has actions similar to DIGOXIN. Mixtures of lanatosides A, B, and C have also been used. (From Martindale, The Extra Pharmacopoeia, 30th ed, p670)
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.
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.
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)
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.
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.
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.
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)
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.
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 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)
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 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 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.
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.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Glycoproteins found on the membrane or surface of cells.
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.
Death of the developing young in utero. BIRTH of a dead FETUS is STILLBIRTH.
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.
A family of serine endopeptidases found in the SECRETORY GRANULES of LEUKOCYTES such as CYTOTOXIC T-LYMPHOCYTES and NATURAL KILLER CELLS. When secreted into the intercellular space granzymes act to eliminate transformed and virus-infected host cells.
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.
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.
Cell surface receptors that bind TUMOR NECROSIS FACTORS and trigger changes which influence the behavior of cells.
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)
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.
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.
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.
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
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
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.
Conceptual response of the person to the various aspects of death, which are based on individual psychosocial and cultural experience.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
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.
Proteins found in any species of helminth.
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.
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 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.
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 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 sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Intracellular fluid from the cytoplasm after removal of ORGANELLES and other insoluble cytoplasmic components.
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 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.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
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.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
A polynucleotide formed from the ADP-RIBOSE moiety of nicotinamide-adenine dinucleotide (NAD) by POLY(ADP-RIBOSE) POLYMERASES.
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.
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.
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.
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.
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.
A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.
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.
A human cell line established from a diffuse histiocytic lymphoma (HISTIOCYTIC LYMPHOMA, DIFFUSE) and displaying many monocytic characteristics. It serves as an in vitro model for MONOCYTE and MACROPHAGE differentiation.
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.
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.
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.
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.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
Proteins from the nematode species CAENORHABDITIS ELEGANS. The proteins from this species are the subject of scientific interest in the area of multicellular organism MORPHOGENESIS.
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.
A group of lysosomal proteinases or endopeptidases found in aqueous extracts of a variety of animal tissues. They function optimally within an acidic pH range. The cathepsins occur as a variety of enzyme subtypes including SERINE PROTEASES; ASPARTIC PROTEINASES; and CYSTEINE PROTEASES.
A family of serine proteinase inhibitors which are similar in amino acid sequence and mechanism of inhibition, but differ in their specificity toward proteolytic enzymes. This family includes alpha 1-antitrypsin, angiotensinogen, ovalbumin, antiplasmin, alpha 1-antichymotrypsin, thyroxine-binding protein, complement 1 inactivators, antithrombin III, heparin cofactor II, plasminogen inactivators, gene Y protein, placental plasminogen activator inhibitor, and barley Z protein. Some members of the serpin family may be substrates rather than inhibitors of SERINE ENDOPEPTIDASES, and some serpins occur in plants where their function is not known.
Proteins prepared by recombinant DNA technology.
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.
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.
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.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Electron microscopy in which the ELECTRONS or their reaction products that pass down through the specimen are imaged below the plane of the specimen.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
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.
A protein of the annexin family isolated from human PLACENTA and other tissues. It inhibits cytosolic PHOSPHOLIPASE A2, and displays anticoagulant activity.
The action of a drug in promoting or enhancing the effectiveness of another drug.
Proteins encoded by the mitochondrial genome or proteins encoded by the nuclear genome that are imported to and resident in the MITOCHONDRIA.
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.
Thin structures that encapsulate subcellular structures or ORGANELLES in EUKARYOTIC CELLS. They include a variety of membranes associated with the CELL NUCLEUS; the MITOCHONDRIA; the GOLGI APPARATUS; the ENDOPLASMIC RETICULUM; LYSOSOMES; PLASTIDS; and VACUOLES.
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).
Peptides composed of between two and twelve amino acids.
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.
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.
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.
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
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.
Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.
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.
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
The process by which chemical compounds provide protection to cells against harmful agents.
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.
A family of non-enveloped viruses infecting mammals (MASTADENOVIRUS) and birds (AVIADENOVIRUS) or both (ATADENOVIRUS). Infections may be asymptomatic or result in a variety of diseases.
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.
The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
Warm-blooded vertebrate animals belonging to the class Mammalia, including all that possess hair and suckle their young.
A species of nematode that is widely used in biological, biochemical, and genetic studies.
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.
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.
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.
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 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.
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.
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.
An inorganic and water-soluble platinum complex. After undergoing hydrolysis, it reacts with DNA to produce both intra and interstrand crosslinks. These crosslinks appear to impair replication and transcription of DNA. The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle.
Compounds which inhibit or antagonize biosynthesis or actions of proteases (ENDOPEPTIDASES).
The reproductive organ (GONADS) in female animals. In vertebrates, the ovary contains two functional parts: the OVARIAN FOLLICLE for the production of female germ cells (OOGENESIS); and the endocrine cells (GRANULOSA CELLS; THECA CELLS; and LUTEAL CELLS) for the production of ESTROGENS and PROGESTERONE.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
A signal-transducing adaptor protein that associates with TNF RECEPTOR complexes. It contains a death effector domain that can interact with death effector domains found on INITIATOR CASPASES such as CASPASE 8 and CASPASE 10. Activation of CASPASES via interaction with this protein plays a role in the signaling cascade that leads to APOPTOSIS.
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.
The artificial induction of GENE SILENCING by the use of RNA INTERFERENCE to reduce the expression of a specific gene. It includes the use of DOUBLE-STRANDED RNA, such as SMALL INTERFERING RNA and RNA containing HAIRPIN LOOP SEQUENCE, and ANTI-SENSE OLIGONUCLEOTIDES.
Components of a cell produced by various separation techniques which, though they disrupt the delicate anatomy of a cell, preserve the structure and physiology of its functioning constituents for biochemical and ultrastructural analysis. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p163)
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.
Proteins to which calcium ions are bound. They can act as transport proteins, regulator proteins, or activator proteins. They typically contain EF HAND MOTIFS.
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 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.)
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.
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.
Proteins which are synthesized in eukaryotic organisms and bacteria in response to hyperthermia and other environmental stresses. They increase thermal tolerance and perform functions essential to cell survival under these conditions.
Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.
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.
Proteins found in any species of virus.
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).
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
The rate dynamics in chemical or physical systems.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
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.
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.
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.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
Proteins involved in the transport of specific substances across the membranes of the MITOCHONDRIA.
All deaths reported in a given population.
Multimeric protein complexes formed in the CYTOSOL that play a role in the activation of APOPTOSIS. They can occur when MITOCHONDRIA become damaged due to cell stress and release CYTOCHROME C. Cytosolic cytochrome C associates with APOPTOTIC PROTEASE-ACTIVATING FACTOR 1 to form the apoptosomal protein complex. The apoptosome signals apoptosis by binding to and activating specific INITIATOR CASPASES such as CASPASE 9.
Electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (OXIDATION-REDUCTION).
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
Postmortem examination of the body.
The processes whereby the internal environment of an organism tends to remain balanced and stable.
The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.
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.
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 outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
Much of her early worked involved Chinese hamster ovary cells, a commonly studied cell line also known as CHO. Using standard ... a pathway by which mammalian cells repair themselves. This discovery was a major breakthrough in understanding the double ... The death of Jeggo's husband almost discouraged her from continuing her research in cancer and radiation biology. Jeggo ... She found that the inability of DNA Ligase IV to repair breaks in stem cell DNA contributes to aging of our cells. Jeggo and ...
Cho YE, Ko JH, Kim YJ, Yim JH, Kim SM, Park JH (Apr 2007). "mHGTD-P mediates hypoxic neuronal cell death via the release of ... and loose specialized surface elements such as microvilli and cell-cell junctions. A shift of fluid out of the cells causes ... which indicates that it may participate in the caspase-independent apoptotic pathway depending on cell type or organism. Human ... It is a mode of cell death defined by characteristic morphological, biochemical and molecular changes. It was first described ...
June 2015). "CXXC5 is a negative-feedback regulator of the Wnt/β-catenin pathway involved in osteoblast differentiation". Cell ... As indicated by its name, the CXXC5 plays a role as a transcription factor in the nucleus of cells, and involved in ... "Entrez Gene: CXXC5 CXXC finger 5". Kim HY, Yoon JY, Yun JH, Cho KW, Lee SH, Rhee YM, et al. ( ... Death and Differentiation. 22 (6): 912-20. doi:10.1038/cdd.2014.238. PMID 25633194. Kim HY, Yang DH, Shin SW, Kim MY, Yoon JH, ...
"HIF2alpha inhibition promotes p53 pathway activity, tumor cell death, and radiation responses". Proceedings of the National ... The GSC niche consists of necessary somatic cells-terminal filament cells, cap cells, escort cells, and other stem cells which ... Diehn, M; Cho, R. W.; Lobo, N. A.; Kalisky, T; Dorie, M. J.; Kulp, A. N.; Qian, D; Lam, J. S.; Ailles, L. E.; Wong, M; Joshua, ... cell-cell interactions between stem cells, as well as interactions between stem cells and neighbouring differentiated cells, ...
CXXC5 is a negative-feedback regulator of the Wnt/β-catenin pathway involved in osteoblast differentiation. Cell Death and ... Wnt5a Is Required for Endothelial Differentiation of Embryonic Stem Cells and Vascularization via Pathways Involving Both Wnt/β ... doi: 10.1038/s41467-018-08230-6. (2019). Park, J, Cho, YH, Shin, WJ, Lee, JH, Lee, SK, Kim, TH, Cha, PH, Yang, JS, Cho, J, Min ... 2014) Choi OM, Cho YH, Choi S, Lee SH, Seo SH, Kim HY, Han GH, Park TS, Min DS, and Choi KY. The small molecule indirubin-3´- ...
Cell death induced by Siglec-8 in the presence of IL-33, in contrast, is mediated primarily by a caspase-dependent pathway, and ... the basophilic leukemia cell line KU812, nor on cells such as HL60 or EoL-3 that have been differentiated towards an eosinophil ... Song DJ, Cho JY, Lee SY, Miller M, Rosenthal P, Soroosh P, Croft M, Zhang M, Varki A, Broide DH (October 2009). "Anti-Siglec-F ... IL-5 stimulation also appears to alter the mode of cell death of eosinophils induced by Siglec-8 ligation in that cell death ...
Estradiol enhances expression of IRS-1 and activity of ERK1/2 and PI3K/Akt pathways in MCF-7 and CHO cells transfected with ... cell growth and initiation of cell death under low growth factor and estrogen conditions are observed in MCF-7 cells with down- ... Overexpression of PTEN in MCF-7 epithelial breast cancer cells inhibits cell growth by inhibiting MAPK pathway. ERK ... LNCaP prostate cancer cells increase cell adhesion and diminish cell motility via IGF-1 independent mechanism, when IRS-1 is ...
Cell Death and Differentiation. 23 (8): 1296-311. doi:10.1038/cdd.2016.6. PMC 4947677. PMID 26990658. Khalife J, Radomska HS, ... activated-NEDD8 is needed in two DNA repair pathways: NER and NHEJ. If activation of NEDD8 is inhibited, cells with induced ... Park HS, Ju UI, Park JW, Song JY, Shin DH, Lee KH, Jeong LS, Yu J, Lee HW, Cho JY, Kim SY, Kim SW, Kim JB, Park KS, Chun YS ( ... The effect of NEDD8 inhibition may be greater for cancer cells than for normal cells if the cancer cells are independently ...
"Association of LETM1 and MRPL36 contributes to the regulation of mitochondrial ATP production and necrotic cell death". Cancer ... Piao L, Li Y, Kim SJ, Byun HS, Huang SM, Hwang SK, Yang KJ, Park KA, Won M, Hong J, Hur GM, Seok JH, Shong M, Cho MH, Brazil DP ... Experiments performed with human cells have been interpreted to indicate that it functions as a component of a Ca2+/H+ ... contribute to two distinct mitochondrial Ca2+ uptake pathways". The Journal of Biological Chemistry. 286 (32): 28444-55. doi: ...
"The C-terminal moiety of HIV-1 Vpr induces cell death via a caspase-independent mitochondrial pathway". Cell Death and ... "HSP72 inhibits apoptosis-inducing factor release in ATP-depleted renal epithelial cells". American Journal of Physiology. Cell ... Joza N, Susin SA, Daugas E, Stanford WL, Cho SK, Li CY, Sasaki T, Elia AJ, Cheng HY, Ravagnan L, Ferri KF, Zamzami N, Wakeham A ... Ferri KF, Jacotot E, Blanco J, Esté JA, Kroemer G (2001). "Mitochondrial control of cell death induced by HIV-1-encoded ...
Zhang L, Chen J, Fu H (July 1999). "Suppression of apoptosis signal-regulating kinase 1-induced cell death by 14-3-3 proteins ... Park HS, Cho SG, Kim CK, Hwang HS, Noh KT, Kim MS, et al. (November 2002). "Heat shock protein hsp72 is a negative regulator of ... Hayakawa T, Matsuzawa A, Noguchi T, Takeda K, Ichijo H (April 2006). "The ASK1-MAP kinase pathways in immune and stress ... induces neuronal differentiation and survival of PC12 cells". The Journal of Biological Chemistry. 275 (13): 9805-13. doi: ...
Goff SP (August 2003). "Death by deamination: a novel host restriction system for HIV-1". Cell. 114 (3): 281-3. doi:10.1016/ ... eukaryotic cells at a high concentration and cleave peptides in an ATP/ubiquitin-dependent process in a non-lysosomal pathway. ... Cho S, Choi YJ, Kim JM, Jeong ST, Kim JH, Kim SH, Ryu SE (June 2001). "Binding and regulation of HIF-1alpha by a subunit of the ... Cho S, Choi YJ, Kim JM, Jeong ST, Kim JH, Kim SH, Ryu SE (June 2001). "Binding and regulation of HIF-1alpha by a subunit of the ...
have reviewed evidence that age-dependent accumulation of DNA damage in both stem cells and cells that comprise the stem cell ... is cell death and replacement a factor in aging?". J Gerontol A Biol Sci Med Sci. 62 (11): 1228-32. Bell DR, Van Zant G (2004 ... Liu, Y., Sanoff, H., Cho, H., Burd, C., Torrice, C., Ibrahim, J., Thomas, N., & Sharpless, N. (2009). Expression of p16INK4a in ... This accumulation is associated with a broad attenuation of DNA repair and response pathways that depends on HSC quiescence. ...
"Distinct p53-independent apoptotic cell death signalling pathways in testicular germ cell tumour cell lines". International ... Such damage will trigger programmed cell death (e.g. apoptosis) in cancer cells. Cisplatin resistance occurs when cancer cells ... Youn, Cha-Kyung; Kim, Mi-Hwa; Cho, Hyun-Ju; et al. (2004-07-15). "Oncogenic H-Ras Up-Regulates Expression of ERCC1 to Protect ... Expression of mutated TP53 causes defects in the apoptotic pathway, allowing cancerous cells to avoid death. Re-expression of ...
Vpr-regulated cell death: insights into mechanism". Cell Death Differ. 12 (Suppl 1): 962-70. doi:10.1038/sj.cdd.4401583. PMID ... cells. Hsp70 member proteins, including Hsp72, inhibit apoptosis by acting on the caspase-dependent pathway and against ... J. Physiol., Cell Physiol. 285 (6): C1483-93. doi:10.1152/ajpcell.00049.2003. PMID 12930708. Park HS, Cho SG, Kim CK, Hwang HS ... It is a mode of cell death defined by characteristic morphological, biochemical and molecular changes. It was first described ...
In particular, JNK can be found in both cell death and survival pathways, with its role in the cell death process being ... Cho YS, Challa S, Moquin D, Genga R, Ray TD, Guildford M, Chan FK (June 2009). "Phosphorylation-driven assembly of the RIP1- ... a type of glial cells located in the brain and the spinal cord. RIPK1 is known to appear in larger quantities in brains from ... Lin Y (2014). "RIP1-Mediated Signaling Pathways in Cell Survival and Death Control". Necrotic Cell Death. Springer New York. pp ...
Cho SD (July 2012). "β-Phenethyl isothiocyanate induces death receptor 5 to induce apoptosis in human oral cancer cells via p38 ... It has also been shown, however, that the LNGFR may signal a cell to die via apoptosis - so therefore cells expressing the ... "Mutations in NTRK3 suggest a novel signaling pathway in human congenital heart disease". Human Mutation. 35 (12): 1459-68. doi: ... Cells which express both the LNGFR and the Trk receptors might therefore have a greater activity - since they have a higher " ...
Cho C, Kim DH, Jung YK (2004). "Calcium binding of ARC mediates regulation of caspase 8 and cell death". Mol. Cell. Biol. 24 ( ... "Inhibition of both the extrinsic and intrinsic death pathways through nonhomotypic death-fold interactions". Mol. Cell. 15 (6 ... and causes cell death in cultured cells". J. Biol. Chem. 275 (4): 2647-53. doi:10.1074/jbc.275.4.2647. PMID 10644725. Li PF, Li ... Cell Death Differ. 12 (6): 682-6. doi:10.1038/sj.cdd.4401631. PMID 15861191. Rual JF, Venkatesan K, Hao T, Hirozane-Kishikawa T ...
102,103 was just as potent at causing adipocyte lysis and cell death as the complete phosphatidylcholine formula, which ... Park SH, Kim DW, Lee MA, Yoo SC, Rhee SC, Koo SH, Seol GH, Cho EY (April 2008). "Effectiveness of mesotherapy on body ... Another pathway, mainly operative in the liver involves methylation of phosphatidylethanolamine with S-adenosyl methionine (SAM ... While phosphatidylcholines are found in all plant and animal cells, they are absent in the membranes of most bacteria, ...
November 2019). "Lipid order and charge protect killer T cells from accidental death". Nature Communications. 10 (1): 5396. doi ... While in most cases activation is dependent on TCR recognition of antigen, alternative pathways for activation have been ... Rudd-Schmidt JA, Hodel AW, Noori T, Lopez JA, Cho HJ, Verschoor S, et al. ( ... cytolytic T cell, CD8+ T-cell or killer T cell) is a T lymphocyte (a type of white blood cell) that kills cancer cells, cells ...
de 2009). «Identification of a novel cyclin required for the intrinsic apoptosis pathway in lymphoid cells». Cell Death Differ. ... Youn, Cha-Kyung; Cho Hyun-Ju, Kim Soo-Hyun, Kim Hong-Beum, Kim Mi-Hwa, Chang In-Youb, Lee Jung-Sup, Chung Myung-Hee, Hahm Kyung ... and human cancer cells». Mol. Cell. Biol. (United States) 22 (23): 8184-98. ISSN 0270-7306. PMC 134072. PMID 12417722. doi: ... de 2001). «C/EBPalpha arrests cell proliferation through direct inhibition of Cdk2 and Cdk4». Mol. Cell (United States) 8 (4): ...
... stimulates proliferation of T cells and inhibits HT29 cell growth". The Journal of Biological Chemistry. 273 (42): 27548-56. ... ISBN 978-0-7817-6519-0. Zhang J, Salcedo TW, Wan X, Ullrich S, Hu B, Gregorio T, Feng P, Qi S, Chen H, Cho YH, Li Y, Moore PA, ... NFκB is a survival factor helping to inhibit apoptosis which triggers a pathway inhibiting caspase 8. When gD from HSV binds to ... Marsters SA, Sheridan JP, Pitti RM, Brush J, Goddard A, Ashkenazi A (April 1998). "Identification of a ligand for the death- ...
... programmed death-ligand 1 and programmed cell death 1 ligand 2, respectively, inhibit the anti-tumor responses of cells in the ... B-cell receptor, JAK/STAT, and perhaps other signaling pathways. In consequence, these cells progressively acquire increased ... Patients who might be intolerant to R-CHO because of general health issues have been treated with just rituximab and ... The neoplastic cells in DLBCL are derived primarily from either germinal center B-cells (i.e. GBC) or activated B-cells (i.e. ...
14-3-3ζ is a major regulator of apoptotic pathways critical to cell survival and plays a key role in a number of cancers and ... The antigenic 14-3-3ζ can directly affect T cell differentiation into Th1 and Th17 cells, and thereby promotes IFN-gamma and IL ... As a result, 14-3-3ζ functions to protect the cell from environmental stresses, such as chemotherapy-induced death, anoikis, ... Qureshi HY, Li T, MacDonald R, Cho CM, Leclerc N, Paudel HK (September 2013). "Interaction of 14-3-3ζ with microtubule- ...
... independent cell death in urothelial cancer cell lines with targeting of an expression signature present in Ta bladder tumors ... and KLF4 and represses pluripotency in human embryonic stem cells". Cell. 137 (4): 647-58. doi:10.1016/j.cell.2009.02.038. PMID ... Cho WC, Chow AS, Au JS (Aug 2009). "Restoration of tumour suppressor hsa-miR-145 inhibits cancer cell growth in lung ... the role of the IGF-I receptor signaling pathway". Journal of Cellular Physiology. 220 (2): 485-91. doi:10.1002/jcp.21796. PMID ...
The Peutz-Jegher gene product LKB1 is a mediator of p53-dependent cell death. „Mol Cell". 7. 6, s. 1307-19, 2001. PMID: ... Complete polarization of single intestinal epithelial cells upon activation of LKB1 by STRAD. „Cell". 116. 3, s. 457-66, 2004. ... Kim CJ, Cho YG, Park JY, Kim TY, Lee JH, Kim HS, Lee JW, Song YH, Nam SW, Lee SH, Yoo NJ, Lee JY, Park WS. Genetic analysis of ... LKB1-dependent signaling pathways. „Annu Rev Biochem". 75, s. 137-63, 2006. DOI: 10.1146/annurev.biochem.75.103004.142702. PMID ...
Cell Death and Differentiation. 21 (11): 1815-24. doi:10.1038/cdd.2014.98. PMC 4211378. PMID 25012505. Sahut-Barnola, Isabelle ... Cho, Yee Sook; Cho-Chung, Yoon S (2000). "Mutations of the gene encoding the protein kinase a type I-alpha regulatory subunit ... used a mouse model to cre-lox knockout the Prkar1a gene specifically from cells of the adrenal cortex and observed that the ... PDE11A4 is the gene encoding phosphodiesterase 11A4, another participant of the cAMP signalling pathway. Diagnosis usually ...
57:51-9. Tang PS, Mura M, Seth R, Liu M. (2008) Acute lung injury and cell death: how many ways can cells die? Am J Physiol 294 ... Am J Respir Cell Mol Biol. 45:88-94. Kang HR, Cho SJ, Lee CG, Homer RJ, Elias JA. (2007) Transforming growth factor (TGF)-beta1 ... Other promising drugs in earlier stages of development act at various steps in the complex molecular pathways underlying ... Furthermore, when phosgene hydrolyzes it forms hydrochloric acid, which can damage the cell surface and cause cell death in the ...
... is induced via ATF4-CHOP pathway and is involved in cell death". The EMBO Journal. 24 (6): 1243-55. doi:10.1038/sj.emboj. ... CHOP-induced apoptosis pathways had been identified in cells infected by Porcine circovirus type 2 (PERK-eIF2α-ATF4 -CHOP-BCL2 ... Lim YJ, Choi JA, Choi HH, Cho SN, Kim HJ, Jo EK, et al. (2011). "Endoplasmic reticulum stress pathway-mediated apoptosis in ... The PERK-ATF4-CHOP pathway can induce apoptosis by binding to the death receptors and upregulating the expression of death ...
... which is an anti-apoptotic gene involved in an evolutionarily conserved pathway in programmed cell death. In the nasopharyngeal ... The fact that mir-16 microRNA loss is observed in a large proportion of cells indicates the change occurred early in cancer ... Cho WC. (2010). "A MicroRNA signature associated with prognosis and progression in chronic lymphocytic leukemia". Expert Opin ... Cell Death Differ. 17 (2): 215-20. doi:10.1038/cdd.2009.69. PMID 19498445. Tsang WP, Kwok TT (2010). "Epigallocatechin gallate ...
FBW7 mutations in leukemic cells mediate NOTCH pathway activation and resistance to gamma-secretase inhibitors. J Exp Med. 2007 ... GSI-I treatment blocks Akt-mediated pro-survival pathways and induces caspase- and ROS-dependent cell death. Cell death in GSI- ... μ GSI-I and ,90% cell death for 2.5. μ GSI-I. The RS4;11 pre-B-cell line was very sensitive to the drug, with cell death ... Z-LLNle-CHO blocks both γ-secretase and proteosome activity, inducing more robust cell death in precursor-B ALL cells than ...
10 FERRI KF., KROEMER G. Organelle-specific initiation of cell death pathways. Nature Cell. Biol., 2001, 3, 255-62. [ Links ]. ... the action of the South American rattlesnake Crotalus durissus terrificus venom on CHO-K1 cell line was analyzed. The cells CHO ... Some of these components can induce in treated cells a type of cell death known as apoptosis (5, 23, 26, 40). Apoptosis is a ... A role for the actin cytoskeleton in cell death and aging in yeast. J. Cell. Biol., 2004, 164, 803-9. [ Links ]. 16 GROENENDYK ...
... glucagon and growth hormone as well as cell growth induced by neuronal excitation in both the central and peripheral nervous ... Somatostatin receptors are activated by somatostatin secreted from nerve and endocrine cells. The Somatostatin Receptors (SSTRs ... Multifunctional 5-aminolevulinic acid prodrugs activating 5 diverse cell-death pathways. Multifunctional 5-aminolevulinic acid ... Normal T-cells expressed SSTR1 and SSTR5 while T-cell leukaemia lines do not. Selective activation of SSTR1 inhibits hormone ...
It is an example of a cell line transfected using our proprietary CBTGS gene screening and amplification system. ... CHO-Anti-Human NGF MAb stable cell line is clonally-derived from a CHO cell line, which has been transfected with an anti-human ... Pathway:. ARMS-mediated activation; Activation of TRKA receptors; Apoptosis; Apoptosis; Axonal growth stimulation; Cell death ... Starting Cells From Frozen Cell Stock:. 1. Remove the packaging cell lines from liquid nitrogen and carry out a quick thaw. ...
... and erastin-induced cell death in renal proximal tubular epithelial cells via distinct signaling mechanisms, Cell Death Differ ... Ac-DEVD-CHO Catalog No. A15816. Quick View .category-products .products-list .btn-quickcart { background: white; border-color ... Mol Cell Biol. 1995 Jun; 15(6):3032-40.. *Russell J.H. (1995) Activation-induced death of mature T cells in the regulation of ... S)-Gossypol acetic acid is a inhibitor of Bcl-2, potently induce cell death in Jurkat cells overexpressing Bcl-2 (IC50, 18.1μM ...
Treatment of THP-1 cells with Z-LLL-CHO resulted in growth arrest and cell death through an apoptotic pathway. Apoptosis was ... reduced cell death in Z-LLL-CHO treated cells. Cells were pretreated with of Boc-D-fmk (100 μm) for 2 h, then with Z-LLL-CHO ( ... Percentage of cell death after treatment with Z-LLL-CHO. A, normal blood monocytes, THP-1 cells, and leukemia cells obtained ... B, Z-LLL-CHO-induced cell death (%) of U937 cells (left) and TF-1 cells (right). Data are means from three separate experiments ...
The mechanisms leading to MST activation and cell death vary depending on stimulus specificity and cell type. Exposure of cells ... Cho S, *Park BC, *Lee do H. (2007) Co-chaperone CHIP promotes aggregation of ataxin-1. Mol Cell Neurosci 34:69-79. ... Percentage of cell death is represented as the mean ± SEM. Cell death was significantly increased upon H2O2 treatment in U6- ... The c-Abl-MST1 Signaling Pathway Mediates Oxidative Stress-Induced Neuronal Cell Death. Lei Xiao, Dongmei Chen, Peng Hu, ...
Distinct and atypical intrinsic and extrinsic cell death pathways between photoreceptor cell types upon specific ablation of ... Cho, Kyoung-In; Haque, Mdemdadul; Wang, Jessica; Yu, Minzhong; Hao, Ying; Qiu, Sunny; Pillai, Indulekha CL; ... (9 authors) ( ... Cell type-specific changes in retinal ganglion cell function induced by rod death and cone reorganization in rats.  Yu, Wan- ... Non-autonomous cell-death is a cardinal feature of the disintegration of neural networks in neurodegenerative diseases, but the ...
Another PCD pathway that we considered as possibly being involved in normal neuronal cell death or in cell death in caspase- or ... 2004) Apoptosome inactivation rescues proneural and neural cells from neurodegeneration. Cell Death Differ 11:1179-1191. ... 2005) Doctor Jekyll and Mister Hyde: autophagy can promote both cell survival and cell death. Cell Death Differ 12:1468-1472. ... 2004) Role of Bcl-2 proteins in a non-apoptotic programmed cell death dependent on autophagy genes. Nat Cell Biol 6:1221-1228. ...
A Nurr1/CoREST pathway in microglia and astrocytes protects dopaminergic neurons from inflammation-induced death. Cell 137: 47- ... A) Frequency of BrdU+ cells of TCRβ+CD8+ cells and frequency of BrdU+ cells of TCRβ+CD8+CXCR3+CD44hi cells found in the lymph ... 4E). We expanded our examination to CD8+ memory T cells. Central memory cells are CCR7+CD62Lhi, whereas effector memory cells ... cells (Fig. 3B). B6 cells were found at an extremely low frequency, whereas abundant Nr4a1−/− cells were found throughout the ...
... cells/mL (H9, P12, PF382, TLOM1, and MT2), 2.5×10 (4) cells/mL (C5MJ) or 1×10 (5) cells/mL (HH). Cell viability was assessed ... Targeting the T-Cell Lymphoma Epigenome Induces Cell Death, Cancer Testes Antigens, Immune-Modulatory Signaling Pathways. Luigi ... Targeting the T-Cell Lymphoma Epigenome Induces Cell Death, Cancer Testes Antigens, Immune-Modulatory Signaling Pathways ... Targeting the T-Cell Lymphoma Epigenome Induces Cell Death, Cancer Testes Antigens, Immune-Modulatory Signaling Pathways ...
... sufficient to kill cells. However, in the absence of cIAPs, a latent RIP1K-dependent pathway is revealed. To fully block cell ... a kinase involved in the apoptosis/necrosis shift in TNF-mediated cell death, was reported to interact with RIP1 (Cho et al., ... Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009. Cell Death Differ. 16:3-11. doi ... zVAD-fmk blocked cell death when cells were stimulated with DLs for 24 h. However, DL-mediated cell death in the presence of ...
Even though large-scale cell culture is more of an industry than a craft, biomanufacturers shouldnt overlook scale-down ... tend to increase in expression under the higher stress conditions of cell culture and activate programmed cell death pathways. ... Also, she has used CRISPR tools to overexpress genes that help increase the productivity of CHO cells in culture. Finally, she ... At the Optimizing Cell Culture Technology conference, a presentation entitled "CRISPR Tools for CHO Cell Engineering" was ...
Mammalian Cell Death Pathways Induced by Different Types of Shear Flow. Timm Tanzeglock, Miroslav Soos, Gregory N. ... Modeling Shear-Induced Cho Cell Death In Rotary Lobe Pump. Hari Kamaraju, Kenneth Wetzel, William J. Kelly. ... Production of Growth Hormone Receptor Antagonist In Nicotiana Tabacum Cells: Process Development, Optimization, Scale-up and ... A 24-Well Plate Microbioreactor Array for High-Throughput Cell Culture Process Development. Yuan Wen, Ning Liu, Xudong Zhang, ...
Recent studies suggested that cell apoptosis and autophagy might play key roles in acupuncture therapy. Therefore, we searched ... These findings demonstrated that acupuncture has a potential role in modulating cell apoptosis and autophagy in animal models, ... aiming to find the potential relationship between acupuncture and cell apoptosis and autophagy. To provide readers with ... "Electroacupuncture inhibits apoptosis in annulus fibrosis cells through suppression of the mitochondria-dependent pathway in a ...
Mesenchymal stem cells (MSCs) expressing EF showed high self-renewal capacity and maintained an undifferentiated state despite ... Combinatorial targeting of survival and cell cycle progression pathways could counteract this aggressive childhood cancer. ... Genetically defined ES models are needed to understand how EF expression changes bone precursor cell differentiation, how ES ... EF expression arrested early chondrocyte and osteoblast differentiation due to changed signaling pathways such as hedgehog, WNT ...
... that astragalin inhibits the proliferation and growth of colon cancer cells in vivo and in vitro via the NF-κB pathway. ... and cell cycle arrest (by modulation of Cyclin D1, Cyclin E, P21, P27, CDK2, CDK4 protein express). Moreover, astragalin ... The results showed that astragalin significantly inhibited the proliferation and diffusion of HCT116 cells by induced apoptosis ... The results showed that astragalin significantly inhibited HCT116 cells proliferation and diffusion by induced apoptosis (by ...
... leading to upregulated transcription of iNOS in activated microglial cells. Modulation of the TLR signaling pathway via GRK2 in ... expression in microglial cells. When mouse MG6 cells were stimulated with the TLR4 ligands lipopolysaccharide (LPS) and ... expression in microglial cells. When mouse MG6 cells were stimulated with the TLR4 ligands lipopolysaccharide (LPS) and ... In this study, we attempted to establish the regulatory role of GRK2 in the Toll-like receptor (TLR) signaling pathway for ...
Fas-induced apoptosis can be associated with two alternate biochemical pathways (38). In type I cells, ligation of Fas ... Soane, L., H. J. Cho, F. Niculescu, H. Rus, M. L. Shin. 2001. C5b-9 terminal complement complex protects oligodendrocytes from ... Cell death as assessed by MTS assay. Cell viability was determined using a CellTiter 96 Aqueous cell proliferation assay ( ... Complement mediated cell death is associated with DNA fragmentation. Cell Death. Differ. 7: 48-58. ...
Genes Cells. 2000 Mar;5(3):155-67.. Bacterial cell death induced by human pro-apoptotic Bax is blocked by an RNase E mutant ... This study implies that the protection of bacterial death induced by Bax is associated with an anti-oxidant pathway and that a ... Department of Biochemistry and Cell Biology, Institute of Gerontology, Nippon Medical School, 1-396, Kosugi-cho, Nakahara-ku, ... We have shown that a trace amount of human Bax induces the cell death of Escherichia coli, accompanied by damage to DNA, and ...
Another [gamma]-secretase inhibitor, Z-Leu-Leu-Nle-CHO, was proven to cause cell death even at minimum concentrations ... CD4.sup.+] T cells were harvested for flow cytometric analysis, RNA extraction, and [gamma]-secretase inhibitor DAPT treatment. ... The stem cells were cultured according to standard protocols (Thomson et al., 1998) and differentiated into immature dorsal ... A High-Throughput Approach to Identify Specific Neurotoxicants/Developmental Toxicants in Human Neuronal Cell Function Assays ...
It seems that Descurainia sophiaoil, as an East Asian folk herbal drug, can suppress the methamphetamine-induced cell... ... Methamphetamine causes cytotoxicity and apoptosis in different cell lines. ... Kim AR, Cho JY, Zou Y, Choi JS, Chung HY (2005) Flavonoids differentially modulate nitric oxide production pathways in ... Results showed that Descurainia sophia oil has cell death-suppressing effects on PC12 cells. It enhanced the cell viability and ...
Scientists have found a way to trick cancer cells into committing suicide. The novel technique potentially offers an effective ... Cell death was correlated with the level of procaspase-3 present in the cells, with more procaspase-3 resulting in cell death ... In cancer cells, however, the signaling pathway to procaspase-3 is broken. As a result, cancer cells escape destruction and ... and Myung-Haing Cho at Seoul National University. The researchers also showed that PAC-1 killed cancer cells in 23 tumors ...
... stable cell line is clonally-derived from a CHO cell line, which has been transfected with an anti-human TNFRSF10D F(ab) gene ... to allow expression of the F(ab). It is an example of a cell line transfected using our proprietary CBTGS gene screening and ... Starting Cells From Frozen Cell Stock:. 1. Remove the packaging cell lines from liquid nitrogen and carry out a quick thaw. ... decoy with truncated death domain; TNF receptor-related receptor for TRAIL; TRAIL receptor with a truncated death domain; TNF- ...
Joo CK, Cho KS, Kim HE, Choi JS, Oh YJ. Protective role for Bcl-2 in experimentally induced cell death of bovine corneal ... Distinctive roles of PHAP proteins and prothymosin-alpha in a death regulatory pathway. Science. 2003 Jan 10;299(5604):223-6. ... A kinetic aggregation assay that enables highly sensitive Ab semiquantification in cells and tissues. Biochemistry 2011 Mar 15 ... Ginsenoside RH-2 induces apoptotic cell death in rat C6 glioma via a reactive oxygen- and caspase-dependent but Bcl-X(L)- ...
CHO cell explanation free. What is CHO cell? Meaning of CHO cell medical term. What does CHO cell mean? ... Looking for online definition of CHO cell in the Medical Dictionary? ... CHO cell growth by targeting both cell death and metabolic pathways that are detrimental to the optimal performance of cells ... CHO cell , definition of CHO cell by Medical dictionary ...
Concentration-dependent and time-dependent effects of YC-1-induced cell death of PC-3 cells. Cells were incubated in the ... Pathways of apoptotic and non-apoptotic death in tumour cells. Nat Rev Cancer 2004;4:592-603. ... Yeo EJ, Chun YS, Cho YS, et al. YC-1: a potential anticancer drug targeting hypoxia-inducible factor 1. J Natl Cancer Inst 2003 ... consistent with induction of cell death. The mode of induction of YC-1-induced cell death was also examined by 4′,6-diamidino-2 ...
However, the clinical implications of the associations among CD8+ T cells infiltration, programmed death receptor ligand-1 (PD- ... Both the low CD8+ T cells infiltration/high PD-L1 expression group and the high CD8+ T cells infiltration/high PD-L1 expression ... CD8+ T cells infiltration was associated with better survival while PD-L1 expression was correlated with PC recurrence. ... Moreover, high infiltration of CD8+ T cells could reduce unfavorable prognostic effect of high co-expression of PD-L1 and CD44/ ...
... has been shown to promote cell growth and inhibit apoptosis, but the underlying ... we found that AEG-1 could inhibit apoptotic cell death in L-78 cells, as assessed by MTT, TUNEL and flow cytometry assay. After ... Zurück zum Zitat Cho SG, Choi EJ. Apoptotic signaling pathways: caspases and stress-activated protein kinases. J Biochem Mol ... Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery. Cell. 1997;91:231-9. PubMedCrossRef ...
... infection induces cell death different from conventional apoptotic/necrotic cell death pathways by interfering with the ... Lu C, Zhu F, Cho YY, et al. Cell apoptosis: requirement of H2A.X in DNA ladder formation, but not for the activation of caspase ... type 1 cell death), autophagy (type 2 cell death), and necrosis (type 3 cell death).11 Apoptosis is characterized by nuclear ... NLFK cells were used to further study the cell death events in CPV-infected cells. Characteristic death events were apparent ...
  • In the cell cycle , apoptosis acts as a fail-safe measure to prevent fidelity and proliferation quality. (
  • Without Nr4a1, the regulation of IRF4 is lost, driving an increase in Irf4 expression and, in turn, resulting in a faster rate of CD8 T cell proliferation and expansion. (
  • Furthermore, it was found that IRF4-transduced CD8 T cells exhibited increased proliferation, suggesting that ectopic expression of IRF4 promotes polyclonal CD8 T cell expansion ( 13 ). (
  • In this study, we evaluated the inhibitory effect of astragalin on proliferation and migration of human colon cancer HCT116 cells in vitro and in vivo . (
  • Our further investigations unveiled astragalin gavage significantly reduced the proliferation of colon cancer xenograft in nude mice, in vivo experiments showed that tumor growth was related to decreased expression of apoptotic proteins in tumor tissues and decreased activity of the NF-κB signaling pathway. (
  • In summary, our results indicated that astragalin inhibits the proliferation and growth of colon cancer cells in vivo and in vitro via the NF-κB pathway. (
  • It enhanced the cell viability and proliferation and also increased the cell cytotoxicity and cell death index in methamphetamine-treated PC12 cells. (
  • Downregulation of cell division cycle 25 homolog C reduces the radiosensitivity and proliferation activity of esophageal squamous cell carcinoma. (
  • Inhibition of NCI-H358 cell proliferation after F3 fraction exposure occurred mainly by apoptosis as evidenced by damaged nuclei, significant DNA fragmentation level and caspase-3 activation in a dose dependent manner. (
  • Inactivation of the Rb tumor suppressor causes context-dependent increases in cell proliferation or cell death. (
  • This led to the postulation that they could also affect growth and differentiation in animals and have potential utility for treating human diseases that involve dysfunctional cell proliferation and/or differentiation [ 3 ]. (
  • Our results showed that oTR inhibited the proliferation of U937 cells by inducing apoptosis via the endoplasmic reticulum stress (ERS) pathway, as evidenced by the increased level of glucose regulated protein 78 (GRP78). (
  • Three cancer cell lines with up- or down-regulation of RCC2 were used to evaluate cell proliferation, apoptosis, Rac1 signaling and sensitivity to a group of nine chemotherapeutic drugs. (
  • Hepatocyte growth factor (HGF), also known as scatter factor (SF), plays an important role in cell:cell adhesion, cell proliferation, motility, and invasiveness of epithelial cells and tumor cells. (
  • HGF-transfected clones showed modestly increased proliferation rates and became more resistant to cell death and apoptosis caused by two anticancer drugs, adriamycin (ADR) and camptothecin (CPT), compared to controlvector-transfected clones. (
  • To examine mechanisms underlying growth-survival decisions during hypoxia, we have compared genetically related transformed and untransformed fibroblast cells in vitro for proliferation, survival, clonogenicity, cell cycle, and p53 expression. (
  • Despite its proapoptotic function, HGTD-P has been observed to coordinate with HIF-1α to promote cell growth and proliferation under hypoxic conditions in cervical cancer. (
  • Cancer cells thus are heavily dependent on ample and continuous availability of glucose for growth, proliferation and invasion. (
  • There are control systems in an organism that prevent proliferation of cells even when nutrient availability is surplus. (
  • Oncogenic mutation within cancer cells favours the intake of comestibles, in particular glucose which is a monosaccharide for uncontrolled cell proliferation. (
  • Previously, we have reported that SPD inhibited the proliferation of MCF-7 human breast cancer cells by inducing apoptotic cell death, while having minimal effects on non-malignant cells. (
  • The subsequent enhanced peptide secretion forced wild type Bon-1 cells in a neoplastic direction demonstrated by increased proliferation and colony formation while cell adhesion was decreased. (
  • The effects of various doses of delphinidin on the proliferation and apoptosis of MDA-MB-453 and BT474 cells were analysed. (
  • Delphinidin inhibited proliferation, promoted apoptosis, and induced autophagy in MDA-MB-453 and BT474 cells in a dose-dependent manner. (
  • AMSBIO can draw upon in-depth expertise in extracellular matrices to provide elegant solutions for studying cell motility, migration, invasion and proliferation. (
  • Using SH-SY5Y cells as an experimental model, we found that supporting with PC12 CM enhanced HA function in SH-SY5Y cell proliferation and adhesion. (
  • Through RP-nano-UPLC-ESI-MS/MS analyses, we identified increased expression of HSP60 and RanBP2 in SH-SY5Y cells grown on HA-modified surface with cotreatment of PC12 CM. Moreover, we also identified factors that were secreted from PC12 cells and may promote SH-SY5Y cell proliferation and adhesion. (
  • Ten metastatic melanoma cell lines were characterized by their proliferation, migration and invasion capabilities. (
  • An aggressiveness score (here named Melanoma AGgressiveness Score: MAGS) was calculated by measuring proliferation, migration, invasion and cell-doubling time in10human melanoma cell lines which were clustered in two distinct groups, according to the corresponding MAGS. (
  • Upon combined treatment, tumor cell proliferation was significantly decreased compared with single treated and untreated tumors. (
  • Taken together, our data show that peptide vaccination with cisplatin treatment leads to decreased tumor cell proliferation and TNFα-induced enhanced cisplatin-mediated killing of tumor cells, together resulting in superior tumor eradication. (
  • This study aimed to determine inhibitory effects on LoVo colon cancer cell proliferation and to clarify the underlying mechanisms in vitro and in vivo. (
  • Using 10-fold lower concentrations (100-500 nM), we found that ATRA inhibits MB (DAOY, D283, D425, and D458) cell proliferation as determined by cell viability [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] and bromodeoxyuridine incorporation assays. (
  • Thus, we demonstrate for the first time that low concentrations of ATRA inhibit MB cell proliferation and induce apoptotic cell death in part by activating caspase-3/poly(ADP-ribose) polymerase 1 effector pathway, and we show that retinoic acids and novel retinoids are potential antitumor agents in MB therapy. (
  • The mitogen-activated protein kinase (MAPK) cascade is a highly conserved module that is involved in various cellular functions, including cell proliferation, differentiation and migration. (
  • ALT inhibited the proliferation of ALL cells in a dose-dependent manner. (
  • Additionally, it was demonstrated that ALT inhibited cell proliferation, colony formation, autophagy, induced apoptosis and reduced tumor growth in vivo through upregulating the expression of adaptor related protein complex 2 subunit mu 1 (AP2M1). (
  • Acute lymphoblastic leukemia (ALL) is the most common type of leukemia, and is characterized by uncontrolled proliferation of immature lymphoid cells [ 1 , 2 ]. (
  • Cell proliferation and death were measured by MTT and LDH assay respectively. (
  • PSO inhibited the proliferation of A549 cells through autophagy but not apoptosis, which was mediated by inducing ROS production. (
  • Apoptosis, or programmed cell death, is an important and active regulatory pathway of cell growth and proliferation. (
  • However, unfortunately, resistant tumor cells are frequently selected during treatment, exemplifying the need for novel treatments that can further sensitize tumors to DR-mediated apoptosis. (
  • 7 , 8 Oncolytic virotherapy means the use of lytic viruses to kill tumor cells while normal cells are not infected by the virus. (
  • Despite the favorable advancement in development of chemotherapeutic drugs, the lack of selectivity to tumor cells and toxic side effects limit their effectiveness [ 1 , 2 ]. (
  • Therefore, oridonin has the potential to be developed as an anticancer agent, and the combination of oridonin with those agents leading to reduction of caspase-9 expression in tumor cells could represent a novel approach to human laryngeal cancer treatment. (
  • Forced RCC2 expression in tumor cells blocked spontaneous- or Staurosporine (STS)-induced apoptosis. (
  • Because chemotherapeutic drugs can kill tumor cells by activating Rac1/JNK pathway, we suspect that tumors with RCC2 overexpression would be more resistant to these drugs. (
  • Tumor cells with forced RCC2 expression indeed had significant difference in drug sensitivity compared to parental cells using a panel of common chemotherapeutic drugs. (
  • This behavior is typical of nearly every common human cancer and strongly implies that within an individual patient, tumor cells are not homogeneous in their treatment sensitivities. (
  • Studies of solid tumor cells have suggested that through induction of apoptosis, hypoxia may select for cells with defective apoptotic regulators such as p53 ( 19 ). (
  • Through understanding the behavior of such hypoxic tumor cells, strategies which better target this potentially dangerous cancer cell population may be devised. (
  • Hypoxia may also induce apoptosis in tumor cells ( 49 , 58 ) and has recently been implicated in the selection for p53-deficient tumor cells with a diminished apoptotic potential in central (hypoxic) areas of solid tumors ( 19 ). (
  • Glucose restriction puts break on speedy multiplying tumor cells as unlike normal cells of the body they are unable to metabolize any other source of fuel. (
  • Lower glucose level induces changes in level of cleaved caspase 3, Bcl-2, p53 and p21 which prompts senescence and apoptosis in rapidly proliferating tumor cells. (
  • Cancer cells are notorious as they are endowed with the ability to divide uncontrollably and generate multitudes of new tumor cells. (
  • Ang-2 release by reduced Pdcd4 in tumor cells increased tube formation of endothelial cells. (
  • The complement system can be specifically targeted to tumor cells due to molecular changes on their surfaces that are recognized by complement directly or via naturally occurring antibodies. (
  • However, tumor cells often overexpress membrane-bound complement inhibitors protecting them from complement attack. (
  • Positive PD-L1 expression in tumor cells was observed in 38.5% (40/104). (
  • A meta-analysis indicated that PD-L1 expression level on tumor cells might be a predictive biomarker of therapeutic response to PD-1/PD-L1-targeted therapy [ 8 ]. (
  • Z-LLNle-CHO blocks both γ-secretase and proteosome activity, inducing more robust cell death in precursor-B ALL cells than either proteosome-selective or γ-secretase-selective inhibitors alone. (
  • These findings show that the action of proteasome inhibitors is mediated primarily through a cytochrome c -dependent pathway and induces apoptosis in leukemic cells that are not differentiated. (
  • A role for cellular inhibitors of apoptosis (IAPs [cIAPs]) in preventing CD95 death has been suspected but not previously explained mechanistically. (
  • Surprisingly, this form of cell death can only be blocked by a combination of RIP1 (receptor-interacting protein 1) kinase and caspase inhibitors. (
  • Treatment of RPE cells with caspase inhibitors and Nec-1 resulted in a near complete rescue from cell death. (
  • Because these mediators may themselves induce both stimulators and inhibitors of apoptosis in endothelial cells ( 19 , 20 , 21 ), it would be extremely difficult to discriminate between direct and indirect effects of VT on apoptosis in tumor necrosis factor-α (TNF-α)-stimulated GMVEC. (
  • Both the caspases inhibitors, ZVAD-fmk and DEVD-cho, inhibited at similar extent apoptosis induced by either DXR or MEN 10755, suggesting an involvement of caspase-3 in this response. (
  • Bcl-2 and its relatives (for example, Bcl-x, E1B 19K, and CED-9) are potent inhibitors of apoptotic cell death ( 1 - 3 ). (
  • Isoproterenol rapidly induced ODC activity in H9c2 cardiomyoblasts by promoting the synthesis of the enzyme protein and this effect was counteracted by inhibitors of the PI3K/Akt pathway. (
  • Additionally, the company offer a number of cell lines and assay kits that can be used to screen for inhibitors of protein-protein interaction, as well as neutralizing antibodies to serve as positive controls for inhibition. (
  • demonstrated that ALT could sensitize human pancreatic cancer cells to EGFR inhibitors [ 11 ]. (
  • Finally, ALT enhances the sensitivity of cancer cells to EGFR inhibitors through inhibition of STAT3 signaling [ 11 ]. (
  • PD-1/PD-L1 pathway inhibitors were approval for the treatment of metastatic NSCLC patients [ 2 ]. (
  • PD-1/PD-L1 pathway inhibitors are only effective in some patients with NSCLC. (
  • We next characterized the morphological mode of PCD in these mice and show that the neurons degenerate by a caspase-independent, nonapoptotic pathway that involves autophagy. (
  • Together, these data indicate that, when key components of the type 1 apoptotic pathway (i.e., caspases and Apaf-1) are perturbed in vivo , developing postmitotic neurons nonetheless undergo quantitatively normal PCD by a caspase-independent pathway involving autophagy and not requiring AIF. (
  • These results demonstrate a fundamental role for RIP1 in CD95 signaling and provide support for a physiological role of caspase-independent death receptor-mediated cell death. (
  • The significance of these caspase-independent DR pathways is debated, and there is a need to provide additional examples in more physiological scenarios. (
  • Tamoxifen-induced toxicity was shown to occur through both caspase-dependent and caspase-independent cell death pathways. (
  • Simultaneous inhibition of caspase-dependent and caspase-independent cell death pathways is required to protect cells from tamoxifen. (
  • In neuronal cells, it additionally stimulates mitochondrial release of AIFM1, which then translocates to the nucleus to effect apoptosis, which indicates that it may participate in the caspase-independent apoptotic pathway depending on cell type or organism. (
  • The results suggest the existence of a second, caspase-independent, pathway for triggering apoptosis. (
  • The ubiquitin-proteasome pathway is the principal mechanism for the degradation of short-lived proteins in eukaryotic cells. (
  • In this pathway, specific proteins are marked for degradation by conjugation to multiple molecules of ubiquitin, which targets proteins for rapid hydrolysis by the 26S proteasome. (
  • The ubiquitin-proteasome pathway was initially regarded as a mechanism of destruction for old and damaged proteins. (
  • Finally, she has used CRISPR-Cas9 to target genes that can interfere with the quality of the protein product, such as host cell proteins that degrade the product or its attached glycan structures. (
  • In addition to targeting genes and regulatory elements that can impact the expression levels and properties of therapeutic proteins, Dr. Kildegaard's group is using CRISPR tools to answer questions about the basic biology of CHO cells. (
  • In addition, astragalin significantly downregulated the expression of key proteins in the NF-κB signaling pathway and inhibited the transcriptional activity of NF-κB P65 stimulated with inflammatory cytokines TNF-α, thereby inhibiting the growth of colon cancer cells in vitro . (
  • Activation of the terminal complement cascade involving C5 to C9 proteins has a beneficial role for oligodendrocytes (OLG) in experimental allergic encephalomyelitis, an animal model of multiple sclerosis, by protecting them from apoptotic cell death. (
  • Cell growth inhibition is essentially due to proteins and peptides isolated from these venoms, some of them are explored in phase I and phase II clinical trials [ 3 ]. (
  • The use of CHO cell line for the production of recombinant proteins used in human therapy has reached a level of industrial production. (
  • Apoptosis is a result of a very complex network of signaling pathways triggered from both inside and outside of the cell and a highly regulated pathway by both pro-apoptotic and anti-apoptotic proteins that promote cell survival or cell death. (
  • Heat shock proteins (HSP) are identified as target antigens of T-cell responses in glaucomatous mice and human glaucoma patients. (
  • Therefore, PrP C may protect against Htt toxicity in neuronal cells by increasing cellular defense proteins, decreasing ROS and increasing proteasome activity thereby increasing Htt degradation. (
  • Programmed death ligand 1 (PD-L1, B7-H1 or CD274) is a member of the growing B7 family of immune proteins that provide signals for both stimulating and inhibiting T cell activation. (
  • We demonstrate sampling of both proteins and mRNA for cell lines as well as human-derived cardiomyocytes and astrocytes. (
  • Here, we report a method for time-resolved, longitudinal extraction and quantitative measurement of intracellular proteins and mRNA from a variety of cell types. (
  • The secreted immunoglobulin footprint of single hybridoma cells, containing ~10 fg of antibody purified in situ, has been probed for 9 properties concurrently by use of detection labels comprising 280 nm combinatorially colored fluorescent latex beads functionalized with proteins. (
  • The PD1:PD-L1/2 Pathway is also involved in regulating autoimmune responses, making these proteins promising therapeutic targets for a number of cancers, as well as multiple sclerosis, arthritis, lupus, and type I diabetes. (
  • AMSBIO offers a comprehensive range of purified, soluble immunoreceptors and proteins involved in key immunosignaling pathways, such as PD-1, PD-L1, PD-L2, CTLA-4, TIGIT, LAG3 and IDO. (
  • Previously, we have shown that synthetic long peptides (SLP) vaccination against human papillomavirus type 16 (HPV16) oncogenic proteins is safe and induces functional T-cell responses in mice and humans. (
  • Protein transduction domains (PTDs) facilitate the delivery of molecules including proteins into cells or tissues. (
  • phagy: eating), autophagy is originally known as destructive mechanism of the cell that degrades unnecessary or dysfunctional proteins or organelles. (
  • When nutrients are limited or deprived in the cells, the autophagy is induced and degrades intracellular materials to produce new proteins and energy. (
  • Anthrax toxin acts by a sequence of events that begins when the protective-antigen (PA) moiety of the toxin binds to either one of two cell-surface proteins, ANTXR1 and ANTXR2, and is proteolytically activated. (
  • The resulting fusion protein transported enzymatic effector proteins into a cell line that expressed the EGF receptor (A431 cells), but not into a line lacking this receptor (CHO-K1 cells). (
  • Addition of excess free EGF blocked transport of effector proteins into A431 cells via the fusion protein, but not via native PA. (
  • PA fusion proteins with altered receptor specificity may be useful in biological research and could have practical applications, including ablation or perturbation of selected populations of cells in vivo. (
  • The use of GSI to induce NOXA induction overcomes the apoptotic resistance of melanoma cells, which commonly express numerous cell survival proteins such as Mcl-1, Bcl-2, and survivin. (
  • The boundary of the cells consists of cross-linked proteins with covalently bound lipids on the outer surface. (
  • In animals the process of programmed cell death, or apoptosis, is thought to be mediated by caspases, a family of cysteine proteases that cleave one another and key intracellular proteins, killing the cell in a controlled way. (
  • Primary ganglion cells treated with homocysteine had elevations in Opa1 and Fis1 proteins, a significantly higher number of mitochondria per length of neurite (0.1781 ± 0.017 vs. 0.1156 ± 0.012), and significantly higher levels of cleaved caspase-3 compared with control. (
  • Among these are externalization of phosphatidylserine (PS) to the cell surface, cleavage and degradation of specific cellular proteins, compaction and fragmentation of nuclear chromatin, and loss of membrane integrity (in late stages). (
  • Interestingly, when THP-1 cells were induced to undergo monocytic differentiation by bryostatin 1, a naturally occurring protein kinase C activator, they were no longer susceptible to apoptosis induced by Z-LLL-CHO. (
  • The protein kinase MST1 (mammalian Ste20-like kinase 1) plays a major role in oxidative stress-induced cell death in primary mammalian neurons. (
  • In mammalian systems, mammalian Ste20-like kinase (MST) is ubiquitously expressed and is best known for its function in promoting cell death. (
  • In this study, we characterize a novel upstream kinase of the MST1 signaling pathway involved in oxidative stress-induced neuronal cell death. (
  • Cormaci G, Mori T, Hayashi T, Su T-P (2007) Protein kinase A activation down-regulates, whereas extracellular signal-regulated kinase activation up-regulates σ-1 receptors in B-104 cells: implication for neuroplasticity. (
  • Cell cycle-dependent Cdc25C phosphatase determines cell survival by regulating apoptosis signal-regulating kinase 1. (
  • Ku is a heterodimeric complex composed of Ku70 and Ku86 subunits that serve as a DNA-binding subunit of the DNA-dependent protein kinase (DNA-PK) complex of the NHEJ pathway ( 12 , 13 ). (
  • The stress kinase pathway is also associated with ER stress-induced apoptosis. (
  • Section I. Kinases and Phosphatases Significance of Protein Kinase A in Cancer Maria V. Nesterova and Y. S. Cho-Chung Protein Kinase C and Cancer Mary E. Reyland The Role of PI3K-Akt Signal Transduction in Virus Infection Samantha Cooray Cyclin-Dependent Kinase 5: A Target for Neuroprotection? (
  • Regulated cell necrosis or necroptosis was examined with 7-AAD and inhibition of receptor-interacting protein 1 (RIP1) kinase using necrostatin-1 (Nec-1). (
  • Human tissue samples of invasive breast cancer and normal breast, as well as breast cancer cell lines, were evaluated for protein kinase D (PKD) expression, to test if altered expression could serve as a marker for invasive breast cancer. (
  • We found that the serine/threonine kinase, PKD1, is highly expressed in ductal epithelial cells of normal human breast tissue, but is reduced in its expression in more than 95% of all analysed samples of human invasive breast tumours. (
  • Jeggo is particularly well known for identifying two components of an enzyme called DNA-dependent protein kinase (DNA-PK) as being important in DNA non-homologous end joining (NHEJ), a pathway by which mammalian cells repair themselves. (
  • Inhibition of c-jun N terminal kinase (JNK) improves functional beta cell mass in human islets and leads to AKT and glycogen synthase kinase-3 (GSK-3) phosphorylation. (
  • Neuroprotection against ischemic brain injury by a small peptide inhibitor of c-Jun N-terminal kinase (JNK) via nuclear and non-nuclear pathways. (
  • C-jun N-terminal kinase regulates the interaction between 14-3-3 and Bad in ethanol-induced cell death. (
  • Differential regulation of the antiapoptotic action of B-cell lymphoma 2 (Bcl-2) and B-cell lymphoma extra-long (Bcl-xL) by c-Jun N-terminal protein kinase (JNK) 1-involved pathway in neuroglioma cells. (
  • The responses of AMP-activated protein kinase (AMPK) and Ornithine decarboxylase (ODC) to isoproterenol have been examined in H9c2 cardiomyoblasts, AMPK represents the link between cell growth and energy availability whereas ODC, the key enzyme in polyamine biosynthesis, is essential for all growth processes and it is thought to have a role in the development of cardiac hypertrophy. (
  • additionally, it is known that the classic AKT/protein kinase B-mammalian target of rapamycin (mTOR) signalling pathway initiates the vesicular double-membrane formation process of autophagy [ 12 ]. (
  • Under this condition, in the hypothalamus, AMP-activated protein kinase (AMPK) known as an energy sensor in the cell, senses the drop and gets activated. (
  • The role of mitogen-activated protein kinase pathways in Alzheimer's disease. (
  • LF inactivates mitogen-activated protein kinase kinases (MEKs) by cleaving near their N termini (3, 5), and we measured LF entry by Western blotting of cell lysates with an anti-MEK1 antibody after incubating cells with LF plus PA or a PA variant. (
  • ALT promotes ROS-mediated inhibition of the Akt/glycogen synthase kinase (GSK)3β pathway and induces endoplasmic reticulum (ER) stress [ 9 ]. (
  • Higher eukaryotic cells primarily repair DSBs by one of two genetically separable pathways, nonhomologous end joining (NHEJ) and homologous recombination (HR). NHEJ repairs broken ends with little or no requirement for sequence homology and involves the XRCC4-LIG4 complex and the DNA-dependent protein kinase (DNA-PK) holoenzyme, consisting of the DNA end-binding heterodimer Ku70-Ku80 and the catalytic subunit DNA-PK cs ( 22 , 23 , 53 ). (
  • Previous studies have shown that caspases and Apaf-1 are required for the normal programmed cell death (PCD) in vivo of immature postmitotic neurons and mitotically active neuronal precursor cells. (
  • Although normally these cells use caspases for PCD, in the absence of caspase activity these neurons undergo a distinct nonapoptotic type of degeneration. (
  • Although this normal programmed cell death (PCD) can occur by distinct morphological pathways ( Clarke, 1990 , 1998 ), the biochemical and molecular pathways involved have been generally considered to require a relatively conserved core of so-called "proapoptotic" genes comprised of Bcl-2 family members, the apoptosome (cytochrome c , Apaf-1, caspase 9) and downstream caspases (e.g., caspase-3). (
  • These studies clearly demonstrate that the extensive PCD of immature postmitotic neurons and mitotically active progenitor cells in the nervous system require cytochrome c , Apaf-1, and caspases. (
  • Here, we discuss the central role of caspases in the regulation of the general pathways of cell-extrinsic and cell-intrinsic T cell apoptosis and programmed necrosis with an overview of their importance for human health. (
  • Apoptosis can be triggered either by death signals acting on death receptors on the cell surface (extrinsic pathway) or by mitochondrial release of proapoptotic factors into the cytosol that leads to apoptosome assembly, activation of caspase-9, and the cleavage of effector caspases (intrinsic pathway) ( 8 ). (
  • Specific inhibition of caspases by Ac-Asp-Glu-Val-Asp-CHO, but not by Ac-Tyr-Val-Ala-Asp-CHO, was accompanied by inhibition of VT-induced apoptosis in FMVEC and TNF-α-treated GMVEC. (
  • Apoptosis can be induced by several activation pathways, which cause the activation of procaspases into active caspases ( 13 , 15 ). (
  • These activities converge in the activation of the so-called death caspases (caspases 3, 6, and 7), which initiate an irreversible process that leads to DNA fragmentation, cell detachment, and death ( 15 , 16 ). (
  • The successive interaction of the FADD-death effector domain molecule with caspase-8 activates a caspase cascade, which ends with downstream activation of caspases (caspase-3 and -7) and cleavage of cellular substrates. (
  • In a cell-free apoptosis system, mitochondria spontaneously released cytochrome c, which activated DEVD-specific caspases, leading to fodrin cleavage and apoptotic nuclear morphology. (
  • Cytochrome c was recently identified as such a factor-it is released from mitochondria in apoptotic cells and can trigger activation of DEVD-specific caspases (DEVDases) and apoptotic effects in cell-free systems containing cytosol ( 16 , 21 ). (
  • Apoptotic signaling pathways: caspases and stress-activated protein kinases. (
  • The Somatostatin Receptors (SSTRs) are expressed in a tissue-specific manner and involved in the regulation of secretion of insulin, glucagon and growth hormone as well as cell growth induced by neuronal excitation in both the central and peripheral nervous systems. (
  • Russell J.H. (1995) Activation-induced death of mature T cells in the regulation of immune responses. (
  • In recent years, however, it has become clear that proteolysis by the proteasome pathway is a crucial mechanism of regulation of many cellular processes, including cell cycle progression, gene expression, and cell differentiation. (
  • however, regulation of IRF4 expression in CD8 + T cells remains unclear. (
  • Our data support a novel and critical role for Nr4a1 in the regulation of CD8 + T cell expansion and effector function through transcriptional repression of Irf4. (
  • To further demonstrate this regulation, we show that small interfering RNA (siRNA)-mediated knockdown of Nr4a1 in CD8 cells in vitro increased the expression of Irf4 , whereas overexpression of Nr4a1 in Nr4a1-deficient CD8 + T cells decreased the expression of Irf4 . (
  • We have previously shown that sublytic C5b-9 complexes, through posttranslational regulation of Bad, inhibit the mitochondrial pathway of apoptosis induced by serum deprivation. (
  • Regulation of the FADD-caspase-8 proapoptotic signaling pathway is mediated through an intrinsic inhibitor, cellular FLIP (c-FLIP) ( 21 , 22 ). (
  • This gene encodes a conserved protein that plays a key role in the regulation of cell division. (
  • Regulation of an ATG7-beclin 1 program of autophagic cell death by caspase-8. (
  • In summary, we used the integration of the data generated by MFA to understand apoptotic behavior and establish a correlation between cell regulation and apoptosis. (
  • It will help us to identify the changes during the onset of apoptosis process will be studied by using proteomics tools to analyze the protein up-regulation or down-regulation in different cell status in the future. (
  • The CD274 - PD-1 pathway is involved in the negative regulation of some immune responses and may play an important role in the regulation of peripheral tolerance. (
  • Epigallocatechin-3-gallate (EGCG): Clinical studies suggest that EGCG has neuroprotective qualities and can significantly suppress toxicity of dopamine neurons through antioxidation, anti-inflammation, iron-chelation, cell death regulation and modulation of signaling pathways (Zhou et al, 2019). (
  • Exposure to either anthracycline induced the up-regulation of several genes known to promote cell cycle arrest and DNA repair (WAF1/p21, GADD45) or apoptosis (bax, Fas). (
  • We summarize the neuronal populations and neural pathways of these three CNCs, which gives evidence for the orchestration within these three CNCs, and the integrative regulation of these three CNCs by different environmental light signals. (
  • Cancer cells bypass growth factor regulation as they acquire genetic mutations and thus exhibit altered signalling pathways which aids in constitutive uptake and metabolism of nutrients which promote cell survival and fuel cell growth. (
  • Regulation of Angiopoietin-2 by Pdcd4 is attained by diverse mechanisms depending on the cell line. (
  • In vitro, PGE2 secreted by MSCs inhibited Kupffer cell apoptosis via TLR4-ERK1/2-caspase3 pathway regulation. (
  • Feedback regulation of SREBP and aromatase in A beta(25-35)-supplemented human neuroblastoma cells. (
  • To evaluate the effect of excess homocysteine on the regulation of retinal ganglion cell mitochondrial dynamics. (
  • The abilities of migration and invasion for EOC cells were significantly reduced after Gal-1 knocked-down in human EOC cell line HO8910, which was accompanied with the suppression of NF-κb pathway activation and with the matrix metalloproteinase-2 and matrix metalloproteinase-9 down-regulation. (
  • Inhibition of c-Abl promotes the degradation of MST1 through C terminus of Hsc70-interacting protein (CHIP)-mediated ubiquitination, and thereby attenuates cell death. (
  • Inhibition of c-Abl by using c-Abl RNAi or STI571 attenuates oxidative stress-induced MST1 activation as well as cell death both in primary cultured neurons and in rat hippocampal neurons. (
  • Genetically defined ES models are needed to understand how EF expression changes bone precursor cell differentiation, how ES arises and through which mechanisms of inhibition it can be targeted. (
  • Functionally, knockdown of Mcl1 or Cdk4 or their combined pharmacologic inhibition resulted in growth arrest and apoptosis in both established human ES cell lines and EF-transformed mouse MSCs. (
  • We concluded that Descurainia sophia oil suppresses the methamphetamine-induced cell death in PC12 cell due to reduction of NO production, inflammation, and inhibition of apoptosis cascade. (
  • Inhibition of upstream activators, such as the cathepsins, may represent a novel approach to block multiple cell death pathways. (
  • 2014) 20-O-beta-D-glucopyranosyl-20(S)-protopanaxadiol suppresses UV-Induced MMP-1 expression through AMPK-mediated mTOR inhibition as a downstream of the PKA-LKB1 pathway. (
  • Modulation of mitochondrial dysfunction-related oxidative stress in fibroblasts of patients with Leigh syndrome by inhibition of prooxidative p66Shc pathway. (
  • Furthermore, whereas partial inhibition of protein synthesis by VT was associated with a considerable number of apoptotic cells, comparable inhibition of protein synthesis by cycloheximide was not. (
  • This suggests that additional pathways, independent of protein synthesis inhibition, may be involved in VT-mediated apoptosis in microvascular endothelial cells. (
  • Various strategies can be employed to cut down glucose accessibility to cancer cells such as inhibition of glucose transporters, adoption of keto diet. (
  • The inhibition of autophagy enhanced the delphinidin-induced apoptosis and antiproliferative effect in both HER-2 positive breast cancer cells. (
  • Our findings suggest potential clinical applications in which autophagic inhibition sensitizes cells to the anticancer effect of delphinidin. (
  • In the present study, we used a lentiviral vector to express short hairpin RNAs for inhibition of apoB production in HepG2 cells. (
  • Oxidative stress influences cell survival and homeostasis, but the mechanisms underlying the biological effects of oxidative stress remain to be elucidated. (
  • The peripheral T-cell lymphomas (PTCL) are a rare and heterogeneous group of non-Hodgkin lymphomas (NHL) associated with a poor prognosis ( 1 ), as only 15%-25% of patients can expect long-term survival following conventional chemotherapy. (
  • Apoptosis and autophagy are two important cellular processes which control cell survival or death [ 4 ] and are also considered as a balanced response to pathogens and other immune stimuli that play an important role in maintaining physiologic homeostasis [ 5 ]. (
  • Acupuncture could regulate multiple molecules and signaling pathways that lead to excitoxicity, oxidative stress, inflammation, and neurons death and survival and also promote neurogenesis, angiogenesis, and neuroplasticity after ischemic damage [ 10 ]. (
  • Combinatorial targeting of survival and cell cycle progression pathways could counteract this aggressive childhood cancer. (
  • Sarcomagenesis was accompanied by upregulation of the CDK4/cyclin D1/pRB axis, and reduced INK4A and P53 expression accelerating cell cycle and survival. (
  • This loss is often correlated with overexpression of several antiapoptotic and cell survival genes that render the cancer cells resistant to apoptosis ( 2 ). (
  • In conclusion, our results indicated that AEG-1 played a crucial role in the carcinogenesis of NSCLC and could inhibit apoptosis via activating cell survival signaling (enhancing the level of anti-apoptotic protein Bcl-2 and the activation of PI3K/Akt pathway). (
  • CD8 + T cells infiltration was associated with better survival while PD-L1 expression was correlated with PC recurrence. (
  • Both the low CD8 + T cells infiltration/high PD-L1 expression group and the high CD8 + T cells infiltration/high PD-L1 expression group show high levels of CD44 + /CD133 + CSCs, but patients with low CD8 + T cells infiltration/high PD-L1 expression had worse survival and higher recurrence risk than those with high CD8 + T cells infiltration/high PD-L1 expression. (
  • Bcl-2 gene promotes haemopoietic cell survival and cooperates with c-myc to immortalize pre-B cells. (
  • bcl-2-immunoglobulin transgenic mice demonstrate extended B cell survival and follicular lymphoproliferation. (
  • Interestingly, as examined by clonogenic survival assay, a 30-minute camptothecin treatment induced significantly higher levels of radiosensitization in the Ku86-deficient Chinese hamster ovary xrs-6 cells than in the hamster Ku86-complemented xrs-6+hamKu86 cells, albeit exhibiting similar drug toxicity in these two cell lines. (
  • Apoptosis, Cell Signaling, and Human Diseases: Molecular Mechanisms, Volumes 1 and 2, present a concise synthesis of recent developments in the understanding of both cell survival and apoptotic pathways. (
  • We showed that NatB subunits were required for elevated EGFR/MAPK signaling and Rb mutant cell survival. (
  • It has been reported that PrP C functions in cell survival, signal transduction, cell adhesion, copper-dependent antioxidant activity, and copper uptake and sequestration ( Roucou and LeBlanc, 2005 ). (
  • Signalling for survival and death in neurones: the role of stress-activated kinases, JNK and p38. (
  • Mutations that cause partial loss of function of killer genes allow the survival of some cells that are programmed to die, and mutations in engulfment genes enhance the frequency of this cell survival. (
  • Furthermore, mutations in engulfment genes alone allow the survival and differentiation of some cells that would normally die. (
  • Evidence for a role of HR in the radioresistance of higher eukaryotes is derived from cell survival experiments with HR-defective mutants. (
  • The relatively high radioresistance of NHEJ-defective mutants in the late-S/G 2 portion of the cell cycle further suggests that HR promotes survival when sister chromatids are present ( 55 , 72 ). (
  • Selective activation of SSTR1 inhibits hormone secretion and cell viability in GH- secreting and PRL-secreting adenomas in vitro. (
  • Apoptotic death of OLG is induced by a variety of factors, both in vitro and in vivo, including TNF-α, nerve growth factor, and the interaction of Fas (CD95) with FasL (CD178) ( 5 , 6 , 7 ). (
  • However, when studied in vitro late apoptotic cells may lose membrane integrity and become necrotic. (
  • 14 This terminal phase of in vitro cell death, called secondary necrosis, occurs in apoptotic cells in the absence of phagocytic cells. (
  • Recently, several investigations demonstrated that venoms and toxins of some species of scorpions, especially those of the Buthidae family, induce cytotoxic antiproliferative effects and apoptosis on cancer cells in vitro and in vivo [ 8 - 12 ]. (
  • However, a major problem encountered in in vitro cultures is cell death via apoptosis. (
  • Since apoptosis leads to the loss of viability of mammalian cells in vitro, especially in serum-free media. (
  • In vitro studies using HUVEC and glomerular microvascular endothelial cells (GMVEC) have indicated that VT susceptibility requires additional stimulation by inflammatory mediators for induction of a sufficiently large number of specific VT receptors on these cells ( 5 , 18 ). (
  • In the vitro experiment, the changes of the mitochondrial membrane potential, expression of superoxide dismutase (SOD), 4-hydroxynonenal (4-HNE), cytochrome c, and cleaved caspase 3 were measured to show the effects of catechin treatment on the NRK-52E cells induced by calcium oxalate monohydrate (COM). (
  • In vitro infection with these strains induces DNA double-strand breaks (DSBs) in cultivated human cells, but the pks island was not proved to cause DNA damage in vivo ( 4 ). (
  • This is because living organisms have a multitude of cell populations that are connected and affect each other compared to a single hypothalamic cell line in vitro. (
  • This process can be mimicked in vitro by growing ES cells in ball-like aggregates called embryoid bodies. (
  • This study provides the first evidence that homocysteine-induced ganglion cell loss involves the dysregulation of mitochondrial dynamics, both in vivo and in vitro. (
  • In vitro experiments were further performed to reveal the function and mechanisms of Gal-1 in invasion and migration of EOC cells. (
  • The N-terminal region of the RNase E protein inhibits bacterial death induced by human Bax as well as paraquat through a unique mechanism that is distinct from RNA digestion. (
  • 2014) A combination of paclitaxel and siRNA-mediated silencing of Stathmin inhibits growth and promotes apoptosis of nasopharyngeal carcinoma cells. (
  • Bcl-2 inhibits cytochrome c release from mitochondria and apoptotic changes in a cell-free system. (
  • The PD-1 ligands are found on most cancers, and PD-1: PD-L2 interaction inhibits T-cell activity and allows cancer cells to escape immune surveillance. (
  • 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. (
  • ALT inhibits TrxR1 activity and activates a ROS-mediated p38 MAPK signaling pathway [ 12 ]. (
  • Bax is a member of the Bcl-2 family and induces apoptosis of mammalian cells. (
  • We have shown that a trace amount of human Bax induces the cell death of Escherichia coli, accompanied by damage to DNA, and that the region of Bax which is lethal to E. coli is also responsible for apoptosis-inducing activity in the mammalian cells. (
  • In the current study, we investigated the role of Ku86 in DNA topoisomerase I-mediated radiosensitization induced by camptothecin in mammalian cells. (
  • Taken together, our data show a novel role of Ku86 in modulating topoisomerase I-mediated radiosensitization, but not cytotoxicity, in mammalian cells. (
  • Indeed, certain topoisomerase I-targeted indolocarbazoles have recently been shown to induce radiosensitization in mammalian cells ( 9 ). (
  • In this study, we wished to explore whether those bacteria were able to induce genetic damage in vivo on the colonic mucosa and to characterize the consequences of this damage on mammalian cells in relation with the number of infecting bacteria. (
  • In addition, infection of various mammalian cells with pks + E. coli induced, at very low multiplicity of infection (MOI), reversible DNA damage response that did not repair all DSBs, leading to chronic mitotic and chromosomal aberrations together with increased frequency of gene mutation and anchorage-independent growth. (
  • Bacterial toxins that act within mammalian cells have receptor-dependent mechanisms to transport their enzymatic components to the cytoplasmic compartment. (
  • Sterol carrier protein-2 (SCP-2) plays a crucial role in the trafficking and metabolism of cholesterol and other lipids in mammalian cells. (
  • Oxidative stress induces the c-Abl-dependent tyrosine phosphorylation of MST1 and increases the interaction between MST1 and FOXO3 (Forkhead box O3), thereby activating the MST1-FOXO signaling pathway, leading to cell death in both primary culture neurons and rat hippocampal neurons. (
  • Exposure of cells to stress and apoptosis-inducing stimuli such as staurosporine, Fas ligase, and oxidative stress activates MST. (
  • Recently, c-Abl has been linked to oxidative stress-induced neuronal cell death through Cdk5/GSK3β activation and Tau hyperphosphorylation or through p73 upregulation. (
  • Moreover, F3 fraction enhanced oxidative and nitrosative stress biomarkers and dissipated mitochondrial membrane potential in lung cancer cells along with significant depletion in cellular enzymatic and non-enzymatic antioxidants. (
  • These findings suggest that F3 fraction could induce apoptosis in lung cancer cells through involvement of oxidative stress and mitochondrial dysfunction. (
  • Mechanical stretch of the tubular epithelium and oxidative stress are believed to be early stress factors leading to tubular cell injury and death. (
  • The intrinsic mitochondrial pathway to apoptosis is further enhanced by oxidative stress. (
  • Stretch appears to play a direct role in oxidative stress in tubular cells, as decreased catalase mRNA was also found when tubular cells were subjected to cyclic mechanical stretch ( 30 ). (
  • Klotho enhances FoxO3-mediated manganese superoxide dismutase expression by negatively regulating PI3K/AKT pathway during tacrolimus-induced oxidative stress. (
  • miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells. (
  • Heat shock protein 22 (HSP22) is known to protect cells against oxidative stress. (
  • However, the protective effects and mechanisms of HSP22 in hippocampal neuronal cells under oxidative stress remain unknown. (
  • 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. (
  • 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. (
  • Lipid hydroperoxides generated under oxidative stress conditions are relatively long-lived intermediates that damage cell membranes and play an important role in redox signaling. (
  • Wild-type MLO dampens the cell wall-restricted hydrogen peroxide burst at points of attempted fungal penetration of the epidermal cell wall, and in subtending mesophyll cells, it suppresses a second oxidative burst and cell death. (
  • Many of the local actions of snake venoms are mediated by a direct action on skeletal and vascular smooth muscle cells, endothelial cells, macrophages, neutrophils, mast cells, and platelets (17). (
  • Protective role for Bcl-2 in experimentally induced cell death of bovine corneal endothelial cells. (
  • 6, Endothelial Cells as Key Determinants of the Tumor Microenvironment. (
  • In this study, the role of apoptosis in verocytotoxin (VT)-mediated endothelial cell death in human glomerular microvascular endothelial cells (GMVEC), human umbilical vein endothelial cells, and foreskin microvascular endothelial cells (FMVEC) was investigated. (
  • VT induced apoptosis in GMVEC and human umbilical vein endothelial cells when the cells were prestimulated with the inflammatory mediator tumor necrosis factor-α (TNF-α). (
  • On the basis of functional (flow cytometry and immunofluorescence microscopy using FITC-conjugated annexin V and propidium iodide), morphologic (transmission electron microscopy), and molecular (agarose gel electrophoresis of cellular DNA fragments) criteria, it was documented that VT induced programmed cell death in microvascular endothelial cells in a dose- and time-dependent manner. (
  • These data indicate that VT can induce apoptosis in human microvascular endothelial cells. (
  • The presence of apoptotic endothelial cells in the glomeruli of kidney biopsy specimens from three patients with the epidemic form of HUS was recently reported ( 11 ). (
  • However, whether VT can directly induce apoptosis in endothelial cells has not been studied. (
  • The presence of caspase 1-like activity and caspase 3 has been demonstrated in human umbilical vein endothelial cells (HUVEC) ( 17 ). (
  • Astrocytes also make a crucial contribution to communication, operating within glial networks through gap junctions and hemichannels and bidirectionally with neurons and endothelial cells via diffusible and surface molecules [ 1 - 4 ]. (
  • Therefore, we analyzed the effect of supernatants from Pdcd4 knock-down cell lines on endothelial cells. (
  • Tube length and junctions of endothelial cells treated with conditioned medium from Pdcd4 knock-down cells were considerably increased. (
  • The inflammatory process in the brain is unique in that the blood-brain barrier (BBB) (tight layer of endothelial cells that separates the brain from regular systemic circulation), during healthy conditions, prevents the infiltration of inflammatory agents and allows only select nutrients and small molecules into the central nervous system (CNS). (
  • Somatostatin receptors are activated by somatostatin secreted from nerve and endocrine cells. (
  • The initiators of the extrinsic cell death pathway are a subclass of TNF superfamily (TNFSF) receptors called death receptors (DRs). A common feature of DR signaling is the formation of a primary plasma membrane-associated death-inducing signaling complex (DISC) and a secondary independent signaling platform in the cytoplasm (complex II). (
  • One is the extrinsic pathway, in which ligation of death receptors by death ligands is followed by recruitment of adaptor molecules and activation of caspase-8 or caspase-10. (
  • While glutamate is the brain's most important excitatory neurotransmitter, L-theanine binds to the same brain cell receptors and blocks them to glutamate's effects. (
  • The actions of many bacterial toxins depend on their ability to bind to one or more cell-surface receptors. (
  • Because of increasing evidence that the Notch signaling network is deregulated in human malignancies, Notch receptors have become attractive targets for selective killing of malignant cells. (
  • By using a small molecule gamma-secretase inhibitor (GSI) consisting of a tripeptide aldehyde, N-benzyloxycarbonyl-Leu-Leu-Nle-CHO, which can block processing and activation of all four different Notch receptors, we identified a specific apoptotic vulnerability in melanoma cells. (
  • Taken together, these results highlight the concept of synthetic lethality in which exposure to GSI, in combination with melanoma cells overexpressing activated Notch receptors, has lethal consequences, producing selective killing of melanoma cells, while sparing normal melanocytes. (
  • In both systems, its actions are exerted extracellularly via membrane-bound receptors on adjacent sites after translocation of the protein from the cytoplasm to the cell surface of adjacent cells. (
  • Necroptosis is initiated when death signals such as TNF-α and Fas bind to their membrane receptors. (
  • Bryostatin 1-induced differentiation of THP-1 cells was associated with growth arrest, acquisition of adherent capacity, and expression of membrane markers characteristic of blood monocytes. (
  • In this article, we report a critical role for Nr4a1 in regulating the expansion, differentiation, and function of CD8 + T cells through direct transcriptional repression of Irf4 . (
  • The effector differentiation of CD8 + T cells is regulated by various transcription factors ( 7 ). (
  • IFN regulatory factor (IRF)4, a member of the IRF family of transcription factors, was recently shown to be vital for sustaining the expansion and effector differentiation of CD8 + T cells ( 8 - 10 ). (
  • The rise in IRF4 resulted in increased proliferative behavior and effector differentiation of CD8 + T cells. (
  • EF expression arrested early chondrocyte and osteoblast differentiation due to changed signaling pathways such as hedgehog, WNT or growth factor signaling. (
  • The caspase-8 inhibitor Z-IETD-FMK inhibited cell death associated with differentiation in a dose-dependent manner. (
  • We concluded that oTR induced apoptosis, promoted the cell differentiation and inhibited DNMT1 activity of U937 cells, suggesting its potential as a therapeutic agent for the treatment of AML. (
  • However, the detailed molecular mechanism underlying its anticancer effect has not been elucidated, and little is known about the effect of differentiation on carcinoma cells. (
  • In the present study, we evaluated the growth inhibitory effects of oTR on human AML U937 cells mediated by the induction of apoptosis and differentiation. (
  • In contrast to neurons, little is known about the intracellular signaling of astrocytes, and the pathways controlling their differentiation and activation have not been elucidated. (
  • By means of STAT transcription factors, cytokines of the interleukin-6 family are key cues in the specification and differentiation of astroglial cells. (
  • This destruction prevents knowledge of prior or future states of the cell, which is particularly important for dynamic cell processes, such as development and differentiation. (
  • Notch signaling regulates cell fate decisions in the epidermis, including influencing stem cell dynamics and growth/differentiation control of cells in skin. (
  • Differentiation of Wharton's jelly-derived mesenchymal stem cells into motor neuron-like cells on three-dimensional collagen-grafted nanofibers. (
  • We showed that NatB regulates the posttranscriptional levels of the highly conserved pathway components Grb2/Drk, MAPK, and PP2AC but not that of the less conserved Sprouty. (
  • Interestingly, NatB increased the levels of positive pathway components Grb2/Drk and MAPK while decreased the levels of negative pathway component PP2AC, which were mediated by the distinct N-end rule branch E3 ubiquitin ligases Ubr4 and Cnot4, respectively. (
  • These results suggest a novel mechanism by which NatB and N-end rule pathways modulate EGFR/MAPK signaling by inversely regulating the levels of multiple conserved positive and negative pathway components. (
  • Signaling via NF-κB and p38 MAPK pathways were both affected by SS-31 treatment. (
  • The dysregulation of miRNA is crucial in neurodegenerative diseases and neuron apoptosis during AD and is closely associated with the MAPK pathway. (
  • Neuronal p38 MAPK signalling: an emerging regulator of cell fate and function in the nervous system. (
  • MAPK pathways in radiation responses. (
  • ALT regulates the p38 MAPK and NF-κB pathways. (
  • While product quality is the predominant focus for matching across scales, as companies gain experience with scale-down modeling of their manufacturing process, they may begin to explore beyond the usual set of process performance parameters, such as cell viability and titer, and look at factors such as carbon dioxide and metabolite profiles. (
  • Studies have demonstrated that silencing certain target genes involved in certain CHO cell apoptotic and metabolic pathways resulted in 40 to 60% improved cell viability as compared with untreated cells. (
  • This is important and necessary to prevent the activation of apoptosis cascade and increase their cell viability and enhance their cellular robustness. (
  • Moreover, when uncoupled from acidosis, hypoxia enhances tumor cell viability and clonogenicity relative to normoxia. (
  • 95% cell viability after sampling, enabling long-term analysis. (
  • Our results demonstrated that LoVo cell viability showed dose- and time-dependence on ${\beta}$ -asarone. (
  • We also demonstrate that the ATRA-induced decrease in cell viability was due to increased cell death by apoptosis, which was accompanied by a 20-fold induction of caspase-3 activity in the most sensitive cell line, D458. (
  • ALL cell lines were treated with 1, 5 and 10 μM ALT, and cell viability was assessed using an MTT assay and RNA sequencing. (
  • The cell viability was measured by MTT assay, and the data were presented as means ± SD from three independent experiments. (
  • The Guava PCA-96 system performs a number of automated cellular assays, including viability, absolute cell counting, three apoptotic assays and a cell cycle assay. (
  • The Guava ViaCount assay rapidly and reliably determines cell concentration and viability. (
  • The system can determine the viability of the cell sample since it can distinguish non-viable cells that will also absorb the second dye. (
  • The Guava ViaCount assay more accurately and precisely determines cell concentrations and viabilities than Trypan Blue exclusion 1 , especially at low cell concentrations, and shows much less operatorto-operator variability, in part because Trypan Blue has been reported to overestimate cell viability 2,3 . (
  • In this study, we attempted to establish the regulatory role of GRK2 in the Toll-like receptor (TLR) signaling pathway for inducible nitric oxide synthase (iNOS) expression in microglial cells. (
  • However, the clinical implications of the associations among CD8 + T cells infiltration, programmed death receptor ligand-1 (PD-L1) expression, and CSCs existence are poorly understood in PC. (
  • Fas death receptor signalling: roles of Bid and XIAP. (
  • 16. Moon NS, Di Stefano L, Dyson N (2006) A gradient of epidermal growth factor receptor signaling determines the sensitivity of rbf1 mutant cells to E2F-dependent apoptosis. (
  • ROS triggered the progression of apoptosis through activation of both the caspase-9-independent mitochondrial pathway and death receptor pathways, and the autophagy had an anti-apoptotic function in oridonin-treated HEp-2 cells. (
  • Although the expression of Fas was increased, an antagonistic anti-Fas antibody ZB4 did not inhibit anthracycline-induced apoptosis, suggesting that the stimulation of the Fas receptor did not play a critical role in the induction of apoptosis in this cell line. (
  • Apoptotic cell death induced by activation of the Fas/Fas-L system requires a multistep cascade of biochemical events: the trimerization of Fas receptor induced by Fas-L stimulates the formation of a death-inducing signaling complex, which consists of the adapter protein FADD and the protease FLICE/caspase-8. (
  • Resident peritoneal macrophages (PEMs) express SIGNR1 on the cell surface as a major mannose receptor. (
  • The binding of Programmed Cell Death Protein 1 (PD-1), a receptor expressed on activated T-cells, to its ligands, PD-L1 and PD-L2, negatively regulates immune responses. (
  • Our results show that the receptor specificity of the transport protein of anthrax toxin may be readily changed, raising the possibility that receptor-redirected forms of protective antigen (PA) and PA homologs may be useful for research and medical applications requiring modification or ablation of designated populations of cells. (
  • Notch receptor-mediated intracellular events represent an ancient cell signaling system, and alterations in Notch expression are associated with various malignancies in which Notch may function as an oncogene or less commonly as a tumor suppressor. (
  • Compared with proliferating normal human melanocytes, melanoma cell lines are characterized by markedly enhanced levels of activated Notch-1 receptor. (
  • Previous studies have suggested that HDL retroendocytosis may play a role in scavenger receptor class B type I (SR-BI)-dependent selective lipid uptake in a cell-specific manner. (
  • This type of necrosis can be inhibited by a chemical named Necrostatin-1 (Nec-1), which suppresses the activity of receptor-interacting protein 1 (RIP1), suggesting that the cell death is molecularly regulated. (
  • Importantly, the EVs secreted by MSCs can transfer a variety of bioactive factors to modulate the function of recipient cells via various mechanisms, including ligand-receptor interactions, direct membrane fusion, endocytosis, or phagocytosis. (
  • AP2M1 is one of the most important cytoplasmic carrier domains in clathrin-mediated endocytosis, and phosphorylation of this subunit stimulates clathrin and supports cell surface receptor incorporation. (
  • Engulfment genes probably act in engulfing cells to promote death, as the expression in engulfing cells of ced-1, which encodes a receptor that recognizes cell corpses, rescues the cell-killing defects of ced-1 mutants. (
  • A common phenotype in all of these mutant mice is a massive overgrowth of cells in the brain (exencephaly) that was attributed in part to reduced PCD of both immature neurons and dividing neuronal precursor cells. (
  • MPP(+) downregulates mitochondrially encoded gene transcripts and their activities in dopaminergic neuronal cells: protective role of Bcl-2. (
  • The effect of normal cellular prion protein (PrP C ) on abnormal protein aggregation was examined by transfecting huntingtin fragments (Htt) into SN56 neuronal-derived cells depleted of PrP C by RNA interference. (
  • Depletion of endogenous PrP C in non-neuronal Caco-2 and HT-29 cells did not affect ROS levels or proteasome activity suggesting that only in neuronal cells does PrP C confer protection against Htt toxicity. (
  • The protective effect of PrP C was further evident in that overexpression of mouse PrP C in SN56 cells transfected with Htt caused a decrease in both the number of cells with Htt granules and the number of apoptotic cells, whereas there was no effect of PrP C expression in non-neuronal NIH3T3 or CHO cells. (
  • Although this could be a direct effect of PrP Sc , it is also possible that, since PrP C specifically prevents pathological protein aggregation in neuronal cells, partial loss of PrP C itself increases PrP Sc aggregation. (
  • There have been numerous models proposed for the neuronal cell loss and spongiform changes in the brain that occur in scrapie, but it is still not clear whether this pathology is due to a loss of functional PrP C or only to a gain of function by PrP Sc . (
  • Furthermore, altered neuronal excitability can predispose individuals to neuronal damage and death ( Leist and Nicotera, 1998 ) so it is possible that loss of PrP C function contributes to scrapie pathogenesis in this way. (
  • It also shows general protection against neuronal death, specifically in the area of the brain that produces dopamine. (
  • 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. (
  • The mechanisms leading to MST activation and cell death vary depending on stimulus specificity and cell type. (
  • There, I studied a mitochondria-initiated apoptosis pathway, specifically looking at the molecular mechanisms behind the activation mechanism of apoptosome. (
  • Expression of astrocyte-elevated gene-1 (AEG-1), a novel oncoprotein, has been shown to promote cell growth and inhibit apoptosis, but the underlying molecular mechanisms and its functional significance in non-small cell lung cancer (NSCLC) remain to be elucidated. (
  • Here we have studied cell death mechanisms of canine parvovirus (CPV) to increase the knowledge on the CPV life cycle in order to facilitate the development of better parvovirus vectors. (
  • Infection arrests cell cycle 21 - 24 and induces cell death through different cell death mechanisms. (
  • We focus principally on cell death mechanisms in T lymphocytes that control the number of T cells of a given antigen specificity represented in the finite T cell niche. (
  • an up-to-date synthesis of information regarding mechanisms of cell cycle control and apoptosis. (
  • To evaluate the mechanism of tamoxifen-induced cell death in human cultured RPE cells, and to investigate concurrent cell death mechanisms including pyroptosis, apoptosis, and necroptosis. (
  • Tamoxifen-induced cell death occurs through concurrent regulated cell death mechanisms. (
  • In the present study, we investigated the mechanisms of cell death induced by doxorubicin (DXR) and the novel disaccharide anthracycline MEN 10755, in a human ovarian cancer cell line (A2780). (
  • Different chemical classes of anticancer drugs can induce tumor cell death by multiple mechanisms. (
  • The present review focuses on recent progress in our understanding of the basic mechanisms underlying HDL biogenesis pathways. (
  • Although all cells seem to be able to generate lipid droplets, their biogenesis, regulatory mechanisms and interactions with other organelles remain largely elusive. (
  • While replacement therapy remained unrealistic, the clinical efficacy of this therapeutic option could be potentially enhanced if we could better decipher the mechanisms underlying some of the beneficial effects of transplanted cells, and work toward augmenting or combining these in a strategic manner. (
  • 2 When administered in animal models, GSIs have a range of biological activities, including an ability to reduce the accumulation of amyloid peptides associated with Alzheimer's disease, and can induce apoptosis in a variety of tumors, included breast cancer cells. (
  • Treatment of human blood monocytes with Z-LLL-CHO did not induce apoptosis or Bcl-2 cleavage in these cells that rarely proliferate. (
  • Numerous studies have shown that suppression of constitutive NF-κB activation by certain small molecules or by genetic manipulation can induce apoptosis, enhance radiosensitization and chemosensitization, suppress invasion, and inhibit metastatic growth in cancer cells, including prostate cancer cells ( 5 ). (
  • Oridonin, a bioactive diterpenoid isolated from Rabdosia rubescens, has been reported to induce apoptosis in human laryngeal cancer HEp-2 cells by our group. (
  • We also observed that neither MEN 10755 nor DXR were able to induce apoptosis in A2780 cells deprived of the nucleus but retaining an intact mitochondrial function (cytoplasts) and that apoptosis induced by either anthracycline was inhibited by cycloheximide, indicating that it is an active process requiring new protein synthesis. (
  • We and others ( 15 , 19 , 21 , 27 ) have demonstrated that stretch induces caspase-dependent apoptosis in tubular epithelial cells. (
  • Induction of apoptosis has also been reported for a variety of cell types ( 7 , 8 , 9 ), including renal tubule-derived epithelial cells ( 10 ). (
  • We conclude that, in a tumor cell line of epithelial origin, the apoptosis following exposure to anthracyclines is an active process requiring protein synthesis and drug interaction with nuclear structures. (
  • We show that a single, short exposure of cultured mammalian epithelial cells to live pks + E. coli at low infectious doses induced a transient DNA damage response followed by cell division with signs of incomplete DNA repair, leading to anaphase bridges and chromosome aberrations. (
  • Mechanistic studies reveal that dysregulated inflammatory/immune responses, uncontrolled activation of coagulation pathways, and increased permeability of alveolar endothelial/epithelial barrier play pivotal roles in the pathogenesis of ARDS [ 3 ]. (
  • Ovarian cancer is the leading cause of death from gynecological malignancies and 90% of ovarian cancer is epithelial ovarian cancer (EOC) [ 1 ]. (
  • This is achieved through molecular pathways of programmed cell death, which maintain selective and specific homeostasis of the numbers of lymphocytes and other immune cells. (
  • This study aimed at identifying new molecular pathways controlling melanoma cell malignancy. (
  • Modulation of the TLR signaling pathway via GRK2 in microglia may be a novel therapeutic target for treatment of neuroinflammatory disorders. (
  • In cancer cells, however, the signaling pathway to procaspase-3 is broken. (
  • Bouchez C and Devin A: mitochondrial biogenesis and mitochondrial reactive oxygen species (ROS): A complex relationship regulated by the cAMP/PKA signaling pathway. (
  • Bioinformatic analyses revealed that EPB41L4A-AS2 may be involved in processes associated with the tumor-associated signaling pathway, especially the TGF-β signaling pathway. (
  • Here we studied the net impact of the cAMP signaling pathway on astrocytes by analyzing the global transcriptome of cultured cells incubated with permeable cAMP analogs. (
  • Our findings show that the overall impact of the cAMP signaling pathway in astrocytes is to promote maturation and restrict developmental and activation features. (
  • The current study is the first demonstration that overexpression of the HGF gene affects chemosensitivity and cell metastasis behaviors, suggesting that HGF signaling pathway is a promising new target of therapeutic intervention of tumors. (
  • Bai T, Dong DS, Pei L. Resveratrol mitigates isoflurane-induced neuroapoptosis by inhibiting the activation of the Akt-regulated mitochondrial apoptotic signaling pathway. (
  • Recent studies suggested that cell apoptosis and autophagy might play key roles in acupuncture therapy. (
  • Therefore, we searched PubMed, Embase, Web of Science, and China National Knowledge Infrastructure (CNKI), aiming to find the potential relationship between acupuncture and cell apoptosis and autophagy. (
  • These findings demonstrated that acupuncture has a potential role in modulating cell apoptosis and autophagy in animal models, suggesting it as a candidate mechanism in acupuncture therapy to maintain physiologic homeostasis. (
  • However, there are few effective and safe ways to regulate cell apoptosis and autophagy in clinical practice right now. (
  • Based on recent studies, the mechanism of acupuncture to treat medical disorders has a high degree of overlap with cell apoptosis and autophagy, which may provide a new direction for the clinical application and basic research. (
  • Up to now, there has been no review to clarify the potential relationship between acupuncture and cell apoptosis and autophagy. (
  • Herein, we performed a review, in particular focused on the therapy of acupuncture, including design method, acupoints selection, acupuncture intervention measure, and related diseases, trying to find out the detailed mechanism and objective evidence for modulation of acupuncture on cell apoptosis and autophagy. (
  • There are three major morphologically and biochemically distinct types of cell death: apoptosis (type 1 cell death), autophagy (type 2 cell death), and necrosis (type 3 cell death). (
  • 15 , 16 Many viruses are known to cause these types of cell death, for example HIV (apoptosis), 17 hepatitis C virus (autophagy), 18 bovine parvovirus (necrosis), 19 and porcine reproductive and respiratory syndrome virus (secondary necrosis). (
  • These collective results suggest that oridonin targets caspase-9 to alter ROS production and autophagy situation to promote HEp-2 cell apoptosis. (
  • Reggiori F and Klionsky DJ: Autophagy in the eukaryotic cell. (
  • Onconase induces autophagy sensitizing pancreatic cancer cells to gemcitabine and activates Akt/mTOR pathway in a ROS-dependent manner. (
  • In this study, we explored the biological activities of delphinidin, the most common of the anthocyanidin monomers, that were related to autophagy in HER-2 positive breast cancer MDA-MB-453 and BT474 cells. (
  • Autophagy was identified as a critical factor that influenced chemotherapy, and the autophagic mechanism in delphinidin-treated cells was investigated. (
  • Collectively, the results showed that delphinidin induced apoptosis and autophagy in HER-2 positive breast cancer cells and that autophagy was induced via the mTOR and AMPK signalling pathways. (
  • This study reported novel functions of delphinidin: the induction of apoptosis and protective autophagy in HER-2-positive MDA-MB-453 and BT474 breast cancer cells and the induction of autophagy through the modulation of the mTOR and AMPK signalling pathways. (
  • Protective role of autophagy in palmitate-induced INS-1 beta-cell death. (
  • Autophagy, a vacuolar degradative pathway, constitutes a stress adaptation that avoids cell death or elicits the alternative cell-death pathway. (
  • This study was undertaken to determine whether autophagy is activated in palmitate (PA)-treated beta-cells and, if activated, what the role of autophagy is in the PA-induced beta-cell death. (
  • Flow cytometry, JC-1 staining and immunofluorescence staining assays were used to measure cell apoptosis and autophagy. (
  • Moreover, the autophagy activator rapamycin, attenuated the pro-apoptotic effects of ALT on BV173 and NALM6 cell lines. (
  • Additionally, ALT impairs the autophagy-lysosome pathway by targeting TFEB [ 12 ]. (
  • However, its effect on autophagy, a nonapoptotic form of programmed cell death, remains to be clarified. (
  • These data highlight some of our results in applying RNAi to augment CHO cell growth by targeting both cell death and metabolic pathways that are detrimental to the optimal performance of cells grown in bioreactors. (
  • In order to bring novel strategies to understand apoptosis in mammalian cell cultures, our study was not only focused on the apoptotic pathway but also expand to metabolic network to set up a link between cell growth and apoptosis. (
  • A comprehensive study of CHO cellular metabolism was made using a metabolic flux network to compare and analyze by metabolic flux analysis (MFA) to get more information on cell metabolism and apoptotic behavior. (
  • Glucose consumed by cells enters Glycolysis which is a series of metabolic pathway by which one molecule of glucose is catabolized into two molecules of pyruvate with net gain of two ATP molecules. (
  • The microbiota generally influences the host in a beneficial fashion by shaping gastrointestinal and immune functions, exerting protection against pathogens, and contributing to metabolic pathways ( 1 ). (
  • Delphinidin causes metabolic stress in breast cancer cells and acts a potential anticancer agent. (
  • By inactivating or otherwise modifying their respective intracellular targets, these intracellular effectors disrupt metabolic pathways and in some cases cause death of the cell. (
  • However, the intracellular damages and the cell death fate induced by venom are unclear. (
  • IRF4-deficient mice cannot clear the intracellular bacterial pathogen Listeria monocytogenes because of intrinsic defects in CD8 T cell expansion and effector function ( 12 ). (
  • The introduction of the truncated 5' end of rne specifically enhanced resistance to paraquat, prevented cell death induced by Bax and decreased the intracellular H2O2 concentration. (
  • Although the initial intracellular targets of different cytotoxic drugs may be heterogeneous, there is increasing evidence indicating that drug-induced cytotoxicity commonly converges on the induction of programmed cell death (apoptosis). (
  • A competition enzyme-linked immunoassay was performed to detect the intracellular concentration of cAMP, based on a standard curve, following the protocol of the manufacturer (Cell Signaling Technology). (
  • Cells respond to specific induction signals by initiating intracellular processes that result in characteristic physiological changes. (
  • However, microarray studies also implicated additional transcriptional targets in GSI-I-dependent cell death, including genes in the unfolded protein response, nuclear factor-κB and p53 pathways. (
  • Modulating T cells functions by down regulating specific genes using RNA interference (RNAi) holds tremendous potential in advancing targeted therapies in many immune related disorders including cancer, inflammation, autoimmunity and viral infections. (
  • For example, to enhance the performance of the CHO cell factories, she has used CRISPR-Cas9 to knockout pro-apoptotic genes, which tend to increase in expression under the higher stress conditions of cell culture and activate programmed cell death pathways. (
  • Also, she has used CRISPR tools to overexpress genes that help increase the productivity of CHO cells in culture. (
  • Genes Cells. (
  • Moreover, numerous genes typically activated in reactive cells, such as scar components and immunological mediators, were repressed by cAMP. (
  • We use the partial mlo resistance alleles and mutations in Ror genes to connect a previously unreported Bgh -triggered hydrogen peroxide (H 2 O 2 ) burst at and cell death of mesophyll cells with the resistance response. (
  • Under a variety of stress conditions, TP53 (p53), stabilized by stress-induced phosphorylation at least on S15 and S20 serine residues, can induce the transcription of genes involved in cell cycle arrest. (
  • TP53 controls transcription of genes involved in both G1 and G2 cell cycle arrest. (
  • E2F7 contributes to G1 cell cycle arrest by repressing transcription of E2F1, a transcription factor that promotes expression of many genes needed for G1/S transition (Aksoy et al. (
  • In the nematode Caenorhabditis elegans programmed cell death requires the killer genes egl-1, ced-4 and ced-3 (refs 1 and 2), and the engulfment of dying cells requires the genes ced-1, ced-2, ced-5, ced-6, ced-7, ced-10 and ced-12 (refs 3,4,5). (
  • Cell lines defective in any of these genes are generally highly IR sensitive (≤7-fold) and have marked deficiencies in DSB repair ( 9 , 28 , 40 , 69 ). (
  • Cells resistant to CD95L/IAP antagonist treatment could be sensitized by short hairpin RNA-mediated knockdown of cellular FLICE-inhibitory protein (cFLIP). (
  • Ku86 is an integral component of the nonhomologous end-joining (NHEJ) pathway of cellular double-strand break repair. (
  • In our project, we applied systems biology methods in a mammalian cell line (CHO TF 70R), to understand the relationship between cellular metabolism and apoptosis in a typical serum free culture medium. (
  • Consistent with the increase in Htt aggregation, PrP C depletion caused an decrease in proteasome activity and a decrease in the activities of cellular defense enzymes compared with control cells whereas reactive oxygen species (ROS) increased more than threefold. (
  • A shift of fluid out of the cells causes cytoplasm condensation, which is followed by convolution of the nuclear and cellular outlines. (
  • Various system-level cellular analyses, such as mapping cell populations at different brain sub-regions, tracing long-distance projection neurons over the entire brain, and calculating neuromuscular junction occupancy across whole muscle, are also readily accomplished by our method. (
  • These data collectively demonstrated that Apaf-1 and the mitochondrial pathway of apoptosis play significant roles in ER stress-induced apoptosis. (
  • Expression of stimuli, such as DNA damage , hypoxia and activation of certain oncoproteins (eg, Myc , Ras) are dependent on the apoptotic pathway of p53 [4] . (
  • Apoptosis in THP-1 cells induced by Z-LLL-CHO involved a cytochrome c -dependent pathway, which included the release of mitochondrial cytochrome c , activation of caspase-9 and -3, and cleavage of Bcl-2 into a shortened 22-kDa fragment. (
  • Likewise, differentiated THP-1 cells were refractory to Z-LLL-CHO-induced cytochrome c release, caspase activation, and Bcl-2 cleavage. (
  • When mouse MG6 cells were stimulated with the TLR4 ligands lipopolysaccharide (LPS) and paclitaxel, we found that interferon regulatory factor 1 (IRF1) protein expression and activation was upregulated, transcription of interferon-β (IFN-β) was accelerated, induction/activation of STAT1 and activation of STAT3 were promoted, and subsequently iNOS expression was upregulated. (
  • The ablation of GRK2 by small interfering RNAs (siRNAs) not only eliminated TLR4-mediated upregulation of IRF1 protein expression and nuclear translocation but also suppressed the activation of the STAT pathway, resulting in negating the iNOS upregulation. (
  • Taken together, our results show that GRK2 regulates the activation of IRF1 as well as the activation of the STAT pathway, leading to upregulated transcription of iNOS in activated microglial cells. (
  • Activation of Fas results in recruitment of the death effector molecule Fas-associated death domain (FADD) to the cytoplasmic tail of Fas ( 14 ), which in turn binds procaspase-8 ( 15 ), leading to formation of a death-inducing signaling complex (DISC). (
  • Recent evidence indicates that c-FLIP L not only functions to block caspase-8 activation but also positively signals the activation of the NF-κB and ERK pathways ( 24 ). (
  • We concluded that the antitumor effects of YC-1 in PC-3 cells include the induction of apoptosis and the suppression of NF-κB activation. (
  • Despite comparable induction of ER stress in both wild type and Apaf-1-deficient cells, activation of caspase-3 was only observed in wild type, but not Apaf-1-deficient, MEFs. (
  • Doxorubicin triggers bioenergetic failure and p53 activation in mouse stem cell-derived cardiomyocytes. (
  • Activation of several B cells is necessary for exosome release.Vol. 29, Iss. (
  • Rac1 regulates a cytokine-stimulated, redox-dependent pathway necessary for NF-kappaB activation. (
  • Kim Y, Morgan M, Choksi S, Liu Z. TNF-induced activation of the Nox1 NADPH oxidase and its role in the induction of necrotic cell death. (
  • These results indicate that cAMP signaling is a key pathway promoting astrocyte maturation and restricting their developmental and activation features. (
  • Strikingly, analysis of glial activation in pro-inflammatory cytokine-administered and genetically-modified mice has shown that JAK-STAT3 signaling is also a key pathway through which astrocytes become reactive [ 6 ]. (
  • However, the precise significance of the cAMP pathway in the maturation and activation of these cells remains elusive. (
  • Apoptosis, an ancient Greek word used to describe the "falling off" of petals from flowers or leaves from trees, is a highly regulated, evolutionarily conserved, and energy-requiring process by which activation of specific signaling cascades ultimately leads to cell death. (
  • We used a cell-free system based on Xenopus egg extracts in which recombinant Bcl-2 prevents protease activation and subsequent apoptotic effects ( 13 - 16 ). (
  • RESULTS: We found that the intrinsic apoptotic pathway was invoked, with the accumulation of cytosolic cytochrome c and processing of the initiator caspase-9.To confirm that apoptosis was induced following caspase-7 activation, the caspase inhibitor Ac-DEVD-CHO was used.CONCLUSIONS: Taken together, these results suggest SPD as a potent antiproliferative agent on MCF-7 cells by inducing apoptosis in a caspase-7-dependent manner. (
  • To confirm that apoptosis was induced following caspase-7 activation, the caspase inhibitor Ac-DEVD-CHO was used. (
  • Immunoblot analyses of lysates obtained from MCF-7 cells treated with SPD at 10-6 M found that caspase-7 was cleaved to the 17-kDa fragment required for its activation (Figure 3). (
  • Most likely, the stimulation of Ang-2 is in part mediated by increased activation of AP-1 but different signal transduction pathways may also be involved since we found opposite activation of PI3K/Akt/mTOR and MAPK7ERK pathways (both known to regulate in Ang-2 expression). (
  • The first one, an increase in ODC activity, is linked to cell growth, whereas the second, AMPK activation, is a homeostatic mechanism that negatively modulates the first. (
  • The signaling enzyme phospholipase D (PLD) and the lipid second messenger it generates, phosphatidic acid (PA), are implicated in many cell biological processes, including Ras activation, cell spreading, stress fiber formation, chemotaxis, and membrane vesicle trafficking. (
  • Regulated on activation normal T cell expressed and secreted. (
  • Furthermore, ATRA-induced cell death in D283, D425, and D458 cells was accompanied by activation of caspase-3, a key executioner of apoptosis. (
  • Silica induces nuclear factor-kappaB activation through TAK1 and NIK in Rat2 cell line. (
  • Cells exposed to 4 μM Cd for 24 h did not show signs of apoptosis, such as DNA fragmentation and caspase-3 activation. (
  • Our results suggest that Gal-1 is associated with poor outcome in EOC and Galectin-1 promotes tumor progression via NF-κB pathway activation in EOC. (
  • Apoptosis was determined using 4′,6-diamidino-2-phenylindole staining, and cell cycle progression was examined by FACScan flow cytometry. (
  • Cancer stem cells (CSCs), a minor subpopulation of cancer cells, play important roles in tumor initiation, progression, and drug resistance. (
  • Immunostaining and quantitative analysis were performed to assess CD8 + T cells infiltration, PD-L1 expression, and their relationship with CD44 + /CD133 + CSCs and disease progression in PC. (
  • Our study highlights an interaction among CD8 + T cells infiltration, PD-L1 expression, and CD44 + /CD133 + CSCs existence, which contributes to PC progression and immune evasion. (
  • Title: Linc00152 promotes malignant progression of glioma stem cells by regulating miR-103a-3p/FEZF1/CDC25A pathway. (
  • Mdm2 overexpression and Cdc25C downregulation delay cell cycle progression through the G2/M phase. (
  • Title: Mdm2 promotes Cdc25C protein degradation and delays cell cycle progression through the G2/M phase. (
  • 2002) E2F integrates cell cycle progression with DNA repair, replication, and G(2)/M checkpoints. (
  • Recent data on novel pathways involved in melanoma development opened new opportunities to identify novel therapeutic targets [ 4 , 5 ], nevertheless additional key players underlying melanoma onset and progression need to be identified. (
  • As GSI-I (Z-LLNle-CHO) is also a derivative of a widely used proteosome inhibitor MG-132, we hypothesized that this compound might be active in precursor-B acute lymphoblastic leukemia (ALL) cell lines and patient samples. (
  • Z-LLNle-CHO), which is structurally similar to the widely used proteosome inhibitor MG-132, and describe its biological activity in precursor-B ALL. (
  • We demonstrated that treatment of THP-1 human monocytic leukemia cells with Z-LLL-CHO, a reversible proteasome inhibitor, induced cell death through an apoptotic pathway. (
  • Induction of apoptosis by protease inhibitor also was detected in U937 and TF-1 leukemia cell lines and cells obtained from acute myelogenous leukemia patients but not in normal human blood monocytes. (
  • X-linked IAP is a direct inhibitor of cell-death proteases. (
  • Furthermore, cotreatment with DNA replication inhibitor aphidicolin abolished both camptothecin-induced cytotoxicity and radiosensitization in the vector-alone, as well as the Ku86-complemented subline cells, indicating both events are initiated by replication-dependent topoisomerase I-mediated DNA damages. (
  • Here, we made unexpected observations that the caspase-9 inhibitor (C9i) enhanced apoptosis in response to selected stimuli, and HEp-2 cells which were made deficient in caspase-9 using siRNA exhibited no resistance to apoptotic signals and actually demonstrated increased apoptotic sensitivity to oridonin. (
  • During apoptosis in intact cells, cytochrome c translocation was similarly blocked by Bcl-2 but not by a caspase inhibitor, zVAD-fmk. (
  • Pre-incubation of cells with this inhibitor reversed apoptosis levels and caspase-7 activity in SPD-treated cells to untreated levels. (
  • When MCF-7 cells were incubated with the caspase-7 inhibitor, DEVD-CHO at (A) 50 μM and (B) 100 μM, prior to SPD treatment, apoptosis levels decreased to control untreated levels as detected by nuclear staining, suggesting the important role played by this executioner caspase in SPD-induced apoptosis. (
  • To confirm that the SPD-induced apoptotic cell death was due to the involvement of caspase-7, cells were also treated with SPD in the presence of the specific inhibitor of caspase-7, Ac-DEVD-CHO [34]. (
  • SPD-treated cells preincubated with the inhibitor exhibited repressed caspase-7 DEVDase activity. (
  • Also, preincubation of MCF-7 cells with this inhibitor at 50 μM to 100 μM inhibited apoptosis and brought apoptotic levels down to the level similar to controls (Figure 5), thus purporting an apoptotic pathway dependent on caspase-7. (
  • Pretreatment with a specific caspase-3 inhibitor, DEVD-CHO, significantly reduced ATRA-induced apoptotic cell death. (
  • From the spectrum of compounds assessed, the naringenin chalcone contained in black pepper was identified as the most potent inhibitor of the growth of prostate cells. (
  • In contrast to DSBs produced by ionizing radiation, DSBs produced by the replication inhibitor aphidicolin are repaired entirely by HR. irs1SF, but not V3, cells show hypersensitivity to aphidicolin treatment. (
  • CHO-Anti-Human NGF MAb stable cell line is clonally-derived from a CHO cell line, which has been transfected with an anti-human NGF MAb gene to allow expression of the MAb. (
  • It is an example of a cell line transfected using our proprietary CBTGS gene screening and amplification system. (
  • The p53 tumor suppressor gene is most frequently mutated in cancer cells (mutation occurs in more than 50% of human cancers) [3] , which makes the restriction mechanism ineffective. (
  • Using CRISPR, her team generates pools of cells such that each pool has a different gene knockout. (
  • Parvoviruses have been used as an antitumor agent, immune cell activator, and as a targeted gene vector. (
  • What pathways are this gene/protein implicaed in? (
  • We used bioinformatics resources (DAvID) to conduct Gene Ontology biological processes and KEGG pathways at the significant level. (
  • Low EPB41L4A-AS2 expression was determined, and overexpression of this gene inhibited cell migration and invasion in the EMT model. (
  • GSEA analysis contrasting gene expression profiles with transcriptome signatures of acutely isolated astrocytes and in situ evaluation of protein levels in these cells showed that cAMP signaling conferred mature and in vivo-like transcriptional features to cultured astrocytes. (
  • In this study, we examined the effects of HGF on these types of biological activities and chemosensitivity in Chinese hamster ovary (CHO) cells by stable transfection of the HGF gene. (
  • Exposed cells exhibited a significant increase in gene mutation frequency and anchorage-independent colony formation, demonstrating the infection mutagenic and transforming potential. (
  • In the present study, using several Pdcd4 knock down cell lines we succeeded to identify angiopoietin-2 (Ang-2) as a gene up-regulated on the mRNA and protein level. (
  • Angiopoietin-2 is a gene regulated by Pdcd4 levels in a multitude of cell lines. (
  • Although ultrasound cavitation must be avoided for safe diagnostic applications, the ability of ultrasound to disrupt cell membranes has taken on increasing significance as a method to facilitate drug and gene delivery. (
  • The most representative cells were also characterized by spheroid formation assay, gene- and protein- expression profiling as well as cytokines secretion and the most relevant pathways identified through bioinformatic analysis were tested by in silico transcriptomic validation on datasets generated from biopsies specimens of melanoma patients. (
  • Gene-expression and protein expression data were collected for SK-MEL-28 and A375 cells by Illumina-, multiplex x-MAP-and mass-spectrometry technology. (
  • Joza et al deleted exon 3 of the aif gene in mouse embryonic stem (ES) cells. (
  • This exon encodes the amino terminus of the protein, and because the aif gene is on the X chromosome, mutation of one aif allele resulted in a complete knockout in male ES cells. (
  • Bid, a BH3-only protein, plays a role in apoptosis initiated by the intrinsic pathway. (
  • The other is the intrinsic pathway, in which the release of cytochrome c from mitochondria triggers the formation of the apoptosome composed of Apaf-1, pro-caspase-9, dATP, and cytochrome c . (
  • In recent years there has been much interest in studying the role played by the Fas system in the induction of apoptosis of cancer cells following exposure to cytotoxic drugs [see Maggi (1998) for review]. (
  • Nr4a1-deficient mice show increases in CD8 T cell effector responses with improved clearance of Listeria monocytogenes . (
  • IRF4-deficient CD8 T cells proliferated less, were more prone to apoptosis, and produced fewer effector molecules, such as IFN-γ ( 11 ). (
  • Furthermore, we found that dysregulation of Irf4 in Nr4a1-deficient CD8 + T cells increased the development of committed effector cells, IFN-γ production, and L. monocytogenes clearance upon infection. (
  • Therefore, Nr4a1 plays a critical role in regulating the proliferative potential and function of effector CD8 T cells through the transcriptional repression of IRF4. (
  • We tested the ability of mPA-EGF to translocate LF and EF, the native effector moieties of anthrax toxin, into A431 cells. (
  • Hypoxia may influence tumor biology in paradoxically opposing ways: it is lethal as a direct stress trigger, yet hypoxic zones in solid tumors harbor viable cells which are particularly resistant to treatment and contribute importantly to disease relapse. (
  • The death of Jeggo's husband almost discouraged her from continuing her research in cancer and radiation biology. (
  • Penelope Jeggo has been very active in various symposiums and conventions where she has discussed her research and given talks on cell biology in relation to radiation biology. (
  • She discussed the importance of low-dose radiation and molecular cell biology. (
  • In this article, we outline some of the recent developments in lipid droplet cell biology. (
  • He works on neural regeneration and stem cell biology. (
  • Dr. Kildegaard discussed her work on accelerated genome engineering of CHO production hosts to improve the yield and quality of therapeutic protein products. (
  • Several studies have showed that animal venoms are a source of bioactive compounds that may inhibit the growth of cancer cells, which makes them useful agents for therapeutic applications. (
  • Pelicano H, Carney D and Huang P: ROS stress in cancer cells and therapeutic implications. (
  • Mammalian cell culture has gained importance in biotechnology for the development of therapeutic and diagnostic agents. (
  • 3:177-182, 1997), this behavior may influence relapse and implicates such cells as potentially important therapeutic targets. (
  • We suggest that the MSC-derived secretome might be an appropriate therapeutic agent for treating aggressive pulmonary disorders because of biological and logistical advantages over live cell therapy. (
  • Furthermore, we found that AEG-1 could inhibit apoptotic cell death in L-78 cells, as assessed by MTT, TUNEL and flow cytometry assay. (
  • The Sirt1 Activators SRT2183 and SRT3025 Inhibit RANKL-Induced Osteoclastogenesis in Bone Marrow-Derived Macrophages and Down-Regulate Sirt3 in Sirt1 Null Cells. (
  • Wound healing assay, cell migration and invasion assays, were used to examine the effects of EPB41L4A-AS2 on tumor cell metastasis in vivo. (
  • This discovery was a major breakthrough in understanding the double strand break repair pathway in mammals. (
  • Oncogene - abstract of article: Paclitaxel (Taxol) upregulates expression of functional interleukin-6 in human ovarian cancer cells through multiple signaling pathways. (
  • Glucose uptake is favoured by alteration in PI3K-Akt-mTOR pathway. (
  • Both scFv9 and scFv42.2 suppress eye toxicity, reduce cell death in brain neurons, protect the structural integrity of dendritic terminals in brain neurons and delay locomotor dysfunction. (
  • Shrinkage and death of neurons, and reductions in the number of synaptic spines and functional synapses contribute to annual reductions of as much as 0.5% to 1.0% in cortical thickness (the cortex is the outermost layer of the brain) and sub-cortical volume in some regions of the brain. (
  • 46 Over time, this free radical damage leads to the death of neurons. (
  • G2019S) LRRK2 activates MKK4-JNK pathway and causes degeneration of SN dopaminergic neurons in a transgenic mouse model of PD. (
  • CHAMPAIGN, Ill. -- Scientists have found a way to trick cancer cells into committing suicide. (
  • As a result, cancer cells escape destruction and grow into tumors. (
  • The researchers tested the compound's efficacy in cell cultures and in three mouse models of cancer. (
  • The researchers also showed that PAC-1 killed cancer cells in 23 tumors obtained from a local hospital. (
  • Although the indazole compound, YC-1, is reported to exert anticancer activities in several cancer cell types, its target and mechanism of action have not been well explored. (
  • The objectives of this study were to ascertain whether YC-1 directly induces apoptosis in prostate cancer cells and to explore the mechanism(s) whereby YC-1 causes cell death. (
  • Hormone-refractory metastatic human prostate cancer PC-3 cells were selected for this study. (
  • Additionally, the NF-κB/RelA complex has been shown to be constitutively activated in prostate tissues from human patients with prostate cancer, in androgen-insensitive human prostate carcinoma cells, and in prostate cancer xenografts ( 3 , 4 ). (
  • In Taiwan, according to the Ministry of Health and Welfare, PC has moved from the tenth leading cause of cancer death in 2006 to the eighth in 2016. (
  • In addition, two human cancer cell lines were found to be infected by CPV. (
  • This necrotic event over apoptotic cell death and infection in human cells provide insightful information when developing CPV as a nanotool for cancer treatments. (
  • 9 Lysis of cancer cells releases tumor-associated antigens that induce anticancer immunity and this type of treatment can also be seen as a cancer vaccine. (
  • The up-regulated levels of topoisomerase I expression in cancer cells provide the molecular basis for selective targeting of cancer cells by using topoisomerase I drugs ( 1 - 3 ). (
  • Recently, it was established that venom toxins from scorpions induced cytotoxic, antiproliferative and apoptogenic effects on cancer cells. (
  • Therefore, the present study aims to investigate the cytotoxic activity of Androctonus australis hector (Aah) scorpion venom and its toxic fractions (FtoxG-50 and F3) on NCI-H358 human lung cancer cells. (
  • The present findings showed that F3 fraction was more cytotoxic towards NCI-H358 lung cancer cells with an IC 50 of 27.05 ± 0.70 μg/mL than venom alone (396.60 ± 1.33 μg/mL) and its toxic fraction FtoxG-50 (45.86 ± 0.91 μg/mL). (
  • Cancer represents a major public health problem and is a leading cause of death worldwide. (
  • 1. Sherr CJ (1996) Cancer cell cycles. (
  • 2. Sherr CJ, McCormick F (2002) The RB and p53 pathways in cancer. (
  • Cancer Cell 2: 103-112. (
  • 10. Du W, Searle JS (2009) The rb pathway and cancer therapeutics. (
  • The biological and molecular events that regulate the invasiveness of breast tumour cells need to be further revealed to develop effective therapies that stop breast cancer from expanding and metastasising. (
  • We further utilised specific PKD1-shRNA and a system to inducibly-express PKD1 to analyse the role of PKD1 in the invasive behaviour of breast cancer cell lines in two-dimensional (2D) and three-dimensional (3D) culture. (
  • Invasive behaviour in breast cancer cell lines has been linked to matrix metalloproteinases (MMPs), so we also determined if PKD1 regulates the expression and activity of these enzymes. (
  • Additionally, PKD1 is not expressed in highly invasive breast cancer cell lines, whereas non-invasive or very low-invasive breast cancer cell lines express PKD1. (
  • PKD1 also regulated the expression of breast cancer cell MMPs, MMP-2, MMP-7, MMP-9, MMP-10, MMP-11, MMP-13, MMP-14 and MMP-15, providing a potential mechanism for PKD1 mediation of the invasive phenotype. (
  • They further suggest that the loss of PKD1 expression increases the malignant potential of breast cancer cells. (
  • Breast cancer cells invade surrounding tissues by breaking through the basal membrane using invadopodia, which participate in proteolytic matrix degradation. (
  • Cytotoxic drugs commonly used in cancer therapy promote tumor cell death by inducing apoptosis, but the cell death pathway(s) is likely dependent on the mechanism of drug action. (
  • Jeggo returned to her research and further researched cancer and DNA a few years after her husband's death. (
  • High glucose condition creates conducive environment for cancer cells to flourish. (
  • Other by products of glycolysis which includes ATP, NADP and NADPH also aids in growth of cancer cells. (
  • It is indeed said that "Sugars feed cancer cells. (
  • Styrylpyrone Derivative (SPD) induces apoptosis in a caspase-7-dependent manner in the human breast cancer cell line MCF-7. (
  • HER-2-positive breast cancer cells (MDA-MB-453 and BT474) were purchased from the Chinese Academy of Sciences (Shanghai, China). (
  • Hypoxia increases susceptibility of non-small cell lung cancer cells to complement attack. (
  • There have been 9,335 deaths from solid cancer and 31,881 deaths from noncancer diseases during the 47-year follow-up. (
  • Of these, 19% of the solid cancer and 15% of the noncancer deaths occurred during the latest 7 years. (
  • We estimate that about 440 (5%) of the solid cancer deaths and 250 (0.8%) of the noncancer deaths were associated with the radiation exposure. (
  • Taken together, these findings for the first time provide evidence that ${\beta}$ -asarone can suppress the growth of colon cancer and the induced apoptosis is possibly mediated through mitochondria/caspase pathways. (
  • Although high concentrations (1-10 microM) of retinoic acid derivatives are generally needed for significant antitumor effects in many cancer cells, we observed that pharmacologically relevant concentrations of ATRA were effective in inducing cell death in human MB cells. (
  • In recent years, ALT has been reported to exert anti-tumor effects in several types of cancer, including lung cancer, gastric cancer, hepatic cancer, B cell acute lymphoblastic leukemia, pancreatic cancer and breast cancer [ 8 ]. (
  • reported that ALT could enhance the sensitivity of lung cancer cells to gemcitabine [ 9 ]. (
  • Lung cancer, especially non-small cell lung cancer (NSCLC), is the most prevalent cancer worldwide [ 1 ]. (
  • Herein, we investigated its anti-proliferative effect and potential approaches of action on human lung cancer A549 cells. (
  • PSO induced apoptosis in breast cancer cells by inhibiting NOTCH1 signaling ( Suman, Das & Damodaran, 2013 ). (
  • Herein, we demonstrated that PSO is an anti-proliferative natural compound on human lung cancer A549 cells. (
  • The cytotoxicity of psoralidin against human lung cancer A549 cells. (
  • We also found that over expression of Gal-1 significantly increased the migration and invasion abilities of human ovarian cancer cell line OVCAR-3 cells [ 7 ]. (
  • and (4) HSP-specific CD4 + T-cell responses and glaucomatous neurodegeneration are both abolished in mice raised in the absence of commensal microbial flora (germ-free (GF) mice), supporting a mechanism of bacteria sensitized T-cell responses underlying the pathogenesis of glaucoma. (
  • It plays an important role during embryonal development as programmed cell death and accompanies a variety of normal involutional processes in which it serves as a mechanism to remove "unwanted" cells. (
  • The modulation of ODC activity by AMPK represents a mechanism that may contribute to control cell growth processes. (
  • The modulation of ODC by AMPK is a mechanism that can regulate cell growth processes. (
  • Several direct transcriptional targets of TP53 are involved in cell cycle arrest but their mechanism of action is still unknown. (
  • This study investigates the mechanism of cell death induced by cadmium (Cd) in Chinese hamster ovary (CHO) cells. (
  • Apoptosis inhibited by DEVD-CHO. (
  • Finally, apoptosis confers cytotoxicity to certain cell types (ie, cytotoxic T lymphocytes and natural killer cells). (
  • Methamphetamine causes cytotoxicity and apoptosis in different cell lines. (
  • In this study, protective effects of Descurainia sophia oil were followed up in methamphetamine-induced cell cytotoxicity in a neuron-like PC12 cell line. (
  • The human medullary thyroid carcinoma cell line TT expresses all SSTR subtypes. (
  • Despite EF-induced toxicity, murine or human mesenchymal stem cells (MSCs) tolerate expression, but only murine EF-transduced MSC displayed sarcoma formation upon transplantation in immunocompromised mice. (
  • Bacterial cell death induced by human pro-apoptotic Bax is blocked by an RNase E mutant that functions in an anti-oxidant pathway. (
  • The testing was performed in collaboration with William Helferich, a professor of food science and human nutrition at the U. of I., and Myung-Haing Cho at Seoul National University. (
  • Aleutian mink disease virus, 25 feline panleukopenia virus (FPLV), 26 human parvovirus B19, 27 - 29 parvovirus H-1, 30 and rat parvovirus 31 have been reported to induce apoptotic cell death while bovine parvovirus infected cells are necrotic. (
  • Compared with the vector-alone sublines, radiation resistance was restored in the human Ku86-complemented sublines without alteration of cell cycle distributions. (
  • Nevertheless, F3 fraction was not cytotoxic at these concentrations on normal human lung fibroblast MRC-5 cells. (
  • In our previous studies, we demonstrated that oTR exerts growth inhibitory and apoptotic effects on the human hepatocellular carcinoma cell line SMMC-7721 and acute promyelocytic leukemia cell line HL-60 through the mitochondrial apoptotic pathway. (
  • Mesenchymal Stem Cell-Derived Factors Restore Function to Human Frataxin-Deficient Cells. (
  • Of 48 mRNA sequences analyzed from a population of cardiomyocytes derived from human induced pluripotent stem cells (hiPSC-CMs), 41 were accurately quantified. (
  • Ceccatelli, S. 2002-11-01 00:00:00 We have previously shown that the neurotoxic compounds colchicine, methylmercury (MeHg) and hydrogen peroxide (H2O2) cause apoptosis in primary cultures of cerebellar granule cells (CGC), characterized by nuclear condensation and high‐molecular weight DNA fragmentation. (
  • A kinetic aggregation assay that enables highly sensitive Ab semiquantification in cells and tissues. (
  • 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay indicated that YC-1 suppresses growth of PC-3 cells in a concentration-dependent and time-dependent manner. (
  • Additionally, hippocampus cell apoptosis was determined using a TUNEL assay and levels of acetylcholinesterase (AChE), reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH‑Px) were evaluated in sera via ELISA. (
  • C) Cells were treated with 5, 10, 20 and 30 µM psoralidin for 24 h, the LDH assay were performed. (
  • The Guava ViaCount Flex reagent used for this assay consists of two DNA-binding fluorescent dyes that differentially stain viable and non-viable (dead or apoptotic) cells based on cell membrane permeability. (
  • Some apoptotic cells can also be distinguished in the Guava ViaCount assay because they show intermediate uptake levels of the membrane impermeant dye, absorbing more dye than the viable cells, but less than dead cells. (
  • The Guava Nexin assay utilizes Annexin V-PE to detect PS on the external membrane of apoptotic cells 12-17 . (
  • Because secondary necrosis is an end stage of apoptosis it can be discriminated from primary necrosis by occurrence of apoptotic and necrotic cell death parameters. (
  • 19 On the other hand apoptosis induced in H-1 infection progresses to a necrotic cell death state in specific cell types. (
  • However, an increase in propidium iodide uptake and depletion of ATP, characteristics of necrotic cell death, were observed. (
  • HGTD-P contains two transmembrane domains that are required for its localization to the mitochondria and induction of cell death. (
  • This system is similar to other cell-free systems based on cytosol derived from apoptotic cultured cells ( 14 , 17 - 20 ), but with one important exception: the spontaneous apoptosis in the Xenopus system depends on the presence of a heavy membrane fraction enriched in mitochondria ( 13 ). (
  • c) from mitochondria into the cytosol in the cell-free apoptosis system. (
  • Their typical characteristic is high consumption of glucose as these cells mostly have defective mitochondria. (
  • Mitochondria within retinal ganglion cell axons underwent systematic ultrastructural analysis to measure area, length, width, and the distance between the mitochondria and the axon wall. (
  • Primary mouse ganglion cells were cultured, treated with homocysteine, and assessed for levels of Opa1 and Fis1 protein, the number of mitochondria per length of neurite, and levels of cleaved caspase-3. (
  • We investigated the involvement of the apoptosome in ER stress-induced cell death pathway using mouse embryonic fibroblasts (MEFs) and mice deficient for Apaf-1. (
  • While the disruption of Rad52 confers no sensitization ( 44 , 73 ), inactivation of Rad54 causes a modest increase in radiosensitivity (∼1.7-fold in mouse embryonic stem cells) that is mainly associated with the late-S/G 2 phase ( 5 , 15 , 16 , 57 ). (
  • Apoptosis is a programmed cell death with known morphological changes in the nucleus (24), actin filaments (16, 27) and endoplasmic reticulum (17, 32). (
  • Morphological studies of CPV-infected Norden laboratory feline kidney (NLFK) cells and canine fibroma cells (A72) displayed characteristic apoptotic events. (
  • It is a mode of cell death defined by characteristic morphological, biochemical and molecular changes. (
  • Later on, it was found to show mostly the morphological features of unregulated necrotic death. (