Fas-Associated Death Domain Protein: 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.Apoptosis: 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.Caspases: 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.Caspase 3: 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.Apoptosis Regulatory Proteins: 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.Caspase 10: A long pro-domain caspase that contains a death effector domain in its pro-domain region. Activation of this enzyme can occur via the interaction of its N-terminal death effector domain with DEATH DOMAIN RECEPTOR SIGNALING ADAPTOR PROTEINS. Caspase 10 plays a role in APOPTOSIS by cleaving and activating EFFECTOR CASPASES. Several isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.Caspase 8: 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.Proto-Oncogene Proteins c-bcl-2: 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.CASP8 and FADD-Like Apoptosis Regulating Protein: An APOPTOSIS-regulating protein that is structurally related to CASPASE 8 and competes with CASPASE 8 for binding to FAS ASSOCIATED DEATH DOMAIN PROTEIN. Two forms of CASP8 and FADD-like apoptosis regulating protein exist, a long form containing a caspase-like enzymatically inactive domain and a short form which lacks the caspase-like domain.Inhibitor of Apoptosis Proteins: 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.Caspase 9: 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.DNA Fragmentation: 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.Signal Transduction: 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.bcl-2-Associated X Protein: 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.In Situ Nick-End Labeling: 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.Cell Line, Tumor: A cell line derived from cultured tumor cells.Caspase Inhibitors: Endogenous and exogenous compounds and that either inhibit CASPASES or prevent their activation.Fas Ligand Protein: 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.Cell Survival: 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.X-Linked Inhibitor of Apoptosis Protein: An inhibitor of apoptosis protein that is translated by a rare cap-independent mechanism. It blocks caspase-mediated cellular destruction by inhibiting CASPASE 3; CASPASE 7; and CASPASE 9.Enzyme Activation: 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.Apoptosis Inducing Factor: 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.Mitochondria: 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)Cells, Cultured: 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.Caspase 6: A short pro-domain caspase that plays an effector role in APOPTOSIS. It is activated by INITIATOR CASPASES such as CASPASE 7; CASPASE 8; and CASPASE 10. Isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.Tumor Suppressor Protein p53: 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.Tumor Cells, Cultured: 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.Jurkat Cells: A CELL LINE derived from human T-CELL LEUKEMIA and used to determine the mechanism of differential susceptibility to anti-cancer drugs and radiation.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Cytochromes c: 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.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.bcl-X Protein: 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.Cell Proliferation: All of the processes involved in increasing CELL NUMBER including CELL DIVISION.Adaptor Proteins, Signal Transducing: 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 enzymesCysteine Proteinase Inhibitors: Exogenous and endogenous compounds which inhibit CYSTEINE ENDOPEPTIDASES.Blotting, Western: 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.Caspase 2: 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.Proteins: 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.Amino Acid Chloromethyl Ketones: Inhibitors of SERINE ENDOPEPTIDASES and sulfhydryl group-containing enzymes. They act as alkylating agents and are known to interfere in the translation process.TNF-Related Apoptosis-Inducing Ligand: 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.Annexin A5: A protein of the annexin family isolated from human PLACENTA and other tissues. It inhibits cytosolic PHOSPHOLIPASE A2, and displays anticoagulant activity.Cell Cycle: 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.Flow Cytometry: 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.Receptors, TNF-Related Apoptosis-Inducing Ligand: 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.Transfection: 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.Poly(ADP-ribose) Polymerases: 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.Death Domain Receptor Signaling Adaptor Proteins: 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.Tumor Necrosis Factor-alpha: 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.Proto-Oncogene Proteins: 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.Antineoplastic Agents: Substances that inhibit or prevent the proliferation of NEOPLASMS.Caspase 1: 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.RNA, Small Interfering: 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.Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.Receptors, Tumor Necrosis Factor: Cell surface receptors that bind TUMOR NECROSIS FACTORS and trigger changes which influence the behavior of cells.Molecular Sequence Data: 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.Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.Membrane Glycoproteins: Glycoproteins found on the membrane or surface of cells.Receptors, Death Domain: 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.Cell Division: The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.Necrosis: 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.NF-kappa B: 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.Reverse Transcriptase Polymerase Chain Reaction: 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.Amino Acid Sequence: 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.Cytochrome c Group: 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)Mice, Inbred C57BLPhosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.Down-Regulation: 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.Mice, Knockout: 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.Reactive Oxygen Species: 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.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Time Factors: Elements of limited time intervals, contributing to particular results or situations.RNA, Messenger: 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.Receptor-Interacting Protein Serine-Threonine Kinases: 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.HeLa Cells: 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.Cysteine Endopeptidases: 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.Up-Regulation: 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.bcl-2 Homologous Antagonist-Killer Protein: 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.BH3 Interacting Domain Death Agonist Protein: A member of the Bcl-2 protein family that reversibly binds MEMBRANES. It is a pro-apoptotic protein that is activated by caspase cleavage.Gene Expression Regulation: 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.HL-60 Cells: A promyelocytic cell line derived from a patient with ACUTE PROMYELOCYTIC LEUKEMIA. HL-60 cells lack specific markers for LYMPHOID CELLS but express surface receptors for FC FRAGMENTS and COMPLEMENT SYSTEM PROTEINS. They also exhibit phagocytic activity and responsiveness to chemotactic stimuli. (From Hay et al., American Type Culture Collection, 7th ed, pp127-8)Caspase 7: 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.Protein Binding: 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.Membrane Potential, Mitochondrial: 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.Protein Structure, Tertiary: 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.Gene Expression Regulation, Neoplastic: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.Intracellular Signaling Peptides and Proteins: 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.Genes, bcl-2: 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.Coenzyme A Ligases: Enzymes that catalyze the formation of acyl-CoA derivatives. EC 6.2.1.Proto-Oncogene Proteins c-akt: 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.Apoptotic Protease-Activating Factor 1: 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.TNF Receptor-Associated Death Domain Protein: A 34 kDa signal transducing adaptor protein that associates with TUMOR NECROSIS FACTOR RECEPTOR TYPE 1. It facilitates the recruitment of signaling proteins such as TNF RECEPTOR-ASSOCIATED FACTOR 2 and FAS ASSOCIATED DEATH DOMAIN PROTEIN to the receptor complex.Fatty Acid Desaturases: A family of enzymes that catalyze the stereoselective, regioselective, or chemoselective syn-dehydrogenation reactions. They function by a mechanism that is linked directly to reduction of molecular OXYGEN.Mutation: 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.DNA Damage: 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.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Myeloid Cell Leukemia Sequence 1 Protein: 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.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Protein-Serine-Threonine Kinases: A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.Ceramides: 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.Antineoplastic Agents, Phytogenic: Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.Models, Biological: 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.Staurosporine: 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)Receptors, Tumor Necrosis Factor, Type I: A tumor necrosis factor receptor subtype that has specificity for TUMOR NECROSIS FACTOR ALPHA and LYMPHOTOXIN ALPHA. It is constitutively expressed in most tissues and is a key mediator of tumor necrosis factor signaling in the vast majority of cells. The activated receptor signals via a conserved death domain that associates with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.Models, Molecular: Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Mitogen-Activated Protein Kinases: 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).T-Lymphocytes: Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.Membrane Proteins: 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.Mice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.bcl-Associated Death Protein: 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.RNA Interference: 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.Neoplasm Proteins: 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.Caspases, Initiator: A subtype of caspases that contain long pro-domain regions that regulate the activation of the enzyme. The pro-domain regions contain protein-protein interaction motifs that can interact with specific signaling adaptor proteins such as DEATH DOMAIN RECEPTORS; DED SIGNALING ADAPTOR PROTEINS; and CARD SIGNALING ADAPTOR PROTEINS. Once activated, the initiator caspases can activate other caspases such as the EFFECTOR CASPASES.DNA-Binding Proteins: 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.Nuclear Proteins: 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.Oxidative Stress: 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).Cell Nucleus: 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)Drug Synergism: The action of a drug in promoting or enhancing the effectiveness of another drug.U937 Cells: 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.Epithelial Cells: Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.TNF Receptor-Associated Factor 1: A signal transducing tumor necrosis factor receptor associated factor that is involved in TNF RECEPTOR feedback regulation. It is similar in structure and appears to work in conjunction with TNF RECEPTOR-ASSOCIATED FACTOR 2 to inhibit APOPTOSIS.Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories for solving biological problems including manipulation of models and datasets.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Sequence Analysis, Protein: A process that includes the determination of AMINO ACID SEQUENCE of a protein (or peptide, oligopeptide or peptide fragment) and the information analysis of the sequence.Tumor Suppressor Proteins: Proteins that are normally involved in holding cellular growth in check. Deficiencies or abnormalities in these proteins may lead to unregulated cell growth and tumor development.Carbon-Sulfur Ligases: Enzymes that catalyze the joining of two molecules by the formation of a carbon-sulfur bond. EC 6.2.Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.p38 Mitogen-Activated Protein Kinases: 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.Disease Models, Animal: 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.Rats, Sprague-Dawley: 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.Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.Drug Resistance, Neoplasm: Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.Sequence Homology, Amino Acid: The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).Serpins: 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.Cycloheximide: Antibiotic substance isolated from streptomycin-producing strains of Streptomyces griseus. It acts by inhibiting elongation during protein synthesis.Mice, Nude: Mutant mice homozygous for the recessive gene "nude" which fail to develop a thymus. They are useful in tumor studies and studies on immune responses.Microscopy, Fluorescence: 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.Recombinant Fusion Proteins: 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.Sequence Alignment: The arrangement of two or more amino acid or base sequences from an organism or organisms in such a way as to align areas of the sequences sharing common properties. The degree of relatedness or homology between the sequences is predicted computationally or statistically based on weights assigned to the elements aligned between the sequences. This in turn can serve as a potential indicator of the genetic relatedness between the organisms.Gene Expression Profiling: The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.Tumor Necrosis Factors: A family of proteins that were originally identified by their ability to cause NECROSIS of NEOPLASMS. Their necrotic effect on cells is mediated through TUMOR NECROSIS FACTOR RECEPTORS which induce APOPTOSIS.Transcription, Genetic: The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.Autophagy: 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.Cyclin-Dependent Kinase Inhibitor p21: A cyclin-dependent kinase inhibitor that mediates TUMOR SUPPRESSOR PROTEIN P53-dependent CELL CYCLE arrest. p21 interacts with a range of CYCLIN-DEPENDENT KINASES and associates with PROLIFERATING CELL NUCLEAR ANTIGEN and CASPASE 3.Breast Neoplasms: Tumors or cancer of the human BREAST.Hydrogen Peroxide: 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.Caspases, Effector: A subclass of caspases that contain short pro-domain regions. They are activated by the proteolytic action of INITIATOR CASPASES. Once activated they cleave a variety of substrates that cause APOPTOSIS.Promoter Regions, Genetic: DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.Etoposide: 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.Xenograft Model Antitumor Assays: In vivo methods of screening investigative anticancer drugs, biologic response modifiers or radiotherapies. Human tumor tissue or cells are transplanted into mice or rats followed by tumor treatment regimens. A variety of outcomes are monitored to assess antitumor effectiveness.Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.MAP Kinase Kinase Kinase 5: A 150-kDa MAP kinase kinase kinase that may play a role in the induction of APOPTOSIS. It has specificity for MAP KINASE KINASE 3; MAP KINASE KINASE 4; and MAP KINASE KINASE 6.Phosphatidylinositol 3-Kinases: Phosphotransferases that catalyzes the conversion of 1-phosphatidylinositol to 1-phosphatidylinositol 3-phosphate. Many members of this enzyme class are involved in RECEPTOR MEDIATED SIGNAL TRANSDUCTION and regulation of vesicular transport with the cell. Phosphatidylinositol 3-Kinases have been classified both according to their substrate specificity and their mode of action within the cell.Immunoblotting: 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.Protein Transport: 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.Mice, Inbred BALB CProtein Synthesis Inhibitors: 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.Colon, Ascending: The segment of LARGE INTESTINE between the CECUM and the TRANSVERSE COLON. It passes cephalad from the cecum to the caudal surface of the right lobe of the LIVER where it bends sharply to the left, forming the right colic flexure.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.MAP Kinase Signaling System: An intracellular signaling system involving the MAP kinase cascades (three-membered protein kinase cascades). Various upstream activators, which act in response to extracellular stimuli, trigger the cascades by activating the first member of a cascade, MAP KINASE KINASE KINASES; (MAPKKKs). Activated MAPKKKs phosphorylate MITOGEN-ACTIVATED PROTEIN KINASE KINASES which in turn phosphorylate the MITOGEN-ACTIVATED PROTEIN KINASES; (MAPKs). The MAPKs then act on various downstream targets to affect gene expression. In mammals, there are several distinct MAP kinase pathways including the ERK (extracellular signal-regulated kinase) pathway, the SAPK/JNK (stress-activated protein kinase/c-jun kinase) pathway, and the p38 kinase pathway. There is some sharing of components among the pathways depending on which stimulus originates activation of the cascade.DNA Primers: 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.Gene Silencing: Interruption or suppression of the expression of a gene at transcriptional or translational levels.Software: Sequential operating programs and data which instruct the functioning of a digital computer.Tumor Necrosis Factor Receptor-Associated Peptides and Proteins: Intracellular signaling peptides and proteins that bind directly or indirectly to the cytoplasmic portion of TUMOR NECROSIS FACTOR RECEPTORS.Adenoviridae: 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.Cell Cycle Proteins: Proteins that control the CELL DIVISION CYCLE. This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS.Culture Media, Serum-Free: CULTURE MEDIA free of serum proteins but including the minimal essential substances required for cell growth. This type of medium avoids the presence of extraneous substances that may affect cell proliferation or unwanted activation of cells.Propidium: Quaternary ammonium analog of ethidium; an intercalating dye with a specific affinity to certain forms of DNA and, used as diiodide, to separate them in density gradients; also forms fluorescent complexes with cholinesterase which it inhibits.Oligonucleotides, Antisense: Short fragments of DNA or RNA that are used to alter the function of target RNAs or DNAs to which they hybridize.Oligopeptides: Peptides composed of between two and twelve amino acids.Drug Screening Assays, Antitumor: Methods of investigating the effectiveness of anticancer cytotoxic drugs and biologic inhibitors. These include in vitro cell-kill models and cytostatic dye exclusion tests as well as in vivo measurement of tumor growth parameters in laboratory animals.Microtubule-Associated Proteins: 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.Gene Deletion: A genetic rearrangement through loss of segments of DNA or RNA, bringing sequences which are normally separated into close proximity. This deletion may be detected using cytogenetic techniques and can also be inferred from the phenotype, indicating a deletion at one specific locus.Cytoprotection: The process by which chemical compounds provide protection to cells against harmful agents.Mitochondrial Membranes: 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).Cell Line, Transformed: Eukaryotic cell line obtained in a quiescent or stationary phase which undergoes conversion to a state of unregulated growth in culture, resembling an in vitro tumor. It occurs spontaneously or through interaction with viruses, oncogenes, radiation, or drugs/chemicals.Phosphatidylserines: 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.Genes, p53: Tumor suppressor genes located on the short arm of human chromosome 17 and coding for the phosphoprotein p53.Immunoprecipitation: The aggregation of soluble ANTIGENS with ANTIBODIES, alone or with antibody binding factors such as ANTI-ANTIBODIES or STAPHYLOCOCCAL PROTEIN A, into complexes large enough to fall out of solution.Transcription Factor CHOP: A CCAAT-enhancer binding protein that is induced by DNA DAMAGE and growth arrest. It serves as a dominant negative inhibitor of other CCAAT-enhancer binding proteins.Proteolysis: Cleavage of proteins into smaller peptides or amino acids either by PROTEASES or non-enzymatically (e.g., Hydrolysis). It does not include Protein Processing, Post-Translational.Colonic Neoplasms: Tumors or cancer of the COLON.Prostatic Neoplasms: Tumors or cancer of the PROSTATE.Neuroblastoma: A common neoplasm of early childhood arising from neural crest cells in the sympathetic nervous system, and characterized by diverse clinical behavior, ranging from spontaneous remission to rapid metastatic progression and death. This tumor is the most common intraabdominal malignancy of childhood, but it may also arise from thorax, neck, or rarely occur in the central nervous system. Histologic features include uniform round cells with hyperchromatic nuclei arranged in nests and separated by fibrovascular septa. Neuroblastomas may be associated with the opsoclonus-myoclonus syndrome. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2099-2101; Curr Opin Oncol 1998 Jan;10(1):43-51)Hepatocytes: The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.Neurons: 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.DNA: 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).Gamma Rays: Penetrating, high-energy electromagnetic radiation emitted from atomic nuclei during NUCLEAR DECAY. The range of wavelengths of emitted radiation is between 0.1 - 100 pm which overlaps the shorter, more energetic hard X-RAYS wavelengths. The distinction between gamma rays and X-rays is based on their radiation source.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Proto-Oncogene Proteins c-myc: Cellular DNA-binding proteins encoded by the c-myc genes. They are normally involved in nucleic acid metabolism and in mediating the cellular response to growth factors. Elevated and deregulated (constitutive) expression of c-myc proteins can cause tumorigenesis.Lymphocytes: White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.MAP Kinase Kinase 4: A mitogen-activated protein kinase kinase with specificity for JNK MITOGEN-ACTIVATED PROTEIN KINASES; P38 MITOGEN-ACTIVATED PROTEIN KINASES and the RETINOID X RECEPTORS. It takes part in a SIGNAL TRANSDUCTION pathway that is activated in response to cellular stress.Gene Knockdown Techniques: 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.Cytokines: Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.Lymphocyte Activation: Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION.Lung Neoplasms: Tumors or cancer of the LUNG.K562 Cells: An ERYTHROLEUKEMIA cell line derived from a CHRONIC MYELOID LEUKEMIA patient in BLAST CRISIS.Acetylcysteine: 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.Cytosol: Intracellular fluid from the cytoplasm after removal of ORGANELLES and other insoluble cytoplasmic components.HCT116 Cells: Human COLORECTAL CARCINOMA cell line.
Fas/Apo [apoptosis]-1 and associated proteins in the differentiating cerebral cortex: induction of caspase-dependent cell death and activation of NF-kappaB. (1/700)The developing cerebral cortex undergoes a period of substantial cell death. The present studies examine the role of the suicide receptor Fas/Apo[apoptosis]-1 in cerebral cortical development. Fas mRNA and protein are transiently expressed in subsets of cells within the developing rat cerebral cortex during the peak period of apoptosis. Fas-immunoreactive cells were localized in close proximity to Fas ligand (FasL)-expressing cells. The Fas-associated signaling protein receptor interacting protein (RIP) was expressed by some Fas-expressing cells, whereas Fas-associated death domain (FADD) was undetectable in the early postnatal cerebral cortex. FLICE-inhibitory protein (FLIP), an inhibitor of Fas activation, was also expressed in the postnatal cerebral cortex. Fas expression was more ubiquitous in embryonic cortical neuroblasts in dissociated culture compared to in situ within the developing brain, suggesting that the environmental milieu partly suppresses Fas expression at this developmental stage. Furthermore, FADD, RIP, and FLIP were also expressed by subsets of dissociated cortical neuroblasts in culture. Fas activation by ligand (FasL) or anti-Fas antibody induced caspase-dependent cell death in primary embryonic cortical neuroblast cultures. The activation of Fas was also accompanied by a rapid downregulation of Fas receptor expression, non-cell cycle-related incorporation of nucleic acids and nuclear translocation of the RelA/p65 subunit of the transcription factor NF-kappaB. Together, these data suggest that adult cortical cell number may be established, in part, by an active process of receptor-mediated cell suicide, initiated in situ by killer (FasL-expressing) cells and that Fas may have functions in addition to suicide in the developing brain. (+info)
Equine herpesvirus-2 E10 gene product, but not its cellular homologue, activates NF-kappaB transcription factor and c-Jun N-terminal kinase. (2/700)We have previously reported on the death effector domain containing E8 gene product from equine herpesvirus-2, designated FLICE inhibitory protein (v-FLIP), and on its cellular homologue, c-FLIP, which inhibit the activation of caspase-8 by death receptors. Here we report on the structure and function of the E10 gene product of equine herpesvirus-2, designated v-CARMEN, and on its cellular homologue, c-CARMEN, which contain a caspase-recruiting domain (CARD) motif. c-CARMEN is highly homologous to the viral protein in its N-terminal CARD motif but differs in its C-terminal extension. v-CARMEN and c-CARMEN interact directly in a CARD-dependent manner yet reveal different binding specificities toward members of the tumor necrosis factor receptor-associated factor (TRAF) family. v-CARMEN binds to TRAF6 and weakly to TRAF3 and, upon overexpression, potently induces the c-Jun N-terminal kinase (JNK), p38, and nuclear factor (NF)-kappaB transcriptional pathways. c-CARMEN or truncated versions thereof do not appear to induce JNK and NF-kappaB activation by themselves, nor do they affect the JNK and NF-kappaB activating potential of v-CARMEN. Thus, in contrast to the cellular homologue, v-CARMEN may have additional properties in its unique C terminus that allow for an autonomous activator effect on NF-kappaB and JNK. Through activation of NF-kappaB, v-CARMEN may regulate the expression of the cellular and viral genes important for viral replication. (+info)
Cell death attenuation by 'Usurpin', a mammalian DED-caspase homologue that precludes caspase-8 recruitment and activation by the CD-95 (Fas, APO-1) receptor complex. (3/700)Apoptotic cell suicide initiated by ligation of CD95 (Fas/APO-1) occurs through recruitment, oligomerization and autocatalytic activation of the cysteine protease, caspase-8 (MACH, FLICE, Mch5). An endogenous mammalian regulator of this process, named Usurpin, has been identified (aliases for Usurpin include CASH, Casper, CLARP, FLAME-1, FLIP, I-FLICE and MRIT). This protein is ubiquitously expressed and exists as at least three isoforms arising by alternative mRNA splicing. The Usurpin gene is comprised of 13 exons and is clustered within approximately 200 Kb with the caspase-8 and -10 genes on human chromosome 2q33-34. The Usurpin polypeptide has features in common with pro-caspase-8 and -10, including tandem 'death effector domains' on the N-terminus of a large subunit/small subunit caspase-like domain, but it lacks key residues that are necessary for caspase proteolytic activity, including the His and Cys which form the catalytic substrates diad, and residues that stabilize the P1 aspartic acid in substrates. Retro-mutation of these residues to functional caspase counterparts failed to restore proteolytic activity, indicating that other determinants also ensure the absence of catalytic potential. Usurpin heterodimerized with pro-caspase-8 in vitro and precluded pro-caspase-8 recruitment by the FADD/MORT1 adapter protein. Cell death induced by CD95 (Fas/APO-1) ligation was attenuated in cells transfected with Usurpin. In vivo, a Usurpin deficit was found in cardiac infarcts where TUNEL-positive myocytes and active caspase-3 expression were prominent following ischemia/reperfusion injury. In contrast, abundant Usurpin expression (and a caspase-3 deficit) occurred in surrounding unaffected cardiac tissue, suggesting reciprocal regulation of these pro- and anti-apoptotic molecules in vivo. Usurpin thus appears to be an endogenous modulator of apoptosis sensitivity in mammalian cells, including the susceptibility of cardiac myocytes to apoptotic death following ischemia/ reperfusion injury. (+info)
TCR engagement regulates differential responsiveness of human memory T cells to Fas (CD95)-mediated apoptosis. (4/700)In this work, we have tried to establish whether human memory T cells may be protected from Fas (CD95)-induced apoptosis when correctly activated by Ag, and not protected when nonspecifically or incorrectly activated. In particular, we wanted to investigate the molecular mechanisms that regulate the fate of memory T cells following an antigenic challenge. To address this issue, we chose an experimental system that closely mimics physiological T cell activation such as human T cell lines and clones specific for viral peptides or alloantigens. We demonstrate that memory T cells acquire an activation-induced cell death (AICD)-resistant phenotype when TCRs are properly engaged by specific Ag bound to MHC molecules. Ag concentration and costimulation are critical parameters in regulating the protective effect. The analysis of the mechanisms involved in the block of CD95 signal transduction pathways revealed that the crucial events are the inhibition of CD95-associated IL-1beta-converting enzyme (ICE)-like protease (FLICE) activation and poly(ADP)-ribose polymerase cleavage, and the mRNA expression of FLICE-like inhibitory protein. Furthermore, we have observed that TCR-mediated neosynthesis of FLICE-like inhibitory protein mRNA is suppressed either by protein tyrosine kinase inhibitors or cyclosporin A. In conclusion, the present analysis of the effects of TCR triggering on the regulation of AICD suggests that AICD could be inhibited in human memory T cells activated in vivo by a foreign Ag, but may become operative when the Ag has been cleared. (+info)
Transcriptional analysis of human herpesvirus-8 open reading frames 71, 72, 73, K14, and 74 in a primary effusion lymphoma cell line. (5/700)We examined the transcription and splicing of open reading frames (ORFs) 71 (K13)-74 of human herpesvirus-8 (HHV-8) in the primary effusion lymphoma cell line BCP-1 (latently infected with HHV-8), using a combination of NORTHERN blot analysis, RT-PCR, and rapid amplification of cDNA ends (PCR-RACE). The three genes encoded by ORFs 71, 72, and 73 [viral FLICE inhibitory protein (v-FLIP), v-cyclin, latent nuclear antigen (LNA)] are transcribed from a common transcription start site in BCP-1 cells uninduced (latent) or induced (lytic) with n-butyrate. The resulting transcript is spliced to yield a 5.32-kb message encoding LNA, v-cyclin, and v-FLIP and a 1.7-kb bicistronic message encoding v-cyclin and v-FLIP. The two genes encoded by ORFs K14 and 74 (v-Ox2 and v-GPCR) are transcribed as a 2.7-kb bicistronic transcript that is induced with n-butyrate. A small (149-bp) intron is spliced from the intragenic noncoding region immediately before the v-GPCR initiating codon. Examination of sequence elements in the promoter of the LNA/v-cyclin/v-FLIP operon revealed TAATGARAT and Octamer binding motifs characteristic of herpesvirus immediate-early genes. Sequence elements in the v-Ox2/v-GPCR promoter included AP1 and Zta-like (EBV Zebra transactivator) binding motifs consistent with the n-butyrate induction of this operon. (+info)
Cell cycle-dependent regulation of FLIP levels and susceptibility to Fas-mediated apoptosis. (6/700)Activation-induced cell death of peripheral T cells results from the interaction between Fas and Fas ligand. Resting peripheral T cells are resistant to Fas-induced apoptosis and become susceptible only after their activation. We have investigated the molecular mechanism mediating the sensitization of resting peripheral T cells to Fas-mediated apoptosis following TCR stimulation. TCR activation decreases the steady state protein levels of FLIP (FLICE-like inhibitory protein), an inhibitor of the Fas signaling pathway. Reconstitution of intracellular FLIP levels by the addition of a soluble HIV transactivator protein-FLIP chimera completely restores resistance to Fas-mediated apoptosis in TCR primary T cells. Inhibition of IL-2 production by cyclosporin A, or inhibition of IL-2 signaling by rapamycin or anti-IL-2 neutralizing Abs prevents the decrease in FLIP levels and confers resistance to Fas-mediated apoptosis following T cell activation. Using cell cycle-blocking agents, we demonstrate that activated T cells arrested in G1 phase contain high levels of FLIP protein, whereas activated T cells arrested in S phase have decreased FLIP protein levels. These findings link regulation of FLIP protein levels with cell cycle progression and provide an explanation for the increase in TCR-induced apoptosis observed during the S phase of the cell cycle. (+info)
Relation of TNF-related apoptosis-inducing ligand (TRAIL) receptor and FLICE-inhibitory protein expression to TRAIL-induced apoptosis of melanoma. (7/700)Past studies have shown that apoptosis mediated by TNF-related apoptosis-inducing ligand (TRAIL) is regulated by the expression of two death receptors [TRAIL receptor 1 (TRAIL-R1) and TRAIL-R2] and two decoy receptors (TRAIL-R3 and TRAIL-R4) that inhibit apoptosis. In previous studies, we have shown that TRAIL but not other members of the tumor necrosis factor family induce apoptosis in approximately two-thirds of melanoma cell lines. Here, we examined whether the expression of TRAIL-R at the mRNA and protein level in a panel of 28 melanoma cell lines and melanocytes correlated with their sensitivity to TRAIL-induced apoptosis. We report that at least three factors appear to underlie the variability in TRAIL-induced apoptosis. (a) Four of nine cell lines that were insensitive to TRAIL-induced apoptosis failed to express death receptors, and in two instances, lines were devoid of all TRAIL-Rs. Southern analysis suggested this was due to loss of the genes for the death receptors. (b) Despite the presence of mRNA for the TRAIL-R, some of the lines failed to express TRAIL-R protein on their surface. This was evident for TRAIL-R1 and more so for the TRAIL decoy receptors TRAIL-R3 and -R4. Studies on permeabilized cells revealed that the receptors were located within the cytoplasm and redistribution from the cytoplasm may represent a posttranslational control mechanism. (c) Surface expression of TRAIL-R1 and -R2 (but not TRAIL-R3 and -R4) showed an overall correlation with TRAIL-induced apoptosis. However, certain melanoma cell lines and clones were relatively resistant to TRAIL-induced apoptosis despite the absence of decoy receptors and moderate levels of TRAIL-R1 and -R2 expression. This may indicate the presence of inhibitors within the cells, but resistance to apoptosis could not be correlated with expression of the caspase inhibitor FLICE-inhibitory protein. mRNA for another TRAIL receptor, osteoprotegerin, was expressed in 22 of the melanoma lines but not on melanocytes. Its role in induction of apoptosis remains to be studied. These results appear to have important implications for future clinical studies on TRAIL. (+info)
Dynamic correlation of apoptosis and immune activation during treatment of HIV infection. (8/700)T cells from HIV infected patients undergo spontaneous apoptosis at a faster rate than those from uninfected patients, are abnormally susceptible to activation induced cell death (AICD), and undergo increased apoptosis in response to Fas receptor ligation. These observations have led to the hypothesis CD4 T cell apoptosis may be a mechanism of CD4 T cell depletion and the pathogenesis of AIDS. Successful treatment of HIV infected patients is accompanied by quantitative and qualitative improvements in immune function reflecting at least partial reversibility of the underlying pathogenesis of HIV. In this report we correlate improvements in markers of immune function with a decrease in apoptosis, and changes in its regulation. Therapy with nelfinavir plus saquinavir in combination with two nucleoside analogue inhibitors of reverse transcriptase dramatically reduces plasma viremia and increases CD4 T cell counts. Coincident with these improvements, CD38 and HLA-DR coexpression on both CD4 and CD8 T cells decrease, and CD45RA and CD62L coexpression increase. Furthermore, spontaneous apoptosis decreases in both CD4 and CD8 T cells (CD4 apoptosis 17.4 vs 2.6%, P=0.005; CD8 apoptosis 15.0 vs 1.0%, P<0.001), as does both Fas mediated apoptosis (CD4 apoptosis 19.0 vs 3.5%, P=0.03; CD8 apoptosis 13.7 vs 1.5%, P=0.002) and CD3 induced AICD (CD4 apoptosis 13.7 vs 3.2%, P=0.001; CD8 apoptosis 29 vs 2.2%, P=0.08). Changes in apoptosis are not associated with changes in Fas receptor expression, but are significantly correlated with changes in activation marker profiles. Although this suggests a possible regulatory role for the apoptosis inhibitory protein FLIP, direct assessment did not reveal quantitative differences in FLIP expression between apoptosis resistant PBL's from HIV negative patients, and apoptosis sensitive PBL's from HIV positive patients. These findings support the hypothesis that apoptosis mediates HIV induced CD4 T cell depletion, but indicate the need for further studies into the molecular regulation of HIV induced apoptosis. (+info)
Induction of apoptosis is the most studied cell death process and it is a tightly regulated physiological event that enables elimination of damaged and unwanted cells. Apoptosis can be induced via activation of either the intrinsic or the extrinsic signalling pathway. The intrinsic pathway involves activation of the mitochondria by stress stimuli, whereas the extrinsic pathway is triggered by ligand induced activation of death receptors such as Fas. Apoptosis induction via Fas activation plays an important role in the function of cytotoxic T lymphocytes and in the control of immune cell homeostasis.. Several studies have shown that anticancer therapies require functional cell death signalling pathways. Irradiation based therapy has been successful in treatment of several malignancies but the usage of high doses has been associated with side effects. Therefore, low dose therapies, that either is optimized for specific delivery or administrated in combination with other treatments, are promising ...
O15519: CASP8 and FADD-like apoptosis regulator; Caspase homolog; CASH; Caspase-eight-related protein; Casper; Caspase-like apoptosis regulatory protein; CLARP; Cellular FLICE-like inhibitory protein; c-FLIP; FADD-like antiapoptotic molecule 1; FLAME-1; Inhibitor of FLICE; I-FLICE; MACH-related inducer of toxicity; MRIT; Usurpin; CASP8 and FADD-like apoptosis regulator subunit p43; CASP8 and FADD-like apoptosis regulator subunit p12; ...
758 Fas is a well characterized member of the death receptor family and its expression correlates with overall patient survival in Cholangiocarcinoma (Shimonishi et al;Hepatology 2000). Cellular FLICE-like inhibitory protein (c-FLIP) is an anti-apoptotic protein that blocks the activation of caspase 8 and apoptosis signaling through death inducing signaling complex (DISC). In our laboratory, we have established a unique Cholangiocarcinoma system with two cell populations that are sensitive (high surface Fas expression) or resistant (low surface Fas expression) to Fas-induced apoptosis (Pan et al; 1999; Am J Path). Fas sensitive, but not Fas resistant cells, undergo apoptosis when exposed to calmodulin (CaM) antagonists via a mechanism similar to Fas-induced death signaling. In an attempt to delineate the role of CaM in Fas mediated signaling, we previously demonstrated a direct interaction between CaM and Fas (Ahn et a; J Biol Chem. 2004) and that CaM is recruited to Fas-induced DISC ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Death receptor (DR) ligation can lead to divergent signaling pathways causing either caspase-mediated cell death or cell proliferation and inflammation. These variations in cellular fate are determined by adaptor proteins that are recruited to the DR signaling complex. FLICE inhibitory protein (FLIP) is an established inhibitor of caspase-8-mediated apoptosis, and it is also involved in NF-kappa B
Melanoma differentiation associated gene-7/interleukin-24 (mda-7/IL-24) is a novel cytokine displaying selective apoptosis-inducing activity in transformed cells without harming normal cells. The present studies focused on clarifying the mechanism(s) by which glutathione S-transferase (GST)-MDA-7 altered cell survival of human renal carcinoma cells in vitro. GST-MDA-7 caused plasma membrane clustering of CD95 and the association of CD95 with procaspase-8. GST-MDA-7 lethality was suppressed by inhibition of caspase-8 or by overexpression of short-form cellular FLICE inhibitory protein, but only weakly by inhibition of cathepsin proteases. GST-MDA-7-induced CD95 clustering (and apoptosis) was blocked by knockdown of acidic sphingomyelinase or, to a greater extent, ceramide synthase-6 expression. GST-MDA-7 killing was, in parallel, dependent on inactivation of extracellular signal-regulated kinase 1/2 and on CD95-induced p38 mitogen-activated protein kinase and c-jun NH2-terminal kinase-1/2 ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
To more characterize the expression of c-FLIP isoforms in human Th cells, we examined the kinetics of c-FLIPS and c-FLIPL on protein amount throughout the early differentiation. c-FLIPL is expressed in Thp cells while c-FLIPS expression becomes noticeable shortly right after activation (Determine 2A). However, we could not detect c-FLIPR isoform on protein degree, which […]. Continue reading ...
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We have examined a large panel of malignant glioma cell lines and identified TRAIL-sensitive and TRAIL-resistant cell lines (5, 7). TRAIL induces apoptosis in the sensitive cell lines through caspase-8-initiated extrinsic and intrinsic pathways (7). Caspase-8-initiated pathways, however, are inhibited in the resistant cell lines due to the recruitment of cellular Fas associate death domain-like IL-1β-converting enzyme-inhibitory protein (c-FLIP) and phosphoprotein enriched in astrocytes 15 kDa/(PEA-15)/phosphoprotein enriched in diabetes (PEA-15/PED) to the death-inducing signaling complex where they inhibit caspase-8 cleavage (46). Conventional chemotherapy agents, such as camptothecin, cisplatin, and etoposide, down-regulates c-FLIP and PED expression and thus sensitizes the resistant glioma cells to TRAIL-induced apoptosis (7). This combination treatment may prove to be effective in clinical treatment of malignant gliomas. In this study, however, we have identified two malignant glioma cell ...
Tumor Necrosis Apoptosis Inducing Ligand (TRAIL) is a death ligand with some specificity for transformed cells. However, some cancer cells develop resistance to TRAIL allowing escape from immune surveillance. Re-sensitization of these cells to TRAIL depends on identifying the mechanism of resistance and applying a targeted corrective. We studied several possible mechanisms of TRAIL resistance beginning with FLICE-Like Inhibitory Protein (FLIP). The short isoform of FLIP (FLIPshort) is an effective inhibitor of caspase 8 activation and therefore overexpression of FLIPshort may be a mechanism of TRAIL resistance. We found that downregulation of FLIP short was sufficient to re-sensitize some prostate carcinoma cells to TRAIL. Another mechanism we investigated is mediated by Elongation Factor 2 (EF2) which acilitates ribosomal translocation along mRNA strands. EF2 can be inactivated by phosphorylation or by ADP-ribosylation, thereby inhibiting protein synthesis. During inhibition of protein ...
Expression of CFLAR (c-FLIP, CASH, CASP8AP1, Casper, CLARP, FLAME, FLIP, I-FLICE, MRIT) in rectum tissue. Antibody staining with HPA019044, CAB022157 and CAB025216 in immunohistochemistry.
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... (vFLIP) that inhibits caspase-8-mediated apoptosis. contaminated cells and renewed MCMV duplication in macrophages partially. Nevertheless, MC159 do not really replace Meters45 completely, as it do not really slow down necroptosis in murine cells, but it decreased TNF-induced necroptosis in MCMV-infected individual HT-29 cells. MC159 differed from M45 in its effect on NF-B also. While MCMV-encoded Meters45 obstructed NF-B account activation by TNF- and interleukin-1 (IL-1), MC159 inhibited TNF- but not really IL-1-activated NF-B account activation in contaminated mouse fibroblasts. These outcomes indicate that the range of MC159t features differs depending on cell type and reflection program and that a cell lifestyle program for the distribution of MCV is normally required to determine the natural relevance of assumed virus-like gene features. IMPORTANCE 398493-79-3 MCV is a human-pathogenic poxvirus that cannot ...
Molluscum contagiosum trojan (MCV) gene encodes a viral FLICE inhibitory proteins (vFLIP) that inhibits caspase-8-mediated apoptosis. contaminated cells and renewed MCMV duplication in macrophages partially. Nevertheless, MC159 do not really replace Meters45 completely, as it do not really slow down necroptosis in murine cells, but it decreased TNF-induced necroptosis in MCMV-infected individual HT-29 cells. MC159 … Continue reading Molluscum contagiosum trojan (MCV) gene encodes a viral FLICE inhibitory proteins. ...
It is postulated that breast cancer stem cells (bCSCs) mediate disease recurrence and drive formation of distant metastases - the principal cause of mortality in breast cancer patients. Therapeutic targeting of bCSCs, however, is hampered by their heterogeneity and resistance to existing therapeutics. In order to identify strategies to selectively remove bCSCs from breast cancers, irrespective of their clinical subtype, we sought an apoptosis mechanism that would target bCSCs yet would not kill normal cells. Suppression of the apoptosis inhibitor cellular FLICE-Like Inhibitory Protein (c-FLIP) partially sensitizes breast cancer cells to the anti-cancer agent Tumour Necrosis Factor-Related Apoptosis Inducing Ligand (TRAIL). Here we demonstrate in breast cancer cell lines that bCSCs are exquisitely sensitive to the de-repression of this pro-apoptotic pathway, resulting in a dramatic reduction in experimental metastases and the loss of bCSC self-renewal. Suppression c-FLIP was performed by siRNA (FLIPi) in
TY - JOUR. T1 - Hypericin induced death receptor-mediated apoptosis in photoactivated tumor cells.. AU - Ali, Seyed Mohamed. AU - Chee, Soo Khee. AU - Yuen, Gan Yik. AU - Olivo, Malini. PY - 2002/6. Y1 - 2002/6. N2 - Nasopharyngeal carcinoma (NPC) is a malignant disease of the head/neck region with a 5-year survival level of approximately 65%. To explore the novel therapeutic strategies in the management of this disease, the potential effects of photodynamic therapy (PDT) in NPC cells were investigated. PDT, a new mode of treatment, is based on the combined use of light-absorbing compounds and light irradiation. Two human NPC cells such as, poorly differentiated (NPC/CNE2) and moderately differentiated (NPC/TW0-1) and other types of tumor cells like colon (CCL-220.1) and bladder (SD) undergo rapid apoptosis when treated with PDT sensitized with hypericin (HY). It has been shown that this compound has a strong photodynamic effect on tumors and viruses. However, the initiating events of PDT ...
Thus, caspase-8 has a crucial pro-survival role in shutting off RIPK1 and preventing it from inducing necroptosis. But how, then, does a cell wherein caspase-8 is activated not die by apoptosis instead? How does it live to develop into a healthy mouse or human? Caspase-8 activates through dimerization; two molecules of caspase-8 are forcefully brought together to form an active complex. The previously mentioned adapter protein FADD is essential for initiating this process of dimerization, but recent evidence has shown that once a few dimers are formed around clusters of FADD, more caspase-8 dimers can form independent of FADD. An important clue comes from the observation that caspase-8 does not only activate when it dimerises with itself to form a homodimer, but can also when it forms a dimer with its cousin, FLIP (FLICE-like Inhibitory Protein), to form a heterodimer. FLIP is similar to caspase-8 but has no protease activity, it is an inactive caspase homologue. The heterodimer is active, but ...
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Nonalcoholic steatohepatitis (NASH) is characterized by progressive liver injury, inflammation, and fibrosis; however, the mechanisms that govern the transition from hepatic steatosis, which is relatively benign, to NASH remain poorly defined. Neuregulin 4 (Nrg4) is an adipose tissue-enriched endocrine factor that elicits beneficial metabolic effects in obesity. Here, we show that Nrg4 is a key component of an endocrine checkpoint that preserves hepatocyte health and counters diet-induced NASH in mice. Nrg4 deficiency accelerated liver injury, fibrosis, inflammation, and cell death in a mouse model of NASH. In contrast, transgenic expression of Nrg4 in adipose tissue alleviated diet-induced NASH. Nrg4 attenuated hepatocyte death in a cell-autonomous manner by blocking ubiquitination and proteasomal degradation of c-FLIPL, a negative regulator of cell death. Adeno-associated virus-mediated (AAV-mediated) rescue of hepatic c-FLIPL expression in Nrg4-deficent mice functionally restored the brake ...
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The protein c-FLIP figures prominently into how the body regulates this process. The protein exists as three different versions, or isoforms. While the roles of c-FLIP-L and c-FLIP-S isoforms are well established, until now relatively little has been known about the role of the c-FLIP-R isoform. Which is why Prof. Ingo Schmitz and the Braunschweig team of researchers decided to take a closer look at this particular isoform. What they found is that it confers protection on immune cells against the apoptosis program. "If c-FLIP-R is activated, lymphocytes are apoptosis-resistant," says the head of the HZIs Systems-oriented Immunology and Inflammation Research work group, who also teaches at the OvGU. "Apoptosis can take place only in the proteins absence ...
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The illustration depicts a wild type mouse and a littermate mutant mouse expressing a constitutive serine phosphorylation mutation in Fas-Associated Death Domain (FADD-D). FADD-D mice exhibit reduced body size. The corresponding confocal images show mislocalization of FADD-D protein. Activated T cells from either wild type or FADD-D mice were stained with FADD antibody (green and pink, respectively) and DAPI (blue).
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Its not only the toughest race in Wyoming, its among the toughest races in the world. It is a national qualifying race for the North American Adventure Racing Series (NAARS) and the United States Adventure Racing Association (USARA). This year, it is part of theAdventure Racing World Series, one of the premier circuits of endurance races on the planet.. This is the third year for the Cowboy Tough, and it will be the third year McGinley Innovations has fielded a team. Sponsored by Black Hills Bentonite, this years lineup is the first (and so far only) all-Casper team to compete in the four-person Coed division.. "From the first year, it has always been my goal to get an all-Casper four-person team, just to support the city that is supporting this race," McGinley said. "Casper and Wyoming have put a lot of work into the Cowboy Tough. It is about showing pride in your community and showing that Casper athletes can compete in world class events." ...
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TRAIL is a potent death-inducing ligand that mediates apoptosis through the extrinsic pathway and serves as an important endogenous tumor suppressor mechanism. Because tumor cells are often killed by TRAIL and normal cells are not, drugs that activate the TRAIL pathway have been thought to have potential clinical value. However, to date, most TRAIL-related clinical trials have largely failed due to the tumor cells having intrinsic or acquired resistance to TRAIL-induced apoptosis. Previous studies to identify resistance mechanisms have focused on targeted analysis of the canonical apoptosis pathway and other known regulators of TRAIL receptor signaling. To identify novel mechanisms of TRAIL resistance in an unbiased way, we performed a genome-wide shRNA screen for genes that regulate TRAIL sensitivity in sublines that had been selected for acquired TRAIL resistance. This screen identified previously unknown mediators of TRAIL resistance including angiotensin II receptor 2, Crk-like protein, ...
Scientists at the Carney Institute for Brain Science have identified one way that a synaptic calcium channel protein in sensory neurons is modulated, providing insight into mechanisms that contribute to chronic pain. The research has the potential to inform new therapeutic targets for abnormal pain conditions. The two-author study was published in the journal eLife on March 26 and reports work of E. Javier López Soto, postdoctoral research associate at Brown University, and Diane Lipscombe, director of the Carney Institute and a professor of neuroscience at Brown.. Lipscombe has been investigating variations in calcium channel proteins since the 1990s. Calcium ion channels produce electrical signals essential for transmission of information between neurons. Scientists have known that ion channels tend to behave differently depending on the type of cell that houses them. Lipscombe and her colleagues had previously found that a process called RNA splicing controls switching between different ...
Siegfried Jost Casper (born 12 January 1929) is a German biologist whose primary research is in limnology and the plant genus Pinguicula (the butterworts). Together with Heinz-Dieter Krausch he has published a basic reference work on the sweet-water flora of central Europe. For many years he studied the East German lake Stechlinsee as well as the river Saale. In 1966 he published a monograph of the genus Pinguicula, a work that is still in use today. He has described at least 14 new species, most recently Pinguicula lippoldii and Pinguicula toldensis in 2007. He has served as head of the Botanical Garden of the Friedrich Schiller University of Jena and since 1990 has been a member of the "Akademie Gemeinnütziger Wissenschaften" in Erfurt. Monographie der Gattung Pinguicula L., (Bibliotheca Botanica, Heft 127/128), 1966, Stuttgart The standard author abbreviation Casper is used to indicate this person as the author when citing a botanical name. Much of the content of this article comes from the ...
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Abstract: Reactive oxygen species (ROS) have been implicated in tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resistance of many cancers. We evaluated the role of peroxiredoxin (Prx) I in TRAIL resistance governed by coupling of nicotinamide adenosine dinucleotide phosphate oxidase (Nox)-derived ROS signaling with the p38 mitogen-activated protein kinase (MAPK)/caspase-signaling cascade in liver cancer cells. Upregulated Prx I expression was found in neoplastic regions of human patient liver, and Prx I knockdown resulted in accelerated TRAIL-induced cell death in SK-Hep-1 human hepatoma cells. The TRAIL cytotoxicity by Prx I knockdown was dependent on activation of caspase-8/3 cascades, which was ablated by addition of inhibitors for p38 MAPK, ROS or Nox, suggesting the association with Nox-driven redox signaling. Furthermore, we found that Nox4 was constitutively expressed in both SK-Hep-1 cells and tumor regions of patient livers, knockdown of Nox4 expression could alleviate ...
Evidence suggests that the signalling events which occur after apoptotic stimulation, define two basic mechanisms for the induction of apoptosis. The first is dependent on signalling via the mitochondria and the second is dependent upon signalling directly from the death receptors. After induction of apoptosis, there is a convergence in signalling at the level of caspase activation and subsequent biochemical and morphological changes. Therefore the efficacy of various inhibitors of apoptosis is dependent upon the initiating signal. In order to understand the apoptotic pathway, the mechanisms by which these inhibitors regulate chemical- and receptor-mediated apoptosis must be understood. The anti-apoptotic oncoprotein, Bcl-2, was shown to inhibit both staurosporine and Fas-mediated apoptosis in a manner which was partially dependent upon the level of Bcl-2 protein expressed. During both staurosporine and Fas-induced apoptosis Bcl-2 acted downstream of caspase-8 activation. High levels of Bcl-2 ...
STANFORD -- The universitys "golden age" lies not in its past, but in its present and future, President Gerhard Casper assured Stanfords new freshmen, transfer students and their parents on the Inner Quad Friday, Sept. 22. The notion of a golden age that once existed in a distant past is common to many civilizations, Casper said in his welcoming address.. The Greek poet Hesiod cited his peoples Golden Age as a time when mortals lived "as if they were gods, their hearts free from all sorrow . . . and without hard work or pain, no miserable old age came their way." From there, Hesiod believed, Greek civilization had declined to a Silver Age, to a Bronze Age, to an intermittent age of Homeric heroes and, eventually, to the poets own period, the Age of Iron. "Of course, individual universities, too, have golden ages," Casper added. "Whether you talk to alumni of Stanford, Chicago, Princeton, Yale, Michigan Berkeley, Harvard - you name it - they will almost invariably assure you that their alma ...
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TY - JOUR. T1 - Regulation in the targeting of TRAIL receptor 1 to cell surface via GODZ for TRAIL sensitivity in tumor cells. AU - Oh, Yumin. AU - Jeon, Y. J.. AU - Hong, G. S.. AU - Kim, I.. AU - Woo, H. N.. AU - Jung, Y. K.. PY - 2012/7. Y1 - 2012/7. N2 - Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and its receptors, TRAIL-R1 (DR4) and TRAIL-R2 (DR5), promote the selective clearing of various malignancies by inducing apoptosis, holding the promise as a potent therapeutic agent for anticancer. Though DR4 and DR5 have high sequence similarity, differential regulation of both receptors in human tumor cells remains largely unexplored. Here, we repot that golgi-specific Asp-His-His-Cys (DHHC) zinc finger protein (GODZ) regulates TRAIL/DR4-mediated apoptosis. Using the SOS protein recruitment-yeast two-hybrid screening, we isolated GODZ that interacted with the death domain of DR4. GODZ binds to DR4, but not to DR5, through the DHHC and the C-terminal transmembrane domain. ...
KSHV is a herpesvirus, and is a large double-stranded DNA virus with a protein covering that packages its nucleic acids, called the capsid, which is then surrounded by an amorphous protein layer called the tegument, and finally enclosed in a lipid envelope derived in part from the cell membrane. KSHV has a genome which is approximately 165,000 nucleic acid bases in length. KSHV is a rhadinovirus, and is remarkable since it has stolen numerous genes from host cells including genes that encode for complement-binding protein, IL-6, BCL-2, cyclin-D, a G protein-coupled receptor, interferon regulatory factor and Flice inhibitory protein (FLIP), as well as DNA synthesis proteins including dihydrofolate reductase, thymidine kinase, thymidylate synthetase, DNA polymerase and many others. While no other human tumor virus possesses these same genes, other tumor viruses target the same cellular pathways illustrating that at a basic level, all tumor viruses appear to attack the same cellular control ...
TY - JOUR. T1 - A genome-wide loss-of-function screen identifies SLC26A2 as a novel mediator of TRAIL resistance. AU - Dimberg, Lina Y.. AU - Towers, Christina G.. AU - Behbakht, Kian. AU - Hotz, Taylor J.. AU - Kim, Jihye. AU - Fosmire, Susan. AU - Porter, Christopher C.. AU - Tan, Aik-Choon. AU - Thorburn, Andrew. AU - Ford, Heide L.. PY - 2017/4/1. Y1 - 2017/4/1. N2 - TRAIL is a potent death-inducing ligand that mediates apoptosis through the extrinsic pathway and serves as an important endogenous tumor suppressor mechanism. Because tumor cells are often killed by TRAIL and normal cells are not, drugs that activate the TRAIL pathway have been thought to have potential clinical value. However, to date, most TRAIL-related clinical trials have largely failed due to the tumor cells having intrinsic or acquired resistance to TRAIL-induced apoptosis. Previous studies to identify resistance mechanisms have focused on targeted analysis of the canonical apoptosis pathway and other known regulators of ...
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Fan, LM, Vinoj, G, Brooks, G and Li, JM (2008) Nox2 modulation of cell cycle inhibitory protein p21cip1 in endothelial cells In: Annual Scientific Conference of the British-Cardiovascular-Society/British-Society-for-Cardiovascular-Research, 2008-06-02 - 2008-06-04, Manchester, ENGLAND. Full text not available from this repository ...
A20 ligase mediates ubiquitination to inhibit caspase-8 cleavage and TRAIL-induced apoptosis, according a study published online in Cancer Discovery.
... a novel FADD-like anti-apoptotic molecule that regulates Fas/TNFR1-induced apoptosis". J. Biol. Chem. 272 (30): 18542-5. doi: ... Caspase-8 is a caspase protein, encoded by the CASP8 gene. It most likely acts upon caspase-3. CASP8 orthologs have been ... protein complex binding. • scaffold protein binding. • protein binding. • identical protein binding. • cysteine-type ... The N-terminal FADD-like death effector domain of this protein suggests that it may interact with Fas-interacting protein FADD ...
... a novel FADD-like anti-apoptotic molecule that regulates Fas/TNFR1-induced apoptosis". J. Biol. Chem. 272 (30): 18542-5. doi: ... Caspase-8 is a caspase protein, encoded by the CASP8 gene. It most likely acts upon caspase-3. CASP8 orthologs have been ... The N-terminal FADD-like death effector domain of this protein suggests that it may interact with Fas-interacting protein FADD ... CASP8 coding sequence". "Entrez Gene: CASP8 caspase 8, apoptosis-related cysteine peptidase". Chun HJ, Zheng L, Ahmad M, Wang J ...
This complex is called the TNFR-1 complex I. Complex-I is then modified by the IAPs (Inhibitor of Apoptosis Proteins) and the ... a protein complex known to regulate transcription of DNA and thus, related to survival processes. The best well-known pathway ... and DR4 induce FADD-dependent apoptosis and activate the NF-kappaB pathway". Immunity. 7 (6): 821-30. doi:10.1016/S1074-7613(00 ... RIPK1 has been shown to interact with: BIRC2, BIRC3, CA11, CASP8, CFLAR, CRADD, RIPK2, RIPK3, RNF11, RNF216, SQSTM1, TNFRSF1A, ...
0 (CASP8 and FADD-Like Apoptosis Regulating Protein); 0 (DNA, Neoplasm). [Em] M s de entrada:. 1712. ... 0 (GNA11 protein, human); 0 (GTP-Binding Protein alpha Subunits); 0 (Membrane Proteins); EC 18.104.22.168 (BRAF protein, human); EC ... Prote na Reguladora de Apoptosis Semelhante a CASP8 e FADD/gen tica. Neoplasias da T nica Conjuntiva/gen tica. DNA de ... Prote na Reguladora de Apoptosis Semelhante a CASP8 e FADD/metabolismo. Linhagem Celular Tumoral. Movimento Celular. Prolifera ...
Can trigger apoptosis via FADD-mediated activation of CASP8. Plays a role in the regulation of the cytoskeleton by binding to ... Either as an adapter protein and/or via its kinase activity, can regulate various signaling pathways (p38 MAP kinase, NF-kappa- ... In addition to serine/threonine-protein kinase activity, also has tyrosine-protein kinase activity and phosphorylates CDK1 at ... and positively regulates ISP via phosphorylation of PPP2R5A which activates FOXO1, which in turn up-regulates the expression of ...
... is thought to proceed via recruitment of the adaptor FADD and caspase-8 to the receptor complex. TNFR1 signaling is also known ... AGFG1 protein, human * Adaptor Proteins, Signal Transducing * CASP8 and FADD-Like Apoptosis Regulating Protein ... Apoptosis induced by TNF-receptor I (TNFR1) is thought to proceed via recruitment of the adaptor FADD and caspase-8 to the ... Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes Cell. 2003 Jul 25;114(2):181-90. doi: ...
casp8 and fadd-like apoptosis regulating protein (1) * cell culture techniques (1) ...
... and apoptosis, (e.g., CASP8, FADD, CTSS), and 16 were down-regulated including genes involved in the complement and coagulation ... 73 proteins were up-regulated. These included proteins involved in protein quality control in the endoplasmic reticulum, e.g., ... The 80 down-regulated proteins included the ribosomal proteins RPL3, RPS8, RPS5 and RPS18.. Conclusion. We developed an in- ... conidia (P-value , 0.05). Of the 56 genes, 40 were up-regulated including genes involved in rearrangement of actin cytoskeleton ...
CASP8, and FADD-like apoptosis regulator (FLIP) but inactivates the proapoptotic protein Bad and caspase 9. Nonetheless, AMP- ... These proteins differ in their tissue distribution, and they are involved in regulating different biological processes such as ... P. Schwertman, A. Lagarou, D. H. W. Dekkers et al., "UV-sensitive syndrome protein UVSSA recruits USP7 to regulate ... Finally, PARylation, mediated by PARP1, regulates some of the NER proteins. First, DDB2 PARylation inhibits its ubiquitination ...
CASP8 and FADD-Like Apoptosis Regulating Protein * Ubiquitin * Colonic Neoplasms * Fever 18 Scopus citations ... Regulation of rad17 protein turnover unveils an impact of rad17-APC cascade in breast carcinogenesis and treatment. Zhou, Z., ... Interplay between arginine methylation and ubiquitylation regulates KLF4-mediated genome stability and carcinogenesis. Hu, D., ...
CASP8 and FADD-Like Apoptosis Regulating Protein * Death Domain Receptor Signaling Adaptor Proteins ... The SCFSkp2 ubiquitin ligase complex modulates TRAIL-R2-induced apoptosis by regulating FLIP(L). Roberts, J. Z., Holohan, C., ... R1095CEM: Klebsiella anti-immunology: exploiting proteins with a eukaryotic SEFIR domain. Bengoechea, J., Moynagh, P. & ...
Can trigger apoptosis via FADD-mediated activation of CASP8. Plays a role in the regulation of the cytoskeleton by binding to ... Either as an adapter protein and/or via its kinase activity, can regulate various signaling pathways (p38 MAP kinase, NF-kappa- ... Gil J and Esteban M. Induction of apoptosis by the dsRNA-dependent protein kinase (PKR): Mechanism of action. Apoptosis 2000; 5 ... In addition to serine/threonine-protein kinase activity, also has tyrosine-protein kinase activity and phosphorylates CDK1 at ...
Negatively regulates hypoxia-induced apoptosis in part by inhibiting the release of cytochrome c from mitochondria in a caspase ... dissociating its interaction with CASP8 and maintaining calcium homeostasis (PubMed:23382383). Negatively regulates oxidative ... Firstly by interacting with FAS and FADD upon FAS activation blocking death-inducing signaling complex (DISC) assembly (PubMed: ... Finally through its role as apoptosis repressor, promotes vascular remodeling through inhibition of apoptosis and stimulation ...
CASP8 and FADD-Like Apoptosis Regulating Protein/genetics/metabolism ; Caspase 8/genetics/metabolism ; DNA Fragmentation/drug ... VPA induced apoptosis via the extrinsic pathway involving engagement of the caspase-8-dependent cascade. Although CLL cells are ... Valproic acid induces apoptosis in chronic lymphocytic leukemia cells through activation of the death receptor pathway and ... RESULTS: Exposure of CLL cells to VPA resulted in dose-dependent cytotoxicity and apoptosis in the 40 CLL patients. VPA ...
These include CASP8- and FADD-like apoptosis regulator (CASP8/CASPER/CLARP), caspase-10 (36, 37), and caspase-1, an interleukin ... a death effector domain-containing protein interacts with caspase-8 and regulates apoptosis. Proc. Natl. Acad. Sci. USA, 94: ... including death effector filament-forming Ced-4-like apoptosis protein, caspase recruitment domain protein 10, and apoptotic ... Shu, H. B., Halpin, D. R., and Goeddel, D. V. Casper is a FADD- and caspase-related inducer of apoptosis. Immunity, 6: 751-763 ...
Viral Proteins/metabolism*. *fas Receptor/metabolism*. Substances. *CASP8 and FADD-Like Apoptosis Regulating Protein ... A viral FLIP (FLICE/caspase-8-Inhibitory Protein), equine herpesvirus type 2 E8 protein, has been shown to inhibit Death ... Although E8-expressing thymocytes were resistant to Fas-mediated apoptosis, the total number of thymocytes in 4-8-week-old E8 ... Thus, the Death receptor-mediated signaling pathway is too complex to be regarded as only an executor for apoptosis. ...
BIRC5 protein, human. *CASP8 and FADD-Like Apoptosis Regulating Protein. *CFLAR protein, human ... Protein kinases C (PKC) have been shown to be important in the regulation of proliferation and apoptosis. In this report, we ... PKCmu prevents CD95-mediated apoptosis and enhances proliferation in pancreatic tumour cells.. Trauzold A1, Schmiedel S, Sipos ... In an attempt to identify the signalling pathways affected by PKCmu, we identified the antiapoptotic proteins c-FLIPL and ...
CASP8 and FADD-Like Apoptosis Regulating Protein. *Carrier Proteins/genetics. *Carrier Proteins/metabolism* ... Recently, cellular FLICE-like inhibitory protein (cFLIP) has been identified as an endogenous inhibitor of Fas- or other ... During tumour progression, cancer cells use diverse mechanisms to escape from apoptosis-inducing stimuli, which may include ... protein was found exclusively in carcinoma cells in all matched sets analysed and approximately three-fold induction was ...
CASP8 and FADD-Like Apoptosis Regulating Protein * Neoplasms * Apoptosis * Down-Regulation 22 Citations (Scopus) ... Vitamin D-binding protein enhances epithelial ovarian cancer progression by regulating the insulin-like growth factor-1/akt ... Role of placental fibrinogen-like protein 1 in gestational diabetes. Kang, L., Li, H. Y., Ou, H. Y., Wu, P., Wang, S. H., Chang ... Primary Cilium-Regulated EG-VEGF Signaling Facilitates Trophoblast Invasion. Wang, C. Y., Tsai, H. L., Syu, J. S., Chen, T. Y ...
Dopamine and cAMP-Regulated Phosphoprotein 32 Stomach Neoplasms CASP8 and FADD-Like Apoptosis Regulating Protein ... The role of DARPP-32 in regulating TRAIL-dependent apoptosis was evaluated by clonogenic survival assay, Annexin V staining, ... The role of DARPP-32 in regulating TRAIL-dependent apoptosis was evaluated by clonogenic survival assay, Annexin V staining, ... The role of DARPP-32 in regulating TRAIL-dependent apoptosis was evaluated by clonogenic survival assay, Annexin V staining, ...
CASP8 and FADD-Like Apoptosis Regulating Protein * Apoptosis Regulatory Proteins * Drug Discovery ... Etoposide induces protein kinase Cδ- and caspase-3-dependent apoptosis in neuroblastoma cancer cells. Day, T. W., Wu, C. H. & ... c-FLIP knockdown induces ligand-independent DR5-, FADD-, caspase-8-, and caspase-9-dependent apoptosis in breast cancer cells. ... RNA interference in cancer: Targeting the anti-apoptotic protein c-FLIP for drug discovery. Day, T. W. & Safa, A. R., Sep 21 ...
CASP8 and FADD-Like Apoptosis Regulating Protein * Staphylococcal Protein A * Death Domain Receptor Signaling Adaptor Proteins ... Targeting the anti-apoptotic protein c-FLIP for cancer therapy. Safa, A. R. & Pollok, K. E., Jun 1 2011, In : Cancers. 3, 2, p ... Cellular FLICE-like inhibitory protein (C-FLIP): A novel target for cancer therapy. Safa, A. R., Day, T. W. & Wu, C. H., Feb 1 ... Role of post-translational modification of the Y box binding protein 1 in human cancers. Prabhu, L., Hartley, A. V., Martin, M ...
CASP8 and FADD-Like Apoptosis Regulating Protein * Apoptosis * Tumor Necrosis Factor-alpha ...
CASP8 and FADD-Like Apoptosis Regulating Protein * Proteasome Endopeptidase Complex * Vitamins * Pancreatic Neoplasms ... Arginase-1 expression in myeloid cells regulates Staphylococcus aureus planktonic but not biofilm infection. Yamada, K. J., ... Vitamin e δ-tocotrienol sensitizes human pancreatic cancer cells to TRAIL-induced apoptosis through proteasome-mediated down- ...
CASP8 and FADD-Like Apoptosis Regulating Protein. *Caspase 8. *Caspase 9. *Caspase Inhibitors ... Matrix attachment regulates Fas-induced apoptosis in endothelial cells: a role for c-flip and implications for anoikis. ... Matrix attachment regulates Fas-induced apoptosis in endothelial cells: a role for c-flip and implications for anoikis. ... Matrix attachment modulates Fas-mediated apoptosis at two different levels: by regulating the expression level of Fas, and by ...
CASP8 and FADD-Like Apoptosis Regulating Protein * Neoplasms * Apoptosis * Down-Regulation 22 引文 斯高帕斯（Scopus） ... STK31 Is a Cell-Cycle Regulated Protein That Contributes to the Tumorigenicity of Epithelial Cancer Cells. Kuo, P-L., Huang, Y ... Functional antagonism between high temperature requirement protein a (HtrA) family members regulates trophoblast invasion. Chen ... Correlation between leucine rich domain and the stability of LRWD1 protein in human NT2/D1 cells. Tsai, Y. C., Teng, Y. N., ...
CASP8 and FADD-Like Apoptosis Regulating Protein (MeSH) * Caspase 8 (MeSH) * Cell Cycle Proteins (MeSH) ... positively and negatively regulating apoptosis, necroptosis, and inflammation. Here, we report an unanticipated cell-death- and ... Receptor-interacting protein kinase (RIPK) 1 functions as a key mediator of tissue homeostasis via formation of Caspase-8 ...
CASP8 and FADD-Like Apoptosis Regulating Protein. Estrogen Receptor alpha. Female. Gene-Environment Interaction ...
Signaling pathwayReceptorsInduces apoptosisGenesInhibitoryInhibitionCysteine peptidaseGeneCFLARProliferationNecrosisNecroptosisCaspase cascadeRIP1StimuliInduction of apoptosisCD95Inhibitor of Apoptosis ProteInhibits apoptosisIntracellularTumor CellsActivationUniProtPhosphorylationRegulationCellsExtrinsicAbstractMitochondriaLigand-induced apoptosisCleavageBindsNegativelyRegulatorAdapterSurvivalDomain ProteinExpression and apoptosisIsoformCell viabilityInteractsBind to the cytoplasmic death domainResistantCASP3Anti-apoptoticDeathKinase activity
- Thus, the Death receptor-mediated signaling pathway is too complex to be regarded as only an executor for apoptosis. (nih.gov)
- Both CD95 and FADD immunoprecipitates were analyzed by Western blotting using monoclonal or polyclonal Abs directed against the components of the DISC (CD95, FADD, and caspase-8) or against the natural antagonist of the death receptor signaling pathway c-FLIP. (nih.gov)
- The main signaling pathway of apoptosis is the mitochondrial pathway and the death receptor pathway. (cusabio.com)
- In the clinical trial of arsenic trioxide treatment of T lymphocytes, it was also found that both were activated simultaneously , and the antibacterial drug chloroiodoquinoline induced autophagic death and apoptosis in leukemia cells and myeloma cells by disrupting the mTOR signaling pathway . (cusabio.com)
- Caspases are involved in the signaling pathway that directs programmed cell death (apoptosis) in activated immune cells. (beds.ac.uk)
- CpG ODN-mediated anti-apoptosis depended on the TLR9-Akt-FoxO3a signaling pathway. (bvsalud.org)
- We investigated the upstream targets of Nox1 and MCP-1 expression and found that Akt-forkhead transcription factors of the O class (FoxO3a) is an important signaling pathway that regulates both genes. (bvsalud.org)
- The binding of this protein to its receptors has been shown to trigger the activation of MAPK8/JNK, caspase 8, and caspase 3. (nih.gov)
- Cellular-FLICE inhibitory protein (c-FLIP) is an inhibitor of apoptosis downstream of the death receptors Fas, DR4, and DR5, and is expressed as long (c-FLIP L ) and short (c-FLIP S ) splice forms. (elsevier.com)
- Intracellular signaling peptides and proteins that bind directly or indirectly to the cytoplasmic portion of TUMOR NECROSIS FACTOR RECEPTORS. (harvard.edu)
- This domain interacts with other DD-containing proteins and couples the death receptors to caspase activation and apoptosis. (wikipathways.org)
- Intracellular signaling adaptor proteins that bind to the cytoplasmic death domain region found on DEATH DOMAIN RECEPTORS. (umassmed.edu)
- Many of the proteins in this class take part in intracellular signaling from TUMOR NECROSIS FACTOR RECEPTORS. (umassmed.edu)
- Members of the tumor necrosis factor receptor (TNFR) superfamily are cell surface cytokine receptors that control critical cell fate decisions such as proliferation, differentiation, and apoptosis. (pnas.org)
- We identified significantly regulated apoptotic genes in several protein families, such as BCL2 proteins, CASPASE proteins, and TNF receptors, and detailed their transcriptional kinetics during the T-cell activation process. (biomedcentral.com)
- The death domain is homologous to the DD of other receptors such as Fas, TRAILR2 (DR5), TNFR1 and TRAILR1 (DR4), so it can bind to these receptors, as well as TRADD and FADD in the TNFR1 signalling complex. (wikipedia.org)
- FADD is a common adaptor shared by several death receptors for signalling apoptosis through recruitment and activation of caspase 8 (refs 1-3). (jefferson.edu)
- Recruited to both Fas- and TNFR-1 receptors in a FADD dependent manner. (genecards.org)
- Activation of TLRs or receptors for proinflammatory cytokines (including IL-1β per se) induces the NF-κB-dependent expression of proIL-1β (33 kDa) as a cytosolic, biologically inactive precursor protein. (jimmunol.org)
- Valproic acid induces apoptosis in chronic lymphocytic leukemia cells through activation of the death receptor pathway and potentiates TRAIL response. (uliege.be)
- Reference : Valproic acid induces apoptosis in chronic lymphocytic leukemia cells through activat. (uliege.be)
- This protein preferentially induces apoptosis in transformed and tumor cells, but does not appear to kill normal cells although it is expressed at a significant level in most normal tissues. (nih.gov)
- In this study, the mechanisms by which As2O3 induces apoptosis in human colorectal adenocarcinoma HT-29 cells were investigated. (bvsalud.org)
- LIMMA (R package) was used to identify differentially abundant genes and proteins. (aspergillus.org.uk)
- Of the 56 genes, 40 were up-regulated including genes involved in rearrangement of actin cytoskeleton (e.g. (aspergillus.org.uk)
- NanoString and shotgun proteomics identified key candidate genes and proteins involved in the early host response to conidia. (aspergillus.org.uk)
- Genes involved in cell volume regulation, nucleosome maintenance, ion transport, energetics, mitochondrion function, transcriptional regulation and apoptosis showed population- and salinity-dependent patterns of expression during acclimation. (biologists.org)
- Transcriptional patterns of a few select genes (BCL2A1, BBC3 and CASP3) were validated at the protein level. (biomedcentral.com)
- Upregulation of NF-κB and IκB family genes (REL, RELA, and RELB, NFKBIA, NFKBIE and NFKB1) at 48 to 96 hours, supported by the increase of phosphorylated RELA (p65), suggests that the involvement of the NF-κB complex in the process of T-cell proliferation is not only regulated at the protein level but also at the transcriptional level. (biomedcentral.com)
- Examination of genes involved in MAP kinase signalling pathway, important in apoptosis, suggests an induction of p38 and ERK1 cascades in T-cell proliferation (at 48 to 96 hours), which was explored using phosphorylation assays for p38 (MAPK14) and ERK1 (MAPK3). (biomedcentral.com)
- This comparative genome-scale, transcriptional analysis of T-cell activation in the CD4+ and CD8+ subsets and the mixed CD3+ population identified many apoptosis genes not previously identified in the context of T-cell activation. (biomedcentral.com)
- We identified several potentially important apoptotic genes based on their patterns of expression and examined the protein expression of a select set of genes, most of which have not been previously discussed in T-cell activation. (biomedcentral.com)
- Polymorphisms in apoptosis- and proliferation-related genes, ionizing radiation exposure, and risk of breast cancer among U.S. Radiologic Technolog. (cdc.gov)
- In a case-control study of 859 cases and 1,083 controls within the U.S. Radiologic Technologists cohort, we assessed breast cancer risk with respect to 16 candidate variants in eight genes involved in apoptosis, inflammation, and proliferation. (cdc.gov)
- Percentage of genes up-regulated (gray bars) and down-regulated (open bars) ≥1.5-fold were grouped into ( A ) functional categories/ontologies or ( B ) ontologies involved in inflammation using Spotfire DecisionSite software based on the Gene Ontology Consortium database. (jimmunol.org)
- Total genes up-regulated and down-regulated in each grouping are represented within the bar. (jimmunol.org)
- Percentages represent genes that were up-regulated following infection. (jimmunol.org)
- Compared to uninfected cells, Shigella- infected epithelial cells, both in the presence and absence of staurosporine, showed significant induced expression of JUN , several members of the inhibitor of apoptosis gene family, nuclear factor κB and related genes, genes involving tumor protein 53 and the retinoblastoma protein, and surprisingly, genes important for the inhibition of the extrinsic pathway of apoptosis. (biomedcentral.com)
- Secretion of these proteins is dependent on a type III secretion system (T3SS), which is encoded by 20 genes in the mxi-spa locus of the virulence plasmid. (biomedcentral.com)
- Probiotic bacteria increased expression of mRNA for clusters of differentiation antigen 2 ( Cd2 ), protein tyrosine phosphatase receptor type C ( Ptprc ), and Toll-like receptor 6 ( Tlr6 ) genes related to T and B cell activation in mouse intestinal tissue. (beds.ac.uk)
- The probiotic bacteria were also associated with reduced mRNA expression of a group of genes ( RelB, Myd88, I κκ a, Jun, Irak2 ) related to nuclear factor of kappa light chains enhancer in B cells (NF-κB) signal transduction pathway-regulated cytokine responses. (beds.ac.uk)
- CGH detected loss of the chromosomal regions that contain the following genes: 8p12-p23 ( DR4 and DR5 ), 2q33-34 ( caspase-8 ), 11q13.3 ( FADD ), 22q11.2 ( Bid ), and 12q24.1-q24.3 ( Smac / DIABLO ) in TRAIL-resistant cell lines. (aacrjournals.org)
- Negatively regulates ISP by inducing the inhibitory phosphorylation of insulin receptor substrate 1 (IRS1) at 'Ser-312' and positively regulates ISP via phosphorylation of PPP2R5A which activates FOXO1, which in turn up-regulates the expression of insulin receptor substrate 2 (IRS2). (uniprot.org)
- Reduction of thymocyte numbers in transgenic mice expressing viral FLICE-inhibitory protein in a Fas-independent manner. (nih.gov)
- A viral FLIP (FLICE/caspase-8-Inhibitory Protein), equine herpesvirus type 2 E8 protein, has been shown to inhibit Death receptor-induced apoptosis by suppressing the activation of FLICE/caspase-8. (nih.gov)
- Recently, cellular FLICE-like inhibitory protein (cFLIP) has been identified as an endogenous inhibitor of Fas- or other receptor-mediated apoptosis and its altered high expression has a suspected association with tumour development or progression. (nih.gov)
- Further analysis revealed that an apoptotic inhibitory complex (AIC) comprised of DR5, FADD, caspase-8, and c-FLIP L exists in MCF-7 cells, and the absence of c-FLIP L from this complex induces DR5- and FADD-mediated caspase-8 activation in the death inducing signaling complex (DISC). (elsevier.com)
- These proliferative effects of TNF are apparently due to enhanced basal expression of the caspase-8/FLICE-inhibitory protein FLIP. (strath.ac.uk)
- FLICE-inhibitory protein is a key regulator of germinal center B cell apoptosis. (nih.gov)
- We found that GC B cells ex vivo display a preformed inactive DISC containing Fas-associated death domain-containing protein (FADD), procaspase-8, and the long isoform of cellular FADD-like IL-1beta-converting enzyme-inhibitory protein (c-FLIP(L)) but not the CD95L. (nih.gov)
- Binding of TNFα to TNF-R1 on the cell surface triggers trimerization of the receptor and exposes intracellular domain of TNF-R1 following the release of an inhibitory protein. (wikipathways.org)
- Likely target for the cowpox virus CRMA death inhibitory protein. (abcam.com)
- Under conditions in which proliferation of CD3-activated human T lymphocytes is increased by recombinant FasL, there was activation of the transcription factors NF-kappaB and AP-1 and recruitment of the caspase-8 inhibitor and FADD-interacting protein FLIP (FLICE-like inhibitory protein). (nih.gov)
- The cellular FLICE-inhibitory protein (c-FLIP) is a modulator of death receptor-mediated apoptosis and plays a major role in T- and B-cell homeostasis. (cdc.gov)
- Overexpression of Short and Raji variants of Cellular FLICE-like inhibitory protein (c-FLIP) is capable of inhibiting apoptosis, while the function of the Long isoform depends of c-FLIPL concentration in cells. (bvsalud.org)
- Cuando las variantes Short y Raji de la proteína Cellular FLICE-like inhibitory protein (c-FLIP) se encuentran sobrexpresadas son capaces de inhibir la apoptosis, mientras la función de la isoforma Long (c-FLIPL), depende de la concentración de esta molécula en las células. (bvsalud.org)
- PURPOSE: Heat shock protein (HSP) 27 protects the cell by controlling apoptosis and immune reactions, and c-FLIP (cellular-FLICE inhibitory protein) inhibits apoptosis by inhibiting caspase-8 activity. (bvsalud.org)
- Stimulation of macrophages with TLR9 agonist prevented apoptosis induced by serum deprivation through increased expression of FLICE-like inhibitory protein (FLIP). (bvsalud.org)
- Combination of rsTRAIL and HU resulted in the phosphorylation of rat sarcoma (RAS), mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK), extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase and in the significant reduction of apoptosis-inhibited molecule Fas associated death domain protein-like interleukin-1 beta-convening enzyme inhibitory protein and cellular inhibitor of apoptosis protein-1 in K562 cells. (bvsalud.org)
- Inhibits viral replication via phosphorylation of the alpha subunit of eukaryotic initiation factor 2 (EIF2S1), this phosphorylation impairs the recycling of EIF2S1 between successive rounds of initiation leading to inhibition of translation which eventually results in shutdown of cellular and viral protein synthesis. (uniprot.org)
- Finally through its role as apoptosis repressor, promotes vascular remodeling through inhibition of apoptosis and stimulation of proliferation, in response to hypoxia (By similarity). (uniprot.org)
- Inhibition of PKCmu with Goe6983 sensitized resistant cells to CD95-induced apoptosis. (nih.gov)
- We further show that detachment-induced cell death, or anoikis, itself results from activation of the Fas pathway by its ligand, Fas-L. Fas-L/Fas interaction, Fas-FADD complex formation, and caspase-8 activation precede the bulk of anoikis in endothelial cells, and inhibition of any of these events blocks anoikis. (nih.gov)
- Inhibition of Fas-mediated apoptosis by the B cell antigen receptor through c-FLIP. (naver.com)
- Fas ligand-induced apoptosis is regulated by nitric oxide through the inhibition of fas receptor clustering and the nitrosylation of protein kinase Cepsilon. (semanticscholar.org)
- The goal of this research was to identify host factors that contribute to apoptosis inhibition in infected cells. (biomedcentral.com)
- Infection of epithelial cells with S. flexneri induces a pro-survival state in the cell that results in apoptosis inhibition in the presence and absence of staurosporine. (biomedcentral.com)
- Apoptosis inhibition is most likely vital to the survival of the bacteria in vivo . (biomedcentral.com)
- We previously observed that probiotic bacteria could prevent inhibition of lymphoproliferation and apoptosis responses of T cells associated with S. enterica infections in orally challenged mice. (beds.ac.uk)
- In the cytosol, Smac interacts with X-linked inhibitor of apoptosis protein to release its inhibition of caspase-3 ( 17 ). (aacrjournals.org)
- Inhibition of TLR9 by small interfering (si) RNA or an inhibitor suppressed CpG ODN-mediated anti-apoptosis. (bvsalud.org)
- PURPOSE: Treatment with arsenic trioxide (As2O3) results in a wide range of cellular effects that includes induction of apoptosis, inhibition of cell growth, promotion or inhibition of cellular differentiation, and inhibition of angiogenesis through a variety of mechanisms. (bvsalud.org)
- These results identify A20 E3 ligase as a therapeutic target whose inhibition can overcome TNF-related apoptosis-inducing ligand resistance in glioblastoma and thus have an impact on ongoing clinical trials of TNF-related apoptosis-inducing ligand-targeted combination cancer therapies. (aacrjournals.org)
- Auf www.antikoerper-online.de finden Sie aktuell 434 Caspase 8, Apoptosis-Related Cysteine Peptidase (CASP8) Antikörper von 38 unterschiedlichen Herstellern. (antikoerper-online.de)
- On www.antibodies-online.com are 406 Caspase 8, Apoptosis-Related Cysteine Peptidase (CASP8) Antibodies from 37 different suppliers available. (antibodies-online.com)
- Caspase-8 is a caspase protein, encoded by the CASP8 gene. (wikipedia.org)
- The CASP8 gene encodes a member of the cysteine - aspartic acid protease ( caspase ) family. (wikipedia.org)
- The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. (nih.gov)
- On complex 1 formation, NF-κB regulated anti-apoptotic gene products efficiently block initiation of apoptosis by complex 2. (wikipathways.org)
- What does this gene/protein do? (cancerindex.org)
- For this reason, potential modification of the relationship between ionizing radiation exposure and breast cancer risk by polymorphic apoptosis gene variants have not been investigated among radiation-exposed women. (cdc.gov)
- BACKGROUND: Reprimo (RPRM), a highly glycosylated protein, is a new downstream effector of p53-induced cell cycle arrest at the G2/M checkpoint, and a putative tumor suppressor gene frequently silenced via methylation of its promoter region in several malignances. (bvsalud.org)
- The protein encoded by this gene is a regulator of apoptosis and is structurally similar to caspase-8. (genecards.org)
- CFLAR (CASP8 And FADD Like Apoptosis Regulator) is a Protein Coding gene. (genecards.org)
- In order to understand the pro-survival effects induced by the bacteria, we utilized apoptosis-specific microarrays to analyze the changes in eukaryotic gene expression in both infected and uninfected cells in the presence and absence of staurosporine, a chemical inducer of the intrinsic pathway of apoptosis. (biomedcentral.com)
- Receptor-interacting serine/threonine-protein kinase 1 (RIPK1) is an enzyme that in humans is encoded by the RIPK1 gene, which is located on chromosome 6. (wikipedia.org)
- CASP8 (Caspase 8) is a Protein Coding gene. (genecards.org)
- Gene Ontology (GO) annotations related to this gene include protein heterodimerization activity . (genecards.org)
- An increase in cell viability by up-regulation in Bcl2 gene, a decrease in apoptosis by enhanced CDK2 gene expression and a decrease in cell cycle arrest at G0/G1 phase were also observed in SW579 cell lines transfected with silenced BTG2 gene. (bvsalud.org)
- The protein encoded by this gene is a member of the TNF-receptor superfamily. (avivasysbio.com)
- CASP10 (Caspase 10) is a Protein Coding gene. (genecards.org)
- Gene Ontology (GO) annotations related to this gene include ubiquitin protein ligase binding and cysteine-type peptidase activity . (genecards.org)
- An important paralog of this gene is CASP8 . (genecards.org)
- In this study, we describe a previously unidentified allele of caspase 8- and FADD-like apoptosis regulator ( Cflar ) (encoding cFLIP) that makes mice of MSM strain resistant to Fas-mediated lethality. (pnas.org)
- Linkage analysis in F2 intercross (B6 x MSM) progeny identified several MSM loci controlling resistance to Fas-mediated death, including the caspase 8- and FADD-like apoptosis regulator ( Cflar ) locus encoding cFLIP. (pnas.org)
- IFN-induced dsRNA-dependent serine/threonine-protein kinase which plays a key role in the innate immune response to viral infection and is also involved in the regulation of signal transduction, apoptosis, cell proliferation and differentiation. (uniprot.org)
- PKCmu prevents CD95-mediated apoptosis and enhances proliferation in pancreatic tumour cells. (nih.gov)
- Protein kinases C (PKC) have been shown to be important in the regulation of proliferation and apoptosis. (nih.gov)
- We found that the knockdown of c-FLIP using small interfering RNA (siRNA) triggered ligand-independent caspase-8- and -9-dependent spontaneous apoptosis and decreased the proliferation of MCF-7 breast cancer cells. (elsevier.com)
- Tumor necrosis factor alpha (TNFα) is a proinflammatory cytokine involved in various biological processes including regulation of cell proliferation, differentiation, apoptosis and immune response. (wikipathways.org)
- Depending on the signal from the B cell antigen receptor, Fas induces either apoptosis or proliferation of B cells in vivo ( 5 ). (pnas.org)
- However, Fas signals do not always result in apoptosis but can also trigger a pathway that leads to proliferation. (nih.gov)
- Activator protein 1 (AP1) 1 , 2 functions in almost all areas of eukaryotic cellular behaviour, from cell cycle proliferation and development to stress response and apoptosis. (pubmedcentralcanada.ca)
- JUN is important for cell proliferation, survival and apoptosis, and accordingly mice lacking JUN die between day 12.5 and 13.5 of embryonal development owing to hepatic failure and heart defects 8 , 9 . (pubmedcentralcanada.ca)
- The effects of knockdown of c-FLIPL on cell viability, proliferation and apoptosis were assessed by comparing with scrambled siRNA-transfected cells. (bvsalud.org)
- Surprisingly, Fadd(-/-) mice die in utero and conditional deletion of FADD leads to impaired lymphocyte proliferation. (jefferson.edu)
- Furthermore, RIP1 deficiency fully restored normal proliferation in Fadd(-/-) T cells but not in Fadd(-/-) B cells. (jefferson.edu)
- It was observed that 131I significantly inhibited cell proliferation, promoted cell apoptosis and cell cycle arrest. (bvsalud.org)
- Although CLL cells are commonly resistant to death receptor-induced apoptosis, VPA significantly increased sensitivity of leukemic cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and led to downregulation of c-FLIP (L) expression. (uliege.be)
- Tumor Necrosis Factor Receptor-Associated Peptides and Proteins" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (harvard.edu)
- This graph shows the total number of publications written about "Tumor Necrosis Factor Receptor-Associated Peptides and Proteins" by people in Harvard Catalyst Profiles by year, and whether "Tumor Necrosis Factor Receptor-Associated Peptides and Proteins" was a major or minor topic of these publication. (harvard.edu)
- Below are the most recent publications written about "Tumor Necrosis Factor Receptor-Associated Peptides and Proteins" by people in Profiles. (harvard.edu)
- Cell death can be divided into two types, apoptosis and necrosis . (cusabio.com)
- Specific conditions can however activate RIPK1, and its kinase activity then regulates assembly of two death-inducing complexes, namely complex IIa (RIPK1-FADD-CASP8) and the complex IIb (RIPK1-RIPK3-MLKL) and these complexes respectively drive apoptosis or necroptosis, a regulated form of necrosis (PubMed:19524513, PubMed:19524512, PubMed:29440439, PubMed:30988283). (icr.ac.uk)
- Apoptosis is a distinct form of cell death that is functionally and morphologically different from necrosis. (wikipathways.org)
- FADD could directly bind to RIP1 (also known as RIPK1), a serine/threonine kinase that mediates both necrosis and NF-κB activation. (jefferson.edu)
- Here we show that Fadd(-/-) embryos contain raised levels of RIP1 and exhibit massive necrosis. (jefferson.edu)
- Therefore, our data demonstrate an unexpected cell-type-specific interplay between FADD and RIP1, which is critical for the regulation of apoptosis and necrosis during embryogenesis and lymphocyte function. (jefferson.edu)
- Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is currently under clinical development as a cancer therapeutic agent. (aacrjournals.org)
- To explore the molecular mechanism via which the chemotherapeutic drug hydroxyurea (HU) enhances K562 cell apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). (bvsalud.org)
- Receptor-interacting protein kinase (RIPK) 1 functions as a key mediator of tissue homeostasis via formation of Caspase-8 activating ripoptosome complexes, positively and negatively regulating apoptosis, necroptosis, and inflammation. (edu.au)
- As a result, the abundant cFLIP L forms enzymatically active heterodimers with caspase 8 (CASP8) in MSMs, which prevents formation of proapoptotic CASP8 p10/p20 and cleaves receptor interacting protein kinase 1 (RIP1), thus setting up a higher threshold for CD95-mediated apoptosis and RIP1-mediated necroptosis. (pnas.org)
- Initiates ripoptocide which describes cell death that is dependent on RIPK1, be it apoptosis or necroptosis (PubMed:31457011). (icr.ac.uk)
- During embryonic development suppresses apoptosis and necroptosis and prevents the interaction of TRADD with FADD thereby limiting aberrant activation of CASP8 (By similarity). (icr.ac.uk)
- In terms of cell death, RIPK1 plays a role in apoptosis and necroptosis. (wikipedia.org)
- The death domain mediates dimerization and activation of its kinase activity during necroptosis and apoptosis (PubMed:29440439). (rcsb.org)
- Recruitment of CASP8, activation of FADD/RIP1 and apoptosis induction, is blunted when RIPK1 becomes ubiquitinated. (wikipathways.org)
- Functional complementation between FADD and RIP1 in embryos and lympho" by Haibing Zhang, Xiaohui Zhou et al. (jefferson.edu)
- Functional complementation between FADD and RIP1 in embryos and lymphocytes. (jefferson.edu)
- To investigate a potential in vivo functional interaction between RIP1 and FADD, null alleles of RIP1 were crossed into Fadd(-/-) mice. (jefferson.edu)
- Notably, RIP1 deficiency allowed normal embryogenesis of Fadd(-/-) mice. (jefferson.edu)
- Conversely, the developmental defect of Rip1(-/-) lymphocytes was partially corrected by FADD deletion. (jefferson.edu)
- Fadd(-/-)Rip1(-/-) double-knockout T cells are resistant to death induced by Fas or TNF-α and show reduced NF-κB activity. (jefferson.edu)
- Upon TNF-α binding, TNF receptor 1 (TNFR1) recruits receptor-interacting protein 1 (RIP1), cellular inhibitor of apoptosis protein 1 and 2 (cIAP1 and cIAP2), and TNFR-associated factor 2 (TRAF2) for the assembly of TNFR1-associated complex I ( 16 ). (aacrjournals.org)
- TRAF2 and RIP1 then detach from TNFR1 and recruit FADD and caspase-8 for the assembly of the cytoplasmic complex II ( 19 ), where the deubiquitinating cylindromatosis removes the polyubiquitin chains from RIP1 to promote caspase-8 cleavage for TNF-α-induced apoptosis ( 20 ). (aacrjournals.org)
- This protein is involved in the programmed cell death induced by Fas and various apoptotic stimuli. (wikipedia.org)
- For this purpose, the proteins associated with either CD95 or FADD were immunoprecipitated in freshly isolated GC B cells or in GC B cells cultured in complete medium without exogenous stimuli for different lengths of time. (nih.gov)
- Many apoptosis-inducing stimuli often induce autophagy, for instance, both apoptosis and autophagy are simultaneously upregulated by treatment in breast cancer cells with ceramide . (cusabio.com)
- Boesen-de Cock, Tepper, de Vries, van Blitterswijk, Borst: Common regulation of apoptosis signaling induced by CD95 and the DNA-damaging stimuli etoposide and gamma-radiation downstream from caspase-8 activation. (antibodies-online.com)
- The most intensively studied inflammasome comprises an oligomeric complex of procaspase-1 with the NLRP3 and ASC adapter proteins that rapidly assembles in response to diverse stress stimuli such as increased reactive oxygen species (ROS) ( 3 ), mitochondrial dysfunction ( 4 ), perturbation of intracellular ion homeostasis ( 5 - 7 ), disruption of lysosomal membrane integrity ( 8 ), and activation of deubiquitinases ( 9 - 11 ). (jimmunol.org)
- However, ectopic expression of Fas did not result in an induction of apoptosis in attached HUVECs, and neither did it sensitize the cells to CH11-mediated killing (see Fig. 6). (nih.gov)
- This study was purposed to investigate the effect of a hypoxia-inducible factor inhibitor (YC-1) on expression of hypoxia-inducible factor 1alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF) as well as induction of apoptosis in leukemic cell lines. (bvsalud.org)
- We demonstrate that in these cells, PKCmu expression strongly correlates with resistance to CD95-induced apoptosis. (nih.gov)
- In CD95-sensitive Colo357 cells, forced overexpression of PKCmu strongly reduced CD95-mediated apoptosis, an effect that could be reversed by pretreatment with Goe6983. (nih.gov)
- Here, we show that GC B cell apoptosis is preceded by the rapid activation of caspase-8 at the level of CD95 death-inducing signaling complex (DISC). (nih.gov)
- A) CD95 or (B) FADD was immunoprecipitated (IP) from 107 freshly isolated GC B cells or at different times after setting the same cells in culture in complete medium as described in Materials and Methods. (nih.gov)
- The immunoprecipitates were washed, subjected to 10% SDS PAGE, and successively probed with the anti-caspase-8, FADD, CD95, and c-FLIP Abs. (nih.gov)
- Cell attachment to extracellular matrix inhibits apoptosis in endothelial cells both in vitro and in vivo, but the molecular mechanisms underlying matrix-induced survival signals or detachment-induced apoptotic signals are unknown. (nih.gov)
- Shigella flexneri inhibits apoptosis in infected epithelial cells. (biomedcentral.com)
- Future characterization of these host factors is required to fully understand how S. flexneri inhibits apoptosis in epithelial cells. (biomedcentral.com)
- Apoptosis can be activated by a variety of cellular signals, including increased intracellular Ca 2+ concentration, reactive oxygen species (ROS) such as hydroxyl radicals caused by oxidative damage, toxins, NO, growth factors, and hormonal stimulation. (cusabio.com)
- Intracellular apoptosis signals usually activate the mitochondrial pathway, stimulate the activation of BH3-only protein to bind to apoptotic proteins such as Bcl-2 , activate Bax/Bak aggregation to the mitochondrial membrane, and release mitochondrial pro-apoptotic proteins including cytochrome C , SMAC/DIABLO. (cusabio.com)
- Conversely, short hairpin RNA-mediated knockdown of endogenous DARPP-32 sensitized the resistant MKN-45 cells to TRAIL-induced apoptosis and enhanced TRAIL-mediated activation of caspase-8, -9, and -3. (elsevier.com)
- This suggests that upregulation of BCL-xL could play a possible role in blocking the mitochondria intrinsic apoptosis pathway, whereas the DARPP-32 effect on the NF-κB/FLIP(S) axis could serve as an additional negative feedback loop that blocks TRAIL-induced activation of caspase-8. (elsevier.com)
- Sequential activation of caspases plays a central role in the execution-phase of cell apoptosis . (wikipedia.org)
- For the death pathway, the caspase-8 zymogen is cleaved into subunits that assemble to form the mature, highly active caspase heterotetramer whereas for the activation pathway, the zymogen appears to remain intact perhaps to limit its proteolytic function but enhance its capability as an adapter protein. (wikipedia.org)
- Can regulate NLRP3 inflammasome assembly and the activation of NLRP3 , NLRP1 , AIM2 and NLRC4 inflammasomes. (rcsb.org)
- Can trigger apoptosis via FADD -mediated activation of CASP8 . (rcsb.org)
- This results in cytochrome C release and activation of other caspases ultimately leading to apoptosis. (wikipathways.org)
- TRAF-2 in complex 1 also activates the MAP kinase cascade, that leads to the activation of JNK, which on prolonged activation is believed to mediate both apoptosis and necrotic cell death. (wikipathways.org)
- There is evidence of an early attempt to signal for apoptosis, which precedes the activation of NF-κB. (wikipathways.org)
- The resulting aggregate called death-inducing signaling complex (DISC) performs CASP8 proteolytic activation. (abcam.com)
- Phosphorylation on Ser-387 during mitosis by CDK1 inhibits activation by proteolysis and prevents apoptosis. (abcam.com)
- The process of proper T-cell activation is strictly monitored and regulated by apoptosis signaling. (biomedcentral.com)
- Yet, regulation of apoptosis, an integral and crucial facet during the process of T-cell activation, is not well understood. (biomedcentral.com)
- Furthermore, it provided a comprehensive temporal analysis of the transcriptional program of apoptosis associated with T-cell activation. (biomedcentral.com)
- However, the regulation of apoptosis and the balance between the anti-apoptotic and pro-apoptotic signalling (which is an essential part of the surveillance machinery) during the process of T-cell activation have not been examined. (biomedcentral.com)
- Nocodazole-induced p53-dependent c-Jun N-terminal kinase activation reduces apoptosis in human colon carcinoma HCT116 cells. (wikipathways.org)
- In addition, Akt activation was involved in CpG ODN-induced phosphorylation of FoxO3a, expression of FLIP, and anti-apoptosis. (bvsalud.org)
- It engages other DD-containing proteins as well as a central (intermediate) region important for NF-kB activation and RHIM-dependent signaling (PubMed:10356400). (rcsb.org)
- Pretreating the HT-29 cells with N-acetyl-L-cysteine, which is a thiol-containing antioxidant, inhibited the As2O3- Induced Apoptosis and Caspase Activation. (bvsalud.org)
- Involved in the activation cascade of caspases responsible for apoptosis execution. (genecards.org)
- Notably, Dox-induced production of mature IL-1β was temporally correlated with caspase-8 activation in WT cells and greatly suppressed in Casp8 −/− Rip3 −/− or Trif −/− BMDC, as well as in WT BMDC treated with the caspase-8 inhibitor, IETD. (jimmunol.org)
- Western blot was performed to analyze the activation of apoptosis-related protein kinases and the expression of apoptosis inhibitor molecules. (bvsalud.org)
- Plays a role in the regulation of the cytoskeleton by binding to gelsolin ( GSN ), sequestering the protein in an inactive conformation away from actin. (rcsb.org)
- This inherently diverse composition of AP1 complexes and their central role in transcriptional regulation places AP1 complexes at a functional epicenter for pathological signal relay in disease, particularly in the context of malignant cellular transformation in which AP1 proteins are often deregulated by oncoprotein signalling 4 - 6 . (pubmedcentralcanada.ca)
- In contrast, NK cells cultivated in IL-2 for 6 days became sensitive to CH11-induced apoptosis without addition of actinomycin D. At this time, a pronounced up-regulation of the Fas protein on the NK cell membrane was detected. (nih.gov)
- Role of Hsp70 in regulation of stress-kinase JNK: implications in apoptosis and aging. (wikipathways.org)
- CONCLUSION: Taken together, these results suggest that the generation of reactive oxygen species (ROS) by As2O3 might play an important role in the regulation of As2O3-induced apoptosis. (bvsalud.org)
- Abgent has over fifteen years of experience producing recombinant proteins in E. coli and mammalian cells (CHO and HEK293, etc), and we have added a powerful yeast expression platform to our menu of services. (abgent.com)
- en] OBJECTIVE: Chronic lymphocytic leukemia (CLL) cells develop chemoresistance over time associated with defects in apoptosis pathway. (uliege.be)
- RESULTS: Exposure of CLL cells to VPA resulted in dose-dependent cytotoxicity and apoptosis in the 40 CLL patients. (uliege.be)
- VPA caused no potentialization of TRAIL-induced apoptosis on normal B cells. (uliege.be)
- Cells in early crisis have short (dysfunctional) telomeres, recognized as DNA damage and undergo p53-dependent apoptosis ( 5 ). (aacrjournals.org)
- Substantial numbers of colon cancer cells have been observed to express Fas/Fas ligand, but are resistant to Fas-mediated apoptosis, suggesting that colonic tumours might develop specific mechanisms to overcome Fas-mediated apoptosis. (nih.gov)
- Matrix attachment regulates Fas-induced apoptosis in endothelial cells: a role for c-flip and implications for anoikis. (nih.gov)
- We demonstrate here that matrix attachment is an efficient regulator of Fas-mediated apoptosis in endothelial cells. (nih.gov)
- Thus, matrix attachment protects cells from Fas-induced apoptosis, whereas matrix detachment results in susceptibility to Fas-mediated cell death. (nih.gov)
- The extracellular signal-regulated kinase (Erk) cascade functions as a survival pathway in adherent cells by regulating c-Flip expression. (nih.gov)
- These studies identify matrix attachment as a survival factor against death receptor-mediated apoptosis and provide a molecular mechanism for anoikis and previously observed Fas resistance in endothelial cells. (nih.gov)
- Thus, although upregulation of Fas may be necessary for anoikis and Fas-mediated apoptosis to take place in detached cells, enhanced Fas expression alone is not sufficient to sensitize adherent HUVECs for Fas-mediated killing. (nih.gov)
- Title: The regulatory protein GADD34 inhibits TRAIL-induced apoptosis via TRAF6/ERK-dependent stabilization of myeloid cell leukemia 1 in liver cancer cells. (nih.gov)
- In human erythroleukemia patient myeloid progenitor stem cells (TF-1) as well as chronic myelogenous leukemia cells (K562), granulocyte-macrophage colony-stimulating factor primes cells for apoptosis. (strath.ac.uk)
- Second, mutant B cell clones with improved affinity for Ag are positively selected by Ag and CD40 ligand (L). This selection step is contingent upon "priming" of GC B cells for apoptosis. (nih.gov)
- TNF-R1 is ubiquitously expressed, whereas TNF-R2 is found typically on cells of the immune system and is highly regulated. (wikipathways.org)
- This signal however is enough to initiate apoptosis in some cells. (wikipathways.org)
- High resistance to treatment is a unique hallmark of malignant melanoma, although the mechanisms by which melanoma cells protect themselves against induced apoptosis remains largely unknown [ 3 ]. (pubmedcentralcanada.ca)
- Here, we identify that primary epithelial cancer cells from colon, breast and lung carcinomas express high levels of the antiapoptotic proteins PED, cFLIP, Bcl-xL and Bcl-2. (nih.gov)
- These cancer cells produced interleukin-4 (IL-4), which amplified the expression levels of these antiapoptotic proteins and prevented cell death induced upon exposure to TRAIL or other drug agents. (nih.gov)
- IL-4 blockade resulted in a significant decrease in the growth rate of epithelial cancer cells and sensitized them, both in vitro and in vivo, to apoptosis induction by TRAIL and chemotherapy via downregulation of the antiapoptotic factors PED, cFLIP, Bcl-xL and Bcl-2. (nih.gov)
- Furthermore, we provide evidence that exogenous IL-4 was able to upregulate the expression levels of these antiapoptotic proteins and potently stabilized the growth of normal epithelial cells rendering them apoptosis resistant. (nih.gov)
- Apoptosis is the process by which cells actively end their lives and is essential for maintaining cellular homeostasis. (cusabio.com)
- Several viral and cellular pro-caspase-8 like proteins, termed FLIPs ( 18 ), contain FADD-interacting DED motifs but inactive protease domains, and they are potent inhibitors of Fas-induced cell death in tissue culture cells and in primary lymphocytes ( 19 - 20 ). (pnas.org)
- The role of interleukin-2 in regulating the sensitivity of natural killer cells for Fas-mediated apoptosis. (nih.gov)
- Highly purified CD56+CD3- natural killer (NK) cells were found to be resistant to the apoptosis-inducing Fas mAb CH11 in the absence or in the presence of interleukin-2 (IL-2) for up to 3 days. (nih.gov)
- The amount of apoptotic and necrotic NK cells was reduced in the presence of Fas-Fc protein. (nih.gov)
- Shan, Li, Newton, Zhao, Li, Guo: A novel protein extracted from foxtail millet bran displays anti-carcinogenic effects in human colon cancer cells. (antikoerper-online.de)
- The present study was undertaken to gain insights into the molecular mechanism of cell death (apoptosis) by guggulsterone, a constituent of Ayurvedic medicinal plant Commiphora mukul, using PC-3 human prostate cancer cells as a model. (isharonline.org)
- Retinol dehydrogenase 12 (RDH12) is a member of the microsomal short-chain dehydrogenase/reductase superfamily of proteins that is highly expressed in photorecep-tor cells. (oatd.org)
- Disease-associated RDH12 variants exhibit lower protein levels when expressed in eukaryotic cells. (oatd.org)
- Entry into epithelial cells is mediated by the Ipa proteins encoded on the 220-kb virulence plasmid. (biomedcentral.com)
- T cells that have been activated, but lacking secondary signals, activate an intrinsic caspase pathway that is arrested by signals from B- cell CLL/lymphoma 2 (BCL) 2 and its related proteins. (beds.ac.uk)
- Polarity of response to transforming growth factor-beta1 in proximal tubular epithelial cells is regulated by beta-catenin. (wikipathways.org)
- miR-29b regulates migration of human breast cancer cells. (wikipathways.org)
- Estradiol-regulated microRNAs control estradiol response in breast cancer cells. (wikipathways.org)
- Functional studies, using an inhibitor of nuclear factor κB (NF-κB), revealed preferential targeting of the cancer stem cell and progenitor population for apoptosis whilst sparing normal stem cells. (biomedcentral.com)
- However, malignant glioma cells express X-linked inhibitor of apoptosis protein ( 16 ) that interacts with caspase-3 and inhibits caspase-8 cleavage of caspase-3 ( 17 ). (aacrjournals.org)
- MATERIALS AND METHODS: RT-PCR, Western blotting, and immunocytochemical staining were performed to determine whether HSP27 mRNA and protein are expressed in PC-3 cells. (bvsalud.org)
- It is concluded that HIF-1alpha mRNA and VEGF mRNA are all expressed in in K562, U937 and Jurkat cells, YC-1 has significant effect on down-regulating the protein expression of HIF-1alpha and VEGF, and induces the apoptosis in U937. (bvsalud.org)
- The mechanism of apoptosis in leukemic cells may involve in up-regulating BAX/BCL-2 ratio and expression of protein caspase-3. (bvsalud.org)
- MATERIALS AND METHODS: To examine the levels of apoptosis, HT-29 cells were treated with As2O3 and then we measured the percentage of Annexin V binding cells, the amount of ROS production and the mitochondrial membrane potential. (bvsalud.org)
- In the death-inducing signaling complex, the C-terminal zinc finger (Znf) domain of the A20 ubiquitin ligase mediates receptor-interacting protein 1 polyubiquitination through lysine-63-linked polyubiquitin chains, which bind to the caspase-8 protease domain and inhibit caspase-8 dimerization, cleavage, and the initiation of TRAIL-induced apoptosis in glioblastoma-derived cell lines and tumor-initiating cells. (aacrjournals.org)
- VPA induced apoptosis via the extrinsic pathway involving engagement of the caspase-8-dependent cascade. (uliege.be)
- Conclusion: Our findings uncover a novel mechanism of TRAIL resistance mediated by DARPP-32, whereby it inhibits the intrinsic apoptosis pathway through upregulation of BCL-xL, and the extrinsic apoptosis pathway through the NF-κB/FLIP(S) axis. (elsevier.com)
- this cleavage was prevented by DARPP-32, thus maintaining NF-κB activity and the expression of its target, FLIP(S) protein. (elsevier.com)
- CASP8 activates apoptotic signal through another mechanism involving BID cleavage to truncated BID (tBID). (wikipathways.org)
- In the death-inducing signaling complex, caspase-8 is cleaved and then initiates apoptosis through cleavage of downstream caspase-3 ( 15 ). (aacrjournals.org)
- The canonical cleavage and processing of proIL-1β into mature IL-1β cytokine (17 kDa) are catalyzed by caspase-1, a pathway regulated by multiprotein inflammasome signaling complexes. (jimmunol.org)
- We show that A20-mediated ubiquitination inhibits caspase-8 cleavage and TRAIL-induced apoptosis in glioblastoma through 2 signaling complexes. (aacrjournals.org)
- This protein binds to several members of TNF receptor superfamily including TNFRSF10A/TRAILR1, TNFRSF10B/TRAILR2, TNFRSF10C/TRAILR3, TNFRSF10D/TRAILR4, and possibly also to TNFRSF11B/OPG. (nih.gov)
- TNF-R1 and TNF-R2 binds membrane-integrated TNF (memTNF) as well as soluble TNF (sTNF) TNF-R1 contains a protein-protein interaction domain, called death domain (DD). (wikipathways.org)
- We have isolated a death domain mutant, termed FasΔ, that selectively binds Daxx but not FADD. (pnas.org)
- An adapter protein, termed FADD or Mort1, binds to the Fas death domain and recruits pro-caspase-8, the zymogen form of an apical cell death protease ( 11 - 12 ). (pnas.org)
- The role of DARPP-32 in regulating TRAIL-dependent apoptosis was evaluated by clonogenic survival assay, Annexin V staining, immunofluorescence, quantitative reverse transcriptase PCR, Western blot, and luciferase reporter assays. (elsevier.com)
- On one hand, it can serve as a cell survival pathway by suppressing apoptosis, for example, the removal of damaged organelles that are a source of genotoxic ROS, or by catabolizing cellular macromolecules to provide a source of nutrients and energy for the starved cell, or by limiting ER stress through the degradation of unfolded protein aggregates. (cusabio.com)
- Exhibits kinase activity-dependent functions that trigger cell death and kinase-independent scaffold functions regulating inflammatory signaling and cell survival (PubMed:11101870, PubMed:25459879). (icr.ac.uk)
- Although both splice variants regulate death receptor (DR)-induced apoptosis by CASP8, the specific role of each isoform is poorly understood. (pnas.org)
- A single nucleotide polymorphism determines protein isoform production of the human c-FLIP protein. (cdc.gov)
- Three different isoforms have been described on the protein level, including the long form c-FLIP(L) as well as 2 short forms, c-FLIP(S) and the recently identified c-FLIP(R). The mechanisms controlling c-FLIP isoform production are largely unknown. (cdc.gov)
- Isoform 7 can enhance NF-kappaB activity but promotes only slight apoptosis. (genecards.org)
- We report that curcumin acts on STAT-3 signal pathway to reduce cell viability and increase apoptosis evaluated by the the amount of activated caspase 3. (bvsalud.org)
- Finally the negative effect of cucumin on cell viability has been impaired in STAT-3i HC11, where STAT-3 protein was greatly reduced by shRNA-interference. (bvsalud.org)
- Microbial infection) Interacts with human herpes simplex virus 1 (HHV-1) protein US11 in an RNA-dependent manner (PubMed:11836380). (rcsb.org)
- Interacts with vaccinia protein E3 (PubMed:25740987). (rcsb.org)
- Microbial infection) Interacts with vaccinia protein E3. (rcsb.org)
- Microbial infection) Interacts with Murid herpesvirus 1 protein RIR1. (rcsb.org)
- Although E8-expressing thymocytes were resistant to Fas-mediated apoptosis, the total number of thymocytes in 4-8-week-old E8 transgenic mice was more than 3-fold less than that in control littermates. (nih.gov)
- Human malignant melanoma cell line UACC903 is resistant to apoptosis while chromosome 6-mediated suppressed cell line UACC903(+6) is sensitive. (pubmedcentralcanada.ca)
- Apoptosis repressor that blocks multiple modes of cell death. (uniprot.org)
- The N-terminal FADD -like death effector domain of this protein suggests that it may interact with Fas-interacting protein FADD. (wikipedia.org)
- Apoptosis induced by the death-inducing ligand FasL (CD95L) is a major mechanism of cell death. (semanticscholar.org)
- Autophagy, also known as type II programmed cell death, a process in which denovo-formed membrane-enclosed vesicles engulf and consume cellular components, has been shown to engage in a complex interplay with apoptosis. (cusabio.com)
- On another hand, it can lead to death itself, either in collaboration with apoptosis or as a back-up mechanism when the former is defective. (cusabio.com)
- the third one is that autophagy acts as enabler of apoptosis, participating in certain morphologic and cellular events that occur during apoptotic cell death, without leading to death in itself . (cusabio.com)
- In this case, both autophagy and apoptosis are regulated to promote cell death. (cusabio.com)
- Fas is a cell surface death receptor that regulates peripheral tolerance and lymphoid homeostasis. (pnas.org)
- Here we show that FADD, which couples Fas to pro-caspase-8, and, Daxx, which couples Fas to the Jun N-terminal kinase pathway, bind independently to the Fas death domain. (pnas.org)
- The cytoplasmic domain of Fas has no enzymatic activity but contains a protein-interaction motif termed the "death domain. (pnas.org)
- JNK has been previously implicated in activating apoptosis in vitro and in vivo ( 24 , 25 ), but its functional role in death-receptor signaling, as assayed by expressing dominant negative proteins, has been controversial ( 21 , 26 - 29 ). (pnas.org)
- The pore-forming protein gasdermin D (GSDMD) was recently identified as the principal executioner of pyroptosis ("fiery death"), a type of proinflammatory programmed cell death driven by inflammasomes. (pnas.org)
- One such protein is HSP27, a 27kDa protein that prevents cell death induced by many pro-apoptotic agents. (bvsalud.org)
- A20 is highly expressed in glioblastomas and, together with the death receptor 5 and receptor-interacting protein 1, forms a plasma membrane-bound preligand assembly complex under physiologic conditions. (aacrjournals.org)