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.
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.
Endogenous and exogenous compounds and that either inhibit CASPASES or prevent their activation.
A long pro-domain caspase that contains a death effector domain in its pro-domain region. Caspase 8 plays a role in APOPTOSIS by cleaving and activating EFFECTOR CASPASES. Activation of this enzyme can occur via the interaction of its N-terminal death effector domain with DEATH DOMAIN RECEPTOR SIGNALING ADAPTOR PROTEINS.
A 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.
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.
A long pro-domain caspase that has specificity for the precursor form of INTERLEUKIN-1BETA. It plays a role in INFLAMMATION by catalytically converting the inactive forms of CYTOKINES such as interleukin-1beta to their active, secreted form. Caspase 1 is referred as interleukin-1beta converting enzyme and is frequently abbreviated ICE.
A 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.
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.
Inhibitors of SERINE ENDOPEPTIDASES and sulfhydryl group-containing enzymes. They act as alkylating agents and are known to interfere in the translation process.
Exogenous and endogenous compounds which inhibit CYSTEINE ENDOPEPTIDASES.
A long pro-domain caspase that contains a caspase recruitment domain in its pro-domain region. Caspase 12 is activated by pro-apoptotic factors that are released during cell stress and by CARD SIGNALING ADAPTOR PROTEINS. It activates APOPTOSIS by cleaving and activating EFFECTOR CASPASES.
A short pro-domain caspase that is almost exclusively expressed in the EPIDERMIS and may play a role in the differentiation of epidermal KERATINOCYTES.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
A serine endopeptidase that has specificity for cleavage at ARGININE. It cleaves a variety of prohormones including PRO-OPIOMELANOCORTIN, proluteinizing-hormone-releasing hormone, proenkephalins, prodynorphin, and PROINSULIN.
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.
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.
Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)
A tumor necrosis factor receptor subtype found in a variety of tissues and on activated LYMPHOCYTES. It has specificity for FAS LIGAND and plays a role in regulation of peripheral immune responses and APOPTOSIS. Multiple isoforms of the protein exist due to multiple ALTERNATIVE SPLICING. The activated receptor signals via a conserved death domain that associates with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.
A 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)
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.
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.
Passages external to the liver for the conveyance of bile. These include the COMMON BILE DUCT and the common hepatic duct (HEPATIC DUCT, COMMON).
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.
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
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.
A CELL LINE derived from human T-CELL LEUKEMIA and used to determine the mechanism of differential susceptibility to anti-cancer drugs and radiation.
A 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.
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.
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.
A member of the Bcl-2 protein family that reversibly binds MEMBRANES. It is a pro-apoptotic protein that is activated by caspase cleavage.
The book composed of writings generally accepted by Christians as inspired by God and of divine authority. (Webster, 3d ed)
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
A cell line derived from cultured tumor cells.
Persons diagnosed as having significantly lower than average intelligence and considerable problems in adapting to everyday life or lacking independence in regard to activities of daily living.
Peptides composed of between two and twelve amino acids.
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.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Established cell cultures that have the potential to propagate indefinitely.
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.
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.
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.
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.
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.
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.
An indolocarbazole that is a potent PROTEIN KINASE C inhibitor which enhances cAMP-mediated responses in human neuroblastoma cells. (Biochem Biophys Res Commun 1995;214(3):1114-20)
A protein of the annexin family isolated from human PLACENTA and other tissues. It inhibits cytosolic PHOSPHOLIPASE A2, and displays anticoagulant activity.
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.
Transport proteins that carry specific substances in the blood or across cell membranes.
A promyelocytic cell line derived from a patient with ACUTE PROMYELOCYTIC LEUKEMIA. HL-60 cells lack specific markers for LYMPHOID CELLS but express surface receptors for FC FRAGMENTS and COMPLEMENT SYSTEM PROTEINS. They also exhibit phagocytic activity and responsiveness to chemotactic stimuli. (From Hay et al., American Type Culture Collection, 7th ed, pp127-8)
A 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.
Physiologically inactive substances that can be converted to active enzymes.
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.
The class of heavy chains found in IMMUNOGLOBULIN D. They have a molecular weight of approximately 64 kDa and they contain about 500 amino acid residues arranged in four domains and an oligosaccharide component covalently bound to the Fc fragment constant region.
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.
Multimeric protein complexes formed in the CYTOSOL that play a role in the activation of APOPTOSIS. They can occur when MITOCHONDRIA become damaged due to cell stress and release CYTOCHROME C. Cytosolic cytochrome C associates with APOPTOTIC PROTEASE-ACTIVATING FACTOR 1 to form the apoptosomal protein complex. The apoptosome signals apoptosis by binding to and activating specific INITIATOR CASPASES such as CASPASE 9.
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.
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.
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.
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.
A death domain receptor signaling adaptor protein that plays a role in signaling the activation of INITIATOR CASPASES such as CASPASE 2. It contains a death domain that is specific for RIP SERINE-THEONINE KINASES and a caspase-binding domain that binds to and activates CASPASES such as CASPASE 2.
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.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Intracellular signaling adaptor proteins that bind to the cytoplasmic death domain region found on DEATH DOMAIN RECEPTORS. Many of the proteins in this class take part in intracellular signaling from TUMOR NECROSIS FACTOR RECEPTORS.
The relationship between the dose of an administered drug and the response of the organism to the drug.
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.
Derivatives of phosphatidic acids in which the phosphoric acid is bound in ester linkage to a serine moiety. Complete hydrolysis yields 1 mole of glycerol, phosphoric acid and serine and 2 moles of fatty acids.
A family of intracellular signaling adaptor proteins that contain caspase activation and recruitment domains. Proteins that contain this domain play a role in APOPTOSIS-related signal transduction by associating with other CARD domain-containing members and in activating INITIATOR CASPASES that contain CARD domains within their N-terminal pro-domain region.
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.
Cysteine proteinase found in many tissues. Hydrolyzes a variety of endogenous proteins including NEUROPEPTIDES; CYTOSKELETAL PROTEINS; proteins from SMOOTH MUSCLE; CARDIAC MUSCLE; liver; platelets; and erythrocytes. Two subclasses having high and low calcium sensitivity are known. Removes Z-discs and M-lines from myofibrils. Activates phosphorylase kinase and cyclic nucleotide-independent protein kinase. This enzyme was formerly listed as EC
A family of serine endopeptidases found in the SECRETORY GRANULES of LEUKOCYTES such as CYTOTOXIC T-LYMPHOCYTES and NATURAL KILLER CELLS. When secreted into the intercellular space granzymes act to eliminate transformed and virus-infected host cells.
Elements of limited time intervals, contributing to particular results or situations.
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.
Proteins encoded by the mitochondrial genome or proteins encoded by the nuclear genome that are imported to and resident in the MITOCHONDRIA.
Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. A mutant or absent p53 protein has been found in LEUKEMIA; OSTEOSARCOMA; LUNG CANCER; and COLORECTAL CANCER.
A 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.
Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.
Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.
The 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.
Cell surface receptors that bind TUMOR NECROSIS FACTORS and trigger changes which influence the behavior of cells.
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.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
Glycoproteins found on the membrane or surface of cells.
Intracellular fluid from the cytoplasm after removal of ORGANELLES and other insoluble cytoplasmic components.
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.
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.
Phosphoric acid esters of inositol. They include mono- and polyphosphoric acid esters, with the exception of inositol hexaphosphate which is PHYTIC ACID.
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.
A subgroup of mitogen-activated protein kinases that activate TRANSCRIPTION FACTOR AP-1 via the phosphorylation of C-JUN PROTEINS. They are components of intracellular signaling pathways that regulate CELL PROLIFERATION; APOPTOSIS; and CELL DIFFERENTIATION.
A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.
A 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.
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.
A chronic disorder of the pilosebaceous apparatus associated with an increase in sebum secretion. It is characterized by open comedones (blackheads), closed comedones (whiteheads), and pustular nodules. The cause is unknown, but heredity and age are predisposing factors.
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).
Proteins prepared by recombinant DNA technology.
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.
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.
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.
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.
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.
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.
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.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
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.
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.
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.
Mitochondria in hepatocytes. As in all mitochondria, there are an outer membrane and an inner membrane, together creating two separate mitochondrial compartments: the internal matrix space and a much narrower intermembrane space. In the liver mitochondrion, an estimated 67% of the total mitochondrial proteins is located in the matrix. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p343-4)
Melanin-containing organelles found in melanocytes and melanophores.
The action of a drug in promoting or enhancing the effectiveness of another drug.
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.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
A 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.
A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts.
The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).
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)
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.
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.
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.
A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.
Synthetic or naturally occurring substances related to coumarin, the delta-lactone of coumarinic acid.
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.
Any of various enzymatically catalyzed post-translational modifications of PEPTIDES or PROTEINS in the cell of origin. These modifications include carboxylation; HYDROXYLATION; ACETYLATION; PHOSPHORYLATION; METHYLATION; GLYCOSYLATION; ubiquitination; oxidation; proteolysis; and crosslinking and result in changes in molecular weight and electrophoretic motility.
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).
Thin structures that encapsulate subcellular structures or ORGANELLES in EUKARYOTIC CELLS. They include a variety of membranes associated with the CELL NUCLEUS; the MITOCHONDRIA; the GOLGI APPARATUS; the ENDOPLASMIC RETICULUM; LYSOSOMES; PLASTIDS; and VACUOLES.
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.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
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).
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.
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.
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.
Antibiotic substance isolated from streptomycin-producing strains of Streptomyces griseus. It acts by inhibiting elongation during protein synthesis.
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.
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.
Compounds which inhibit or antagonize biosynthesis or actions of proteases (ENDOPEPTIDASES).
A state of insufficient flesh on the body usually defined as having a body weight less than skeletal and physical standards. Depending on age, sex, and genetic background, a BODY MASS INDEX of less than 18.5 is considered as underweight.
Compounds that inhibit cell production of DNA or RNA.
The proportion of patients with a particular disease during a given year per given unit of population.
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.
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.
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.
Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.
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.
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.
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.
A large multisubunit complex that plays an important role in the degradation of most of the cytosolic and nuclear proteins in eukaryotic cells. It contains a 700-kDa catalytic sub-complex and two 700-kDa regulatory sub-complexes. The complex digests ubiquitinated proteins and protein activated via ornithine decarboxylase antizyme.
Techniques or methods of patient care used by nurses as primary careproviders.
The process of cleaving a chemical compound by the addition of a molecule of water.
A fractionated cell extract that maintains a biological function. A subcellular fraction isolated by ultracentrifugation or other separation techniques must first be isolated so that a process can be studied free from all of the complex side reactions that occur in a cell. The cell-free system is therefore widely used in cell biology. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p166)
That portion of the electromagnetic spectrum immediately below the visible range and extending into the x-ray frequencies. The longer wavelengths (near-UV or biotic or vital rays) are necessary for the endogenous synthesis of vitamin D and are also called antirachitic rays; the shorter, ionizing wavelengths (far-UV or abiotic or extravital rays) are viricidal, bactericidal, mutagenic, and carcinogenic and are used as disinfectants.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
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.
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
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.
Preparations of cell constituents or subcellular materials, isolates, or substances.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Various physiological or molecular disturbances that impair ENDOPLASMIC RETICULUM function. It triggers many responses, including UNFOLDED PROTEIN RESPONSE, which may lead to APOPTOSIS; and AUTOPHAGY.
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.
Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.
A light microscopic technique in which only a small spot is illuminated and observed at a time. An image is constructed through point-by-point scanning of the field in this manner. Light sources may be conventional or laser, and fluorescence or transmitted observations are possible.
Adenine nucleotides which contain deoxyribose as the sugar moiety.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.
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.
Nuclear matrix proteins that are structural components of the NUCLEAR LAMINA. They are found in most multicellular organisms.
A genus of small, two-winged flies containing approximately 900 described species. These organisms are the most extensively studied of all genera from the standpoint of genetics and cytology.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
Proteins found in any species of insect.
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.
Coronary artery bypass surgery on a beating HEART without a CARDIOPULMONARY BYPASS (diverting the flow of blood from the heart and lungs through an oxygenator).
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.
Property of membranes and other structures to permit passage of light, heat, gases, liquids, metabolites, and mineral ions.
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.
Proteins found in the nucleus of a cell. Do not confuse with NUCLEOPROTEINS which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus.
An interleukin-1 subtype that is synthesized as an inactive membrane-bound pro-protein. Proteolytic processing of the precursor form by CASPASE 1 results in release of the active form of interleukin-1beta from the membrane.
A lysosomal cysteine proteinase with a specificity similar to that of PAPAIN. The enzyme is present in a variety of tissues and is important in many physiological and pathological processes. In pathology, cathepsin B has been found to be involved in DEMYELINATION; EMPHYSEMA; RHEUMATOID ARTHRITIS, and NEOPLASM INVASIVENESS.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
An antibiotic produced by Pseudomonas cocovenenans. It is an inhibitor of MITOCHONDRIAL ADP, ATP TRANSLOCASES. Specifically, it blocks adenine nucleotide efflux from mitochondria by enhancing membrane binding.
An island in Polynesia, in the south Pacific Ocean. It was discovered in 1767 by Philip Carteret, uninhabited until 1790 when settled by mutineers from the English ship, Bounty. The settlement was discovered in 1808; the population was removed temporarily to Tahiti in 1831 and to Norfolk Island (between New Caledonia and New Zealand) in 1856. Some later returned to Pitcairn and their descendents constitute the present population of this British colony. The island is named for the midshipman who first sighted it from the ship. (From Webster's New Geographical Dictionary, 1988, p958 & Room, Brewer's Dictionary of Names, 1992, p422)
A malignant neoplasm occurring in young children, primarily in the liver, composed of tissue resembling embryonal or fetal hepatic epithelium, or mixed epithelial and mesenchymal tissues. (Stedman, 25th ed)
Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.
The process by which chemical compounds provide protection to cells against harmful agents.
One of the non-essential amino acids commonly occurring in the L-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter.
A tetrameric enzyme that, along with the coenzyme NAD+, catalyzes the interconversion of LACTATE and PYRUVATE. In vertebrates, genes for three different subunits (LDH-A, LDH-B and LDH-C) exist.
A ubiquitously expressed protein kinase that is involved in a variety of cellular SIGNAL PATHWAYS. Its activity is regulated by a variety of signaling protein tyrosine kinase.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in enzyme synthesis.
A subclass of ubiquitously-expressed lamins having an acidic isoelectric point. They are found to remain bound to nuclear membranes during mitosis.
An indole-dione that is obtained by oxidation of indigo blue. It is a MONOAMINE OXIDASE INHIBITOR and high levels have been found in urine of PARKINSONISM patients.
A type I keratin found associated with KERATIN-8 in simple, or predominately single layered, internal epithelia.
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)
A tripeptide with many roles in cells. It conjugates to drugs to make them more soluble for excretion, is a cofactor for some enzymes, is involved in protein disulfide bond rearrangement and reduces peroxides.
A group of acylated oligopeptides produced by Actinomycetes that function as protease inhibitors. They have been known to inhibit to varying degrees trypsin, plasmin, KALLIKREINS, papain and the cathepsins.
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.
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
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.
A c-jun amino-terminal kinase that is activated by environmental stress and pro-inflammatory cytokines. Several isoforms of the protein with molecular sizes of 43 and 48 KD exist due to multiple ALTERNATIVE SPLICING.
A system of cisternae in the CYTOPLASM of many cells. In places the endoplasmic reticulum is continuous with the plasma membrane (CELL MEMBRANE) or outer membrane of the nuclear envelope. If the outer surfaces of the endoplasmic reticulum membranes are coated with ribosomes, the endoplasmic reticulum is said to be rough-surfaced (ENDOPLASMIC RETICULUM, ROUGH); otherwise it is said to be smooth-surfaced (ENDOPLASMIC RETICULUM, SMOOTH). (King & Stansfield, A Dictionary of Genetics, 4th ed)
Agents that emit light after excitation by light. The wave length of the emitted light is usually longer than that of the incident light. Fluorochromes are substances that cause fluorescence in other substances, i.e., dyes used to mark or label other compounds with fluorescent tags.

MycN sensitizes neuroblastoma cells for drug-induced apoptosis. (1/2199)

Amplification of the MYCN gene is found in a large proportion of neuroblastoma and considered as an adverse prognostic factor. To investigate the effect of ectopic MycN expression on the susceptibility of neuroblastoma cells to cytotoxic drugs we used a human neuroblastoma cell line harboring tetracycline-controlled expression of MycN. Neither conditional expression of MycN alone nor low drug concentrations triggered apoptosis. However, when acting in concert, MycN and cytotoxic drugs efficiently induced cell death. Apoptosis depended on mitochondrial permeability transition and activation of caspases, since the mitochondrion-specific inhibitor bongkrekic acid and the caspase inhibitor zVAD-fmk almost completely abrogated apoptosis. Loss of mitochondrial transmembrane potential and release of cytochrome c from mitochondria preceded activation of caspase-8 and caspase-3 and cleavage of PARP. CD95 expression was upregulated by treatment with cytotoxic drugs, while MycN cooperated with cytotoxic drugs to increase sensitivity to CD95-induced apoptosis and enhancing CD95-L expression. MycN overexpression and cytotoxic drugs also synergized to induce p53 and Bax protein expression, while Bcl-2 and Bcl-X(L) protein levels remained unchanged. Since amplification of MYCN is usually associated with a poor prognosis, these findings suggest that dysfunctions in apoptosis pathways may be a mechanism by which MycN-induced apoptosis of neuroblastoma cells is inhibited.  (+info)

Tumor necrosis factor alpha regulation of the FAS-mediated apoptosis-signaling pathway in synovial cells. (2/2199)

OBJECTIVE: Fas-mediated apoptosis is observed in synoviocytes of patients with rheumatoid arthritis (RA), but not in those of patients with osteoarthritis (OA). The present study was conducted to elucidate the mechanisms that initiate induction of Fas-mediated apoptosis in RA synoviocytes. METHODS: Cultured OA synoviocytes, which are insensitive to Fas-mediated apoptosis in spite of Fas antigen expression, were used in these experiments. Synovial cell proliferation and cytotoxicity studies were performed using MTS and lactate dehydrogenase release assays. Surface expression of Fas antigen was analyzed by flow cytometry. The expression and function of apoptosis-signaling molecules, such as caspase 8 and caspase 3, were examined by immunoblot analysis. RESULTS: Tumor necrosis factor alpha (TNFalpha) induced proliferation of cultured OA synoviocytes. Fas ligation with anti-Fas monoclonal antibody (mAb) resulted in cytotoxic activity against cultured OA synoviocytes that had been pretreated with TNFalpha for 5 days, but not those pretreated for 2 days. In contrast, anti-Fas mAb did not show a cytotoxic effect against untreated cultured OA synoviocytes. A gradual up-regulation of caspase 8 and caspase 3, which played a role in the caspase cascade for Fas-mediated apoptosis, was observed in TNFalpha-treated cultured OA synoviocytes. In addition, Fas ligation to TNFalpha-treated cultured OA synoviocytes induced activation of caspase 8 and caspase 3, with subsequent cleavage of poly(ADP-ribose) polymerase (PARP), a substrate of activated caspase 3. More importantly, Z-IETD-FMK, a caspase 8 inhibitor, and Ac-DEVD-CHO, a caspase 3 inhibitor, almost completely inhibited Fas-mediated apoptosis of TNFalpha-treated cultured OA synoviocytes, whereas Ac-YVAD-CHO, a caspase 1 inhibitor, did not. CONCLUSION: Our results clearly demonstrate that TNFalpha stimulates synovial cells to proliferate as well as sensitizes the cells for Fas-mediated apoptosis, at least in part by up-regulation and activation of caspase 8 and caspase 3. These findings suggest that TNFalpha may be one of the factors providing sensitization of synovial cells to Fas-mediated apoptosis in RA.  (+info)

Solution structure of BID, an intracellular amplifier of apoptotic signaling. (3/2199)

We report the solution structure of BID, an intracellular cross-talk agent that can amplify FAS/TNF apoptotic signal through the mitochondria death pathway after Caspase 8 cleavage. BID contains eight alpha helices where two central hydrophobic helices are surrounded by six amphipathic ones. The fold resembles poreforming bacterial toxins and shows similarity to BCL-XL although sequence homology to BCL-XL is limited to the 16-residue BH3 domain. Furthermore, we modeled a complex of BCL-XL and BID by aligning the BID and BAK BH3 motifs in the known BCL-XL-BAK BH3 complex. Additionally, we show that the overall structure of BID is preserved after cleavage by Caspase 8. We propose that BID has both BH3 domain-dependent and -independent modes of action in inducing mitochondrial damage.  (+info)

Solution structure of the proapoptotic molecule BID: a structural basis for apoptotic agonists and antagonists. (4/2199)

Members of the BCL2 family of proteins are key regulators of programmed cell death, acting either as apoptotic agonists or antagonists. Here we describe the solution structure of BID, presenting the structure of a proapoptotic BCL2 family member. An analysis of sequence/structure of BCL2 family members allows us to define a structural superfamily, which has implications for general mechanisms for regulating proapoptotic activity. It appears two criteria must be met for proapoptotic function within the BCL2 family: targeting of molecules to intracellular membranes, and exposure of the BH3 death domain. BID's activity is regulated by a Caspase 8-mediated cleavage event, exposing the BH3 domain and significantly changing the surface charge and hydrophobicity, resulting in a change of cellular localization.  (+info)

Targeted disruption of caspase genes in mice: what they tell us about the functions of individual caspases in apoptosis. (5/2199)

Cysteine proteases of the caspase family are crucial mediators of apoptosis. All mammalian cells contain a large number of caspases. Although many caspases are activated in a cell committed to apoptosis, recent data from caspase gene knockout mice suggest that individual caspases may be involved in the cell and stimulus-specific pathways of cell death. The gene disruption studies also establish the functional hierarchy between two structurally distinct classes of caspases. The present review discusses these recent findings and elaborates on how these mutant mouse models have helped the understanding of the mechanisms that govern programmed cell death in the immune and other systems.  (+info)

Ordering of ceramide formation, caspase activation, and mitochondrial changes during CD95- and DNA damage-induced apoptosis. (6/2199)

To evaluate the role of ceramide (Cer) in apoptosis signaling, we examined Cer formation induced by CD95, etoposide, or gamma-radiation (IR) in relation to caspase activation and mitochondrial changes in Jurkat T cells. The Cer response to all three stimuli was mapped in between caspases sensitive to benzoyloxycarbonyl-VAD-fluoromethylketone (zVAD-fmk) and acetyl-DEVD-aldehyde (DEVD-CHO). Cer production was independent of nuclear fragmentation but associated with the occurrence of other aspects of the apoptotic morphology. Caspase-8 inhibition abrogated Cer formation and apoptosis induced by CD95 but did not affect the response to etoposide or IR, placing CD95-induced Cer formation downstream from caspase-8 and excluding a role for caspase-8 in the DNA damage pathways. CD95 signaling to the mitochondria required caspase-8, whereas cytochrome c release in response to DNA damage was caspase-independent. These results indicate that the caspases required for the Cer response to etoposide and IR reside at or downstream from the mitochondria. Bcl-2 overexpression abrogated the Cer response to etoposide and IR and reduced CD95-induced Cer accumulation. We conclude that the Cer response to DNA damage fully depends on mitochondrion-dependent caspases, whereas the response to CD95 partially relies on these caspases. Our data imply that Cer is not instrumental in the activation of inducer caspases or signaling to the mitochondria. Rather, Cer formation is associated with the execution phase of apoptosis.  (+info)

Caspase-8 is required for cell death induced by expanded polyglutamine repeats. (7/2199)

We show here that caspase-8 is required for the death of primary rat neurons induced by an expanded polyglutamine repeat (Q79). Expression of Q79 recruited and activated caspase-8. Inhibition of caspase-8 blocked polyglutamine-induced cell death. Coexpression of Q79 with the caspase inhibitor CrmA, a dominant-negative mutant of FADD (FADD DN), Bcl-2, or Bcl-xL, but not an N-terminally tagged Bcl-xL, prevented the recruitment of caspase-8 and inhibited polyglutamine-induced cell death. Furthermore, Western blot analysis revealed the presence of activated caspase-8 in the insoluble fraction of affected brain regions from Huntington's disease (HD) patients but not in those from neurologically unremarkable controls, suggesting the relocation and activation of caspase-8 during the pathogenesis of HD. These results suggest an essential role of caspase-8 in HD-related neural degenerative diseases.  (+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. (8/2199)

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)

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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
Active Caspase 3 FITC Staining Kit(Caspase 3FITC染色试剂盒)(ab65613)在活细胞中检测激活型caspase 3,基于流式、显微镜或荧光读板仪。
Active Caspase 2 FITC Staining Kit (ab65612). Active caspase 2 detection in living cells by flow, microscopy or fluorescent plate reader.
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
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 ...
CASP10; MCH4; Caspase-10; CASP-10; Apoptotic protease Mch-4; FAS-associated death domain protein interleukin-1B-converting enzyme 2; FLICE2; ICE-like apoptotic protease ...
RTN3 can recruit Fas-associated death domain (FADD), thus initiating the ER-stress activated apoptosis. It also interacts with the β-secretase and its aggregation is critically associated with Alzheimers disease. Here, we first investigated the solution conformation of hRTN3, subsequently characterized its binding with hFADD. The results reveal: (1) both hRTN3 N- and C-termini are intrinsically unstructured. Nevertheless, the C-terminus contains two short helix-populated regions. (2) The unstructured hRTN3 C-terminus can bind to hFADD as shown by ITC. Further NMR investigation successfully identified the binding involved hRTN3 residues. (3) Although upon hRTN3-binding, the perturbed hFADD residues were distributed over the whole sequence, the majority of the significantly perturbed are over its death effector domain, very different from the previously observed binding mode for FADD. This study also implies a possible linkage between Alzheimers disease and ER-stress activated apoptosis. © ...
SWISS-MODEL Repository entry for Q297U0 (FADD_DROPS), Fas-associated death domain protein. Drosophila pseudoobscura pseudoobscura (Fruit fly)
Yan, Q., McDonald, J. M., Zhou, T. and Song, Y. (2013), Structural insight for the roles of fas death domain binding to fadd and oligomerization degree of the fas-fadd complex in the death-inducing signaling complex formation: A computational study. Proteins, 81: 377-385. doi: 10.1002/prot.24193 ...
Effects of ponicidin on the activity of caspase-3 in MKN28 cells. After treatment, the activity of caspase-3 in MKN28 cells was analyzed by the caspase-3 assay
Caspase-9兔多克隆抗体(ab52298)可与小鼠, 大鼠样本反应并经ELISA, IHC, ICC/IF实验严格验证,被6篇文献引用。所有产品均提供质保服务,中国75%以上现货。
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A bid given to the balancing power market to increase generation or reduce consumption. When the bid is activated, the party carrying out the regulation sells regulating power to Fingrid.. ...
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The death receptor (DR)-mediated apoptosis pathway is thought to be unique to vertebrates. However, the presence of DR-encoding genes in the sea urchin and the basal chordate amphioxus prompted us to reconsider, especially given that amphioxus contains 14 DR proteins and hundreds of death domain (DD)-containing adaptor proteins. To understand how the extrinsic apoptotic pathway was originally established and what the differences in signaling are between invertebrates and vertebrates, we performed functional studies of several genes that encode DDs in the amphioxus Branchiostoma belcheri tsingtauense (Bbt). First, we observed that the increased abundance of Bbt Fas-associated death domain 1 (BbtFADD1) in HeLa cells resulted in the formation of death effector filamentous structures in the cytoplasm and the activation of the nuclear factor κB pathway, whereas BbtFADD2 protein was restricted to the nucleus, although its death effector domain induced apoptosis when in the cytoplasm. We further ...
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 ...
Activation and Inhibition of ApoptosisSeveral mechanisms have been identified in mammalian cells for the induction of apoptosis. These mechanisms include factors that lead to perturbation of the mitochondria leading to leakage of cytochrome c or factors that directly activate members of the death receptor family. Fas is a member of the tumor necrosis factor (TNF) receptor superfamily, a family of transmembrane receptors that include neurotrophin receptor (p75NTR), TNF-R1, and a variety of other cell surface receptors. Fas Ligand (Fas L) transmits signals to Fas on a target cell by inducing trimerization of Fas. Activation of Fas causes the recruitment of Fas-associated protein with death domain (FADD) via interactions between the death domain of Fas and FADD and is followed by pro-caspase-8 binding to FADD via interactions between the death effector domains (DED) of FADD and pro-caspase-8 leading to the activation of caspase-8. Activation of caspase-8 leads to the activation of other
Lapatinib, a HER2/EGFR inhibitor, is the most recently approved targeted therapy for metastatic breast cancer. Based on clinical evidence that lapatinib enhances efficacy of capecitabine in breast cancer patients, we hypothesized that lapatinib could augment the anti-cancer activity of agents in other tumor types such as colon cancer. Using in vitro cell death and apoptosis assays, we found lapatinib to have minimal effect on chemotherapy-induced cytotoxicity in colon cancer cell lines. However, elevated concentrations of lapatinib (5-10μM) significantly enhanced the pro-apoptotic effects of TRAIL and agonistic TRAIL receptor antibodies. In vivo, xenografted colon tumors from mice treated with lapatinib/TRAIL combinations exhibited more immunostaining for cleaved caspase-8, an apical caspase in the extrinsic cell death pathway, compared to tumors from mice treated with lapatinib or TRAIL alone. Furthermore, the combination therapy suppressed tumor growth, whereas single agent treatments had ...
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Caspase detection antibodies and assays are used to help detect and study caspase activation in Apoptotic cells via immunoprecipitation and immunoblotting techniques.
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Antho 50 induces caspase 3 activation and UHRF1 down-regulation independently of p53 and p73.B CLL cells were incubated with Antho 50 at 75 μg/mL for the ind
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Studies of tumour necrosis factor receptor-1 in tumour necrosis factor receptor associated periodic sysndrome (TRAPS): United Kingdom
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 ...
Activation of Fas receptor by Fas ligand causes caspase 8 activation and apoptosis in cells and is an important mechanism by which normal tissue homeostasis and function are maintained. Activation of caspase 8 is preceded by the formation of a death-inducing signalling complex (DISC), and a number of redundant mechanisms regulate DISC formation in vivo. Fas receptor is widely expressed in tissues, and dysfunction of the regulatory mechanisms in Fas receptor signalling has been reported in several diseases including autoimmune disease and cancer. This review aims to identify and discuss the various mechanisms employed by cells to alter their sensitivity to Fas-mediated apoptosis by regulating DISC formation. We also discuss a number of defects identified with Fas receptor signalling and the associated pathologies.
Fingerprint Dive into the research topics of Se-Methyl-L-selenocysteine Induces Apoptosis via Endoplasmic Reticulum Stress and the Death Receptor Pathway in Human Colon Adenocarcinoma COLO 205 Cells. Together they form a unique fingerprint. ...
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; ...
During the maturation process, spermatids must eliminate most of their cytoplasm to become small, highly motile sperm with their characteristic small DNA-packed head and tail for swimming. In fruit flies, caspases contribute to the elimination of the cytoplasm in a process called individualization, which begins in the head and ends with the elimination of the cytoplasmic contents into a waste bag from the tail end. Kaplan et al. identified Scotti (abbreviated soti), in a yeast two-hybrid screen for partners of the adaptor Klhl10, which is part of the E3 ligase complex required for individualization, and confirmed this interaction by coimmunoprecipitation from transfected S2 cells. Spermatids from soti-null mutant flies failed to mature, and immunostaining for active caspase showed that the abundance of activated caspase was abnormally high and that the developing spermatids failed to generate waste bags. In flies double homozygous for soti and cullin3 (cul3) or klhl10, caspase activation ...
Cellular caspase-8 (FLICE)-like inhibitory protein (cFLIP) was originally identified as an inhibitor of death-receptor signalling. However, this Review discusses new data indicating that cFLIP is also required for the survival and proliferation of T cells following T-cell-receptor stimulation. Cellular caspase-8 (FLICE)-like inhibitory protein (cFLIP) was originally identified as an inhibitor of death-receptor signalling through competition with caspase-8 for recruitment to FAS-associated via death domain (FADD). More recently, it has been determined that both cFLIP and caspase-8 are required for the
The IUPHAR/BPS Guide to Pharmacology. Caspase 1 - C14: Caspase. Detailed annotation on the structure, function, physiology, pharmacology and clinical relevance of drug targets.
The IUPHAR/BPS Guide to Pharmacology. Caspase 6 - C14: Caspase. Detailed annotation on the structure, function, physiology, pharmacology and clinical relevance of drug targets.
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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 ...
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Few things can be considered to be more important to a cell than its threshold for apoptotic cell death, which can be modulated up or down, but rarely in both directions, by a single enzyme. Therefore, it came as quite a surprise to find that one enzyme, glycogen synthase kinase-3 (GSK3), has the pe …
BioAssay record AID 306845 submitted by ChEMBL: Induction of apoptosis in U937 cells assessed as caspase 3 cleavage at 3 uM by Western blot.
The intracellular redox position is intently connected to the levels of professional-inflammatory cytokines, IL-1β, IL-23 and TNF-α which are the major factors of inflammatory responses. IFN-γ has also been shown to be linked with swelling although TNF-α has been researched thoroughly for its function in the inflammatory method and generation of ROS.Maintaining the earlier mentioned information into thought, we evaluated the level of IL-1β and IL-seventeen employing ELISA even though IFN-γ, IL-23 and TNF-α mRNA expression fold transform was identified utilizing qRT-PCR. We located that IL-1β ranges had been considerably larger in the two diabetic teams as in MEDChem Express 415903-37-6 contrast to the wholesome handle topics. The IL-1β is typically expressed by in-filtering macrophages, once activated they synthesize larger volume of nitric oxide as well. Curiously, there have been outstanding discrepancies in both NO and cytokine levels in the patients of higher age teams with glucose ...
Explore EarlyTox Caspase-3/7 NucView 488 Assay Kits that enables detection of apoptosis within intact cell populations through the use of NucView 488 Caspase-3 substrate.
Caspase-7 is a member of the caspase (cysteine aspartate protease) family of proteins, and has been shown to be an executioner protein of apoptosis. Sequential activation
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Scientists at the NYU Langone Medical Center and the Laura and Isaac Perlmutter Cancer Center are researching a form of cancer treatment called necroptosis.
The Loss of Functional Caspase-12 in Europe Is a Pre-Neolithic Event. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Biological Description: Necrostatin 2 is a potent necroptosis inhibitor with EC50 of 50 nM.IC50 Value: 50 nM (EC50) [1]Target: TNF-alphaNecrostatin 2 is a potent in vitro necroptosis inhibitors (exemplified by 1, EC50-0.05 uM) that also were efficacious in an animal model of ...
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Sequential activation of caspases plays a central role in the execution-phase of cell apoptosis. Caspases exist as inactive ... Cowling V, Downward J (October 2002). "Caspase-6 is the direct activator of caspase-8 in the cytochrome c-induced apoptosis ... "Entrez Gene: CASP8 caspase 8, apoptosis-related cysteine peptidase".. *^ a b c Chun HJ, Zheng L, Ahmad M, Wang J, Speirs CK, ... Caspase 3. Pro-apoptotic:. BAX. BAK1/Bcl-2 homologous antagonist killer. Bcl-2-associated death promoter. Anti-apoptotic:. Bcl- ...
Fas and Fas-ligand interact to trigger the caspase cascade, leading to cell apoptosis. Patients with ALPS have a defect in this ... CEDS: Caspase 8 deficiency state. No longer considered a subtype of ALPS but distinct disorder ... 129 (4): 534-8. doi:10.1111/j.1365-2141.2005.05496.x. PMID 15877736.. [unreliable medical source?] ... 105 (6): 2443-8. doi:10.1182/blood-2004-09-3542. PMID 15542578.. [unreliable medical source?] ...
... caspase-11 or caspase-5 in humans, which is responsible for some of the effects that had been attributed to caspase-1, ... The 2011 paper showed that mice lacking the gene that encodes caspase-1 also carry a mutation in a neighboring caspase gene, ... Dixit was among the first scientists to demonstrate that other immune caspases besides death caspases are incorporated into the ... In particular, caspase-1 activates cytokines of the interleukin-1 family, which are immune effectors that initiate an immune ...
Caspase-independent apoptosis[edit]. The characterization of the caspases allowed the development of caspase inhibitors, which ... Caspases. Caspases play the central role in the transduction of ER apoptotic signals. Caspases are proteins that are highly ... The apoptosome cleaves the pro-caspase to its active form of caspase-9, which in turn cleaves and activates pro-caspase into ... There are two types of caspases: initiator caspases, caspase 2,8,9,10,11,12, and effector caspases, caspase 3,6,7. The ...
... has been shown to interact with Caspase 8. GRCh38: Ensembl release 89: ENSG00000114446 - Ensembl, May 2017 GRCm38: ... "Recruitment and activation of caspase-8 by the Huntingtin-interacting protein Hip-1 and a novel partner Hippi". Nat. Cell Biol ... "Recruitment and activation of caspase-8 by the Huntingtin-interacting protein Hip-1 and a novel partner Hippi". Nat. Cell Biol ... "Interaction of HIPPI with putative promoter sequence of caspase-1 in vitro and in vivo". Biochem. Biophys. Res. Commun. 353 (1 ...
Caspase-3, caspase-8, and caspase-9 have been reported to be modified by O-GlcNAc. Caspase-8 is modified near its cleavage/ ... Hyper-O-GlcNAcylation in PDAC cells appeared to be anti-apoptotic, inhibiting cleavage and activation of caspase-3 and caspase- ... deoxy-GlcNAc Reveals O-GlcNAc Modification of the Apoptotic Caspases That Can Block the Cleavage/Activation of Caspase-8". ... GlcNAc with 5S-GlcNAc accelerated caspase activation while pharmacological raising of O-GlcNAc with thiamet-G inhibited caspase ...
... binds to the death receptors DR4 (TRAIL-RI) and DR5 (TRAIL-RII). The process of apoptosis is caspase-8-dependent. Caspase ... doi:10.1016/1074-7613(95)90057-8. PMID 8777713.. *^ Pitti RM, Marsters SA, Ruppert S, Donahue CJ, Moore A, Ashkenazi A (May ... However, as of 2013, these have not shown significant survival benefit.[8] TRAIL has also been implicated as a pathogenic or ... "Differential cleavage of Mst1 by caspase-7/-3 is responsible for TRAIL-induced activation of the MAPK superfamily". Cellular ...
... initiating the caspase cascade. The activated caspases can go on to cleave intracellular proteins such as inhibitor of caspase- ... "Death receptor recruitment of endogenous caspase-10 and apoptosis initiation in the absence of caspase-8". Journal of ... Since activation of caspase 8 requires FADD in order to bring the procaspase 8 molecules into close proximity to one another to ... Caspase 8 then cleaves RIPK1, leading to inhibition of this signalling, inhibiting cell death. FADD knockout in mouse embryos ...
"The marine lipopeptide somocystinamide A triggers apoptosis via caspase 8". Proceedings of the National Academy of Sciences. ...
Hu WH, Johnson H, Shu HB (April 2000). "Activation of NF-kappaB by FADD, Casper, and caspase-8". J. Biol. Chem. 275 (15): 10838 ... In 2000, he and his colleagues showed that FADD, Casper (caspase-8-related protein), and caspase-8 play important roles in NF- ... They also cloned and identified a novel AIF-homologous molecule called AMID, which can lead the way to caspase-independent ... induces caspase-independent apoptosis". J. Biol. Chem. 277 (28): 25617-23. doi:10.1074/jbc.M202285200. PMID 11980907. Xu LG, ...
... caspase 1 and caspase 8). In comparison to their mammalian counterparts, viral serpins contain significant deletions of ... 16 (6): 761-8. doi:10.1016/j.sbi.2006.10.005. PMID 17079131. Law RH, Zhang Q, McGowan S, Buckle AM, Silverman GA, Wong W, ... 31 (8): 427-35. doi:10.1016/j.tibs.2006.06.005. PMID 16820297. Jin L, Abrahams JP, Skinner R, Petitou M, Pike RN, Carrell RW ( ... 92 (8): 2696-706. doi:10.1182/blood.V92.8.2696. PMID 9763552. Gooptu B, Hazes B, Chang WS, Dafforn TR, Carrell RW, Read RJ, ...
Initiator caspases: responsible for the activation of effector caspases. These caspases are activated through oligomerization ... FLIPL's pseudo-caspase has two tandem DEDs that are very similar to the N-terminus of capase-8, but in which there is an ... Studying caspases is important since they don't only control apoptosis but also inhibit it, depending on the necessity of the ... This type of apoptosis depends on the pDED of the HIP-1, and it consists in the activation of caspase-3, an enzyme that is ...
... the activation of caspase-9, caspase-3 and the decrease of Bcl-2. Those phenomena indicate the role of mitochondrial in the ... This can stimulate the apoptosis by activating downstream caspase-3 or by cleaving Bid. As a result, the cleavage of Bid (tBid ... Furthermore, the increase in caspase-8 activation is also observed. ... 148 (2): 203-8. doi:10.1007/s12011-012-9364-2. PMID 22367705. S2CID 16035022. Li GQ, Chen XG, Wu XP, Xie JD, Liang YJ, Zhao XQ ...
Wang M, Qanungo S, Crow MT, Watanabe M, Nieminen AL (2005). "Apoptosis repressor with caspase recruitment domain (ARC) is ... NOL3 has been shown to interact with SFRS9 and Caspase 8. GRCh38: Ensembl release 89: ENSG00000140939 - Ensembl, May 2017 ... Ekhterae D, Platoshyn O, Zhang S, Remillard CV, Yuan JX (2003). "Apoptosis repressor with caspase domain inhibits cardiomyocyte ... "Apoptosis repressor with caspase recruitment domain is required for cardioprotection in response to biomechanical and ischemic ...
A latest study indicated that ECP caused cytotoxicity in HL-60 and HeLa cells via caspase-3 like activity. Accordingly, ... ECP triggers apoptosis by caspase-8 activation through mitochondria-independent pathway. Increases in chromatin condensation, ... 8 (12): 1778-95. doi:10.1111/j.1600-0854.2007.00650.x. PMID 17944807. Chang KC, Lo CW, Fan TC, Chang MD, Shu CW, Chang CH, ... 267 (3): 391-5. doi:10.1007/s00405-009-1103-8. PMID 19760211. Yuksel H, Yilmaz O, Sogut A, et al. (2009). "Correlation of ...
The caspase-independence of necroptosis allows the cell to bypass caspase activation, decreasing the time during which the ... in a caspase-independent fashion in the presence of viral caspase inhibitors to restrict virus replication. In addition to ... Conversely, caspase 8 inhibition of necroptosis can be bypassed by the necroptotic machinery through the anti-apoptotic protein ... The best characterized example of this co-regulation is the ability of caspase 8 to inhibit the formation of the necrosome by ...
"RIPK1 blocks early postnatal lethality mediated by caspase-8 and RIPK3". Cell. 157 (5): 1189-202. doi:10.1016/j.cell.2014.04. ...
"AID and Caspase 8 Shape the Germinal Center Response through Apoptosis". The Journal of Immunology. 191 (12): 5840-5847. doi: ...
On the other hand, activated caspases cleave several components of the NF-κB pathway, including RIP, IKK, and the subunits of ... Nevertheless, TRADD binds FADD, which then recruits the cysteine protease caspase-8. A high concentration of caspase-8 induces ... 8: 1675. doi:10.3389/fimmu.2017.01675. PMC 5712345. PMID 29234328. Rolski F, Błyszczuk P (2015). "TNF and its receptors in the ... 66 (8): 1403-8. doi:10.1016/S0006-2952(03)00490-8. PMID 14555214. Ghada A. Abd El Latif, Tumor necrosis factor alpha and ...
Chaudhary PM, Eby MT, Jasmin A, Kumar A, Liu L, Hood L (2000). "Activation of the NF-kappaB pathway by caspase 8 and its ... 13 (1): 13-8. PMID 11801527. Castellino AM, Parker GJ, Boronenkov IV, Anderson RA, Chao MV (1997). "A novel interaction between ... 22 (8): 2536-43. doi:10.1128/MCB.22.8.2536-2543.2002. PMC 133739. PMID 11909948. Gajate C, Mollinedo F (2005). "Cytoskeleton- ... 57 (2-3): 117-8. doi:10.1159/000133127. PMID 1655358. Schall TJ, Lewis M, Koller KJ, Lee A, Rice GC, Wong GH, Gatanaga T, ...
Chaudhary PM, Eby MT, Jasmin A, Kumar A, Liu L, Hood L (2000). "Activation of the NF-kappaB pathway by caspase 8 and its ... 19 (3): 2180-8. doi:10.1128/MCB.19.3.2180. PMC 84010. PMID 10022904. Lin X, Cunningham ET, Mu Y, Geleziunas R, Greene WC (1999 ... doi:10.1016/S1074-7613(00)80027-8. PMID 10072079. Ninomiya-Tsuji J, Kishimoto K, Hiyama A, Inoue J, Cao Z, Matsumoto K (1999 ...
Chaudhary PM, Eby MT, Jasmin A, Kumar A, Liu L, Hood L (September 2000). "Activation of the NF-kappaB pathway by caspase 8 and ... 278 (52): 52914-8. doi:10.1074/jbc.C300407200. PMID 14578343. Machida N, Umikawa M, Takei K, Sakima N, Myagmar BE, Taira K, ... 12 (8): 622-31. doi:10.1016/S0960-9822(02)00764-9. PMID 11967148. S2CID 9977605. Fong A, Zhang M, Neely J, Sun SC (October 2002 ... 8 (2): e57903. doi:10.1371/journal.pone.0057903. PMC 3585282. PMID 23469100. Roth Flach RJ, Skoura A, Matevossian A, Danai LV, ...
Chaudhary PM, Eby MT, Jasmin A, Kumar A, Liu L, Hood L (September 2000). "Activation of the NF-kappaB pathway by caspase 8 and ...
Alcivar A, Hu S, Tang J, Yang X (Jan 2003). "DEDD and DEDD2 associate with caspase-8/10 and signal cell death". Oncogene. 22 (2 ... Alcivar A, Hu S, Tang J, Yang X (2003). "DEDD and DEDD2 associate with caspase-8/10 and signal cell death". Oncogene. 22 (2): ... Schickling O, Stegh AH, Byrd J, Peter ME (2002). "Nuclear localization of DEDD leads to caspase-6 activation through its death ... DEDD has been shown to interact with: CFLAR, Caspase 8, and FADD. GRCh38: Ensembl release 89: ENSG00000158796 - Ensembl, May ...
The activation of caspase 3 and 9 by the apoptosome starts a proteolitic cascade that eventually leads to the degradation of ... Chaudhary PM, Eby MT, Jasmin A, Kumar A, Liu L, Hood L (September 2000). "Activation of the NF-kappaB pathway by caspase 8 and ... Lin Y, Devin A, Rodriguez Y, Liu ZG (October 1999). "Cleavage of the death domain kinase RIP by caspase-8 prompts TNF-induced ... FLIP then binds to caspase-8, forming a caspase-8 FLIP heterodimer in the cytosol that disrupts the activity of caspase-8 and ...
gp120 induces mitochondrial-death proteins like caspases which may influence the upregulation of the death receptor Fas leading ... "Tubular cell HIV-1 gp120 expression induces caspase 8 activation and apoptosis". Ren Fail. 31 (4): 303-12. doi:10.1080/ ... "Tubular Cell HIV-1 gp120 Expression Induces Caspase 8 Activation and Apoptosis". Renal Failure. 31 (4): 303-312. doi:10.1080/ ... and it is also known to activate STAT1 and induce interleukins IL-6 and IL-8 secretion in neuronal cells. HIV envelope gene HIV ...
Genetic abnormalities frequently occur in a tumor-suppressor gene called caspase 8. Inactivation of this gene will result in ...
Xkr8 was activated directly by caspases and required a caspase-3 cleavage site for its function. CED-8, the only Caenorhabditis ... Chen, Yu-Zen; Mapes, James; Lee, Eui-Seung; Skeen-Gaar, Riley Robert; Xue, Ding (2013-01-01). "Caspase-mediated activation of ... Thus, there is a link between caspase activation and PS externalization, which triggers phagocytosis of apoptotic cells. Ho, ... is a substrate of the CED-3 caspase. Cleavage of CED-8 by CED-3 activates its proapoptotic function and generates a carboxyl- ...
A follow-up study researched to determine if the caspases were involved in the apoptosis seen in the previous study as well as ... The study confirmed that there was cleavage of caspase-3, -8, and -9. All three of these cysteine proteases play an important ... 8 (3): 343-52. PMID 9056677. Archived from the original on 2014-04-26. Thyrell L, Erickson S, Zhivotovsky B, et al. (February ... 21 (8): 1251-62. doi:10.1038/sj.onc.1205179. PMID 11850845. Peginterferon alfa-2b in the U.S. National Library of Medicine's ...
... of the presenilin 1/beta-catenin interaction and preservation of the heterodimeric presenilin 1 complex following caspase ... 2 (8). doi:10.1101/cshperspect.a006239. PMC 3405821. PMID 22908189.. *^ Su DM, Zhang Q, Wang X, He P, Zhu YJ, Zhao J, Rennert ... doi:10.1016/S0896-6273(01)00512-8. PMID 11719200.. *^ Buxbaum JD, Choi EK, Luo Y, Lilliehook C, Crowley AC, Merriam DE, Wasco W ... 279 (24): 25333-8. doi:10.1074/jbc.M312710200. PMID 15087467.. *^ Phiel CJ, Wilson CA, Lee VM, Klein PS (May 2003). "GSK-3alpha ...
CASP16P: encoding protein Caspase 16, pseudogene. *CCDC113: encoding protein Coiled-coil domain-containing protein 113 ...
... condensed apoptotic nuclei and a 2-4 fold increase in cortical precursors that stained immunopositive for cleaved caspase-3.[30 ... Brain-derived neurotrophic factor (BDNF), or abrineurin,[5] is a protein[6] that, in humans, is encoded by the BDNF gene.[7][8] ... 11 (8): 1169-80. doi:10.1017/S1461145708009309. PMID 18752720.. *^ Xiu MH, Hui L, Dang YF, Hou TD, Zhang CX, Zheng YL, Chen DC ... 8: 170. doi:10.3389/fncel.2014.00170. PMC 4064707. PMID 24999318.. *^ Heinonen I, Kalliokoski KK, Hannukainen JC, Duncker DJ, ...
... the Smac mimetic promotes formation of a RIPK1-dependent caspase-8-activating complex, leading to apoptosis. Recent studies ... 8 (3): 197-204. doi:10.1007/s10456-005-9010-0. PMID 16328160. Mercurio, Arthur M; Bachelder, Robin E; Bates, Richard C; Chung, ... STAT3 and RANTES contribute to the maintenance of drug resistance by upregulating anti-apoptotic signals and inhibiting caspase ...
The resulting deconstruction of cellular components is primarily carried out by specialized proteases known as caspases, but ... 278 (1): 311-8. doi:10.1074/jbc.M206279200. PMID 12401807.. *^ a b c Gille C, Goede A, Schlöetelburg C, Preissner R, Kloetzel ... 4 (8): 1015-8. doi:10.4161/cc.4.8.1900. PMID 16082197.. *^ a b Shringarpure R, Grune T, Mehlhase J, Davies KJ (January 2003). " ... 7 (8): 742-9. doi:10.1038/ncb0805-742. PMID 16056265.. *^ Sadanandom A, Bailey M, Ewan R, Lee J, Nelis S (October 2012). "The ...
HR has some similarities to animal pyroptosis, such as a requirement of caspase-1-like proteolytic activity of VPEγ, a cysteine ... November 2004). "VPEgamma exhibits a caspase-like activity that contributes to defense against pathogens". Current Biology. 14 ... When the cytoplasmic receptors MDA5 and RIG-I recognize a virus the conformation between the caspase-recruitment domain (CARD) ... 8 (4): 652-8. PMID 8152260.. *^ Klingemann HG (2010). "Development and testing of NK cell lines". In Lotze MT, Thompson AW (eds ...
Nevertheless, TRADD binds FADD, which then recruits the cysteine protease caspase-8. A high concentration of caspase-8 induces ... On the other hand, activated caspases cleave several components of the NF-κB pathway, including RIP, IKK, and the subunits of ... 17 (8): 884-886. doi:10.1096/fj.02-0670fje.. *^ Pedersen BK (December 2009). "The diseasome of physical inactivity - and the ... 60 (14): 756-8. doi:10.1007/BF01716573. PMID 6181289.. *^ Pennica D, Nedwin GE, Hayflick JS, Seeburg PH, Derynck R, Palladino ...
"Critical loss of CBP/p300 histone acetylase activity by caspase-6 during neurodegeneration". primary. The EMBO Journal. 22 (24 ... 82 (8): 850-2. doi:10.1136/jnnp.2009.200253. PMID 20551479.. *^ a b Swoboda KJ, Scott CB, Crawford TO, Simard LR, Reyna SP, ... 12 (8): 1261-8. doi:10.1002/pmic.201200010. PMID 22577027.. *^ Gräff J, Rei D, Guan JS, Wang WY, Seo J, Hennig KM, Nieland TJ, ... 19 (8): 1492-506. doi:10.1093/hmg/ddq023. PMID 20097677.. *^ Dewey CM, Cenik B, Sephton CF, Johnson BA, Herz J, Yu G (June 2012 ...
... to upregulate the activity of caspase-8. This causes cross talking of apoptotic signaling between caspase-8 and caspase-9 ... 39 (7-8): 1489-1499. doi:10.1016/j.biocel.2007.01.022. Quach, H; Ritchie, D; Stewart, A K; Neeson, P; Harrison, S; Smyth, M J; ... 79: 114-8. doi:10.1038/sj.bjc.6690020. PMC 2362163 . PMID 10408702. Bartlett, J. Blake; Dredge, Keith; Dalgleish, Angus G. (1 ... 87 (3): 503-8. doi:10.1111/j.1365-2141.1994.tb08304.x. PMID 7527645. Schafer, Peter (1 June 2012). "Apremilast mechanism of ...
... condensed apoptotic nuclei and a 2-4 fold increase in cortical precursors that stained immunopositive for cleaved caspase-3.[27 ... 11 (8): 1169-80. doi:10.1017/S1461145708009309. PMID 18752720.. *^ Xiu MH, Hui L, Dang YF, Hou TD, Zhang CX, Zheng YL, Chen DC ... 8: 170. doi:10.3389/fncel.2014.00170. PMC 4064707. PMID 24999318.. *^ Heinonen I, Kalliokoski KK, Hannukainen JC, Duncker DJ, ... 75 (8): e794-801. doi:10.4088/JCP.13m08772. PMID 25191916.. *^ Ray MT, Shannon Weickert C, Webster MJ (May 2014). "Decreased ...
Caspase 9 can then go on to activate caspase 3 and caspase 7, which are responsible for destroying the cell from within. ... Caspase 3. Pro-apoptotic:. BAX. BAK1/Bcl-2 homologous antagonist killer. Bcl-2-associated death promoter. Anti-apoptotic:. Bcl- ... Apoptosis & Caspase 3 - PMAP The Proteolysis Map-animation. *UMich Orientation of Proteins in Membranes families/superfamily-78 ... This release of cytochrome c in turn activates caspase 9, a cysteine protease. ...
Angiotensinogen · Caspase · F12 · Kimotripsinogen · Pepsinogen · Proelastase · Prokarboksipolipeptidase · Prolipase · ... 3 HSD · .4 · .5 · .6 · .7 · .8 · .9 · .10 · .11 · .12 · .13 · .14 · .15 · .16 · .17 · .18 · .19 · .20 · .21 · .22 · .23 · .24 · ... 1 PA · .2 · .3 · .4 · .5 · .6 · .7 · .8 · .9 · .10 · .11 · .12 · .13 · .14 · .15 · .16 · .17 · .18 · .19 · .20 · .21 · .22 α- ... 1 Rsk · .2 PDK · .3 · .4 · .5 · .6 · .7 · .8 · .9 · .10 · .11 · .12 · .13 · .14 · .15 · .16 · DAPK · .18 · .19 · .20 · .21 · . ...
This protein was reported to be specifically cleaved by CASP3-like caspases, which thus leads to a dramatic activation of CDK2 ... and may be instrumental in the execution of apoptosis following caspase activation. However p21 may inhibit apoptosis and does ... 8: 14728. doi:10.1038/ncomms14728. PMID 28317845.. *^ Yu, Z.-K.; Gervais, J. L. M.; Zhang, H. (1998). "Human CUL-1 associates ... 437 (7062): 1173-8. doi:10.1038/nature04209. PMID 16189514.. *^ Frouin I, Maga G, Denegri M, Riva F, Savio M, Spadari S, ...
"Crocetin prevents retinal degeneration induced by oxidative and endoplasmic reticulum stresses via inhibition of caspase ... 2E,4E,6E,8E,10E,12E,14E)-2,6,11,15-Tetramethylhexadeca-2,4,6,8,10,12,14-heptaenedioic acid[2] ... InChI=1S/C20H24O4/c1-15(11-7-13-17(3)19(21)22)9-5-6-10-16(2)12-8-14-18(4)20(23)24/h5-14H,1-4H3,(H,21,22)(H,23,24)/b6-5+,11-7+, ... InChI=1/C20H24O4/c1-15(11-7-13-17(3)19(21)22)9-5-6-10-16(2)12-8-14-18(4)20(23)24/h5-14H,1-4H3,(H,21,22)(H,23,24)/b6-5+,11-7+,12 ...
"A novel form of DAP5 protein accumulates in apoptotic cells as a result of caspase cleavage and internal ribosome entry site- ... 273 (48): 31901-8. doi:10.1074/jbc.273.48.31901. PMID 9822659.. *^ Harris TE, Chi A, Shabanowitz J, Hunt DF, Rhoads RE, ... 273 (48): 31901-8. doi:10.1074/jbc.273.48.31901. PMID 9822659.. *. Ensinger C, Obrist P, Mikuz G, Merkx G, Smeets D, Bänziger R ...
Non obstante, a TRADD únese a FADD, o cal despois recruta a cisteína protease caspase-8. Unha alta concentración de caspase-8 ... Por outra parte, as caspases activadas clivan varios compoñentes da vía NF-κB, incluíndo a RIP, IKK, e as propias subunidades ... Wochenschr. 60 (14): 756-8. PMID 6181289. doi:10.1007/BF01716573.. *↑ Pennica D, Nedwin GE, Hayflick JS, Seeburg PH, Derynck R ... doi:10.1016/S0006-2952(03)00490-8.. *↑ Selwood T, Jaffe EK (2011). "Dynamic dissociating homo-oligomers and the control of ...
Excess progenitor cell proliferation that leads to gross brain abnormalities is often lethal, as seen in caspase-3 or caspase-9 ... Kuida, K (1998). "Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9". Cell. 94: 325-337 ... to cells (such as feedback from neighbors, stress or DNA damage), mitochondria release caspase activators that trigger the cell ... Kroemer G, Martin SJ (2005). "Caspase-independent cell death". Nature Medicine. 11 (7): 725-30. doi:10.1038/nm1263. PMID ...
Martinon F, Burns K, Tschopp J (2002). "The inflammasome: a molecular platform triggering activation of inflammatory caspases ... 8] 이 덕분에 망막 조직은 면역 특권 지역으로서 유지될 수 있다. 망막에서 다른 신체 부위처럼 면역 반응이 활성하면 망막 작용에 부정적인 영향이 크기 때문인데, [9] [10] [11] 이를 망막색소상피 세포가 외부 흐름을 ... "DICER1/Alu RNA dysmetabolism induces Caspase-8-mediated cell death in age-related macular degeneration". 》PNAS》 111 (45): 16082 ... Brian M. Kevany and Krzysztof Palczewski, Phagocytosis of Retinal Rod and Cone Photoreceptors, Physiology (Bethesda), 25(1): 8- ...
It is an energy dependent process mediated by proteolytic enzymes called caspases, which trigger cell death through the ... 8] Cytosolic components that leak through the damaged plasma membrane into the extracellular space can incur an inflammatory ...
Executioner Caspases (Caspase 3, Caspase 6 and Caspase 7). Once initiator caspases are activated, they produce a chain reaction ... Caspase-1, Caspase-4, Caspase-5 and Caspase-11 are considered 'Inflammatory Caspases'.[7] ... Caspase-1, Caspase-4 and Caspase-5 in humans, and Caspase-1 and Caspase-11 in mice play important roles in inducing cell death ... or direct activation of Executioner Caspases (Caspase 3, Caspase 6 and Caspase 7) to degrade cellular components as shown in ...
"Caspase 8 small interfering RNA prevents acute liver failure in mice". Proc Natl Acad Sci USA 100 (13): 7797-802. PMC 164667. ... ISBN 978-0-521-73444-8.. *↑ Matzke MA, Matzke AJM. (2004). "Planting the Seeds of a New Paradigm.". PLoS Biol 2 (5): e133. PMC ... doi:10.1016/S0168-9525(01)02367-8.. *↑ 66,0 66,1 Lucy A, Guo H, Li W, Ding S (2000). "Suppression of post-transcriptional gene ... doi:10.1007/s00425-003-1005-8.. *↑ Le L, Lorenz Y, Scheurer S, Fötisch K, Enrique E, Bartra J, Biemelt S, Vieths S, Sonnewald U ...
This complex then cleaves procaspase-9, activating caspase-9 and eventually inducing apoptosis via caspase-3 activation. Hsp70 ... 2 (8): 469-75. doi:10.1038/35019501. PMID 10934466.. *^ Gupta S, Deepti A, Deegan S, Lisbona F, Hetz C, Samali A (July 2010). ... The protein is then free to fold on its own, or to be transferred to other chaperones for further processing.[8] HOP (the Hsp70 ... 1 (1): 23-8. doi:10.1379/1466-1268(1996)001,0023:AHSGTT,2.3.CO;2. PMC 313013. PMID 9222585.. ...
a b Nikolaev A. APP Binds DR6 to Cause Axon Pruning and Neuron Death via Distinct Caspases. Nature. 19. februar 2009;457(7232): ... 1987;1(1):3-8. PMID 3331112.. *. Maurer Ulrike; Maurer Konrad (2003). Alzheimer: The Life of a Physician and the Career of a ... 2006;21(8):722-8. doi:10.1002/gps.1552. PMID 16858741. *^ An Estimate of the Worldwide Prevalence and Direct Costs of Dementia ... Arkiveret fra originalen 8. januar 2012. Hentet 28. november 2016.. *. Can Alzheimer's Disease Be Prevented? (PDF). US ...
Ubiquitin ligases transfer ubiquitin to its pendant, proteins, and caspases, which engage in proteolysis in the apoptotic cycle ... 61 (8-9). ISSN 0214-6282.. *^ Sekhar, Rajagopal V; Patel, Sanjeet G (2011). "Deficient synthesis of glutathione underlies ... 20 (8): 668. doi:10.1002/anie.198106681.. *^ Drauz, Karlheinz; Grayson, Ian; Kleemann, Axel; Krimmer, Hans-Peter; ... ISBN 0-8493-0462-8.. . *^ "Nomenclature and symbolism for amino acids and peptides (IUPAC-IUB Recommendations 1983)", Pure Appl ...
Stegh AH, Barnhart BC, Volkland J, Algeciras-Schimnich A, Ke N, Reed JC, Peter ME (Feb 2002). "Inactivation of caspase-8 on ... doi:10.1016/0092-8674(95)90530-8. PMID 7774010.. *^ Jiao Y, Lu Y, Li XY (Jan 2015). "Farnesoid X receptor: a master regulator ... 278 (22): 20420-8. doi:10.1074/jbc.M302505200. PMID 12660231.. *. Pircher PC, Kitto JL, Petrowski ML, Tangirala RK, Bischoff ED ... 284 (5418): 1365-8. doi:10.1126/science.284.5418.1365. PMID 10334993.. *. Bramlett KS, Yao S, Burris TP (Dec 2000). " ...
Caspase. *Caspase 1. *Caspase 2. *Caspase 3. *Caspase 4. *Caspase 5. *Caspase 6 ... 383 (7-8): 1285-9. doi:10.1515/BC.2002.144. PMID 12437118.. *. Wex T, Bühling F, Wex H, et al. (2001). "Human cathepsin W, a ... 167 (4): 2172-8. doi:10.4049/jimmunol.167.4.2172. PMID 11490002.. *. Wex T, Levy B, Wex H, Brömme D (2000). "Human cathepsins W ...
Also, it is extensively used in research for the detection of DNA damage,[34][35] caspase cleavage and apoptosis.[36] In ... Apoptosis (quantification, measurement of DNA degradation, mitochondrial membrane potential, permeability changes, caspase ... This process is called color compensation, which calculates a fluorochrome as a percentage to measure itself[8]. ...
Toisc go bhfuil an liosta bunaithe ar an leagan Béarla i 'Wikipedia en' beidh an leagan Béarla ar dtús agus an leagan Gaeilge ina dhiaidh. Tá súil agam, nuair atá méid áirithe den liosta aistrithe go Gaeilge gur féidir liosta i nGaeilge a chumadh nó i nGaeilge agus i mBéarla. ...
"Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9". Cell. 94 (3): 325-37. doi:10.1016/ ... 44 (2): 271-8. doi:10.1002/ajpa.1330440209. PMID 816206.. *^ Weiner, S; Monge, J; Mann, A (September 2008). "Bipedalism and ... 978-0-07-139011-8. .. *^ Smart, IH; McSherry, GM (June 1986). "Gyrus formation in the cerebral cortex in the ferret. I. ... Rakic, P (8 July 1988). "Specification of cerebral cortical areas". Science. 241 (4862): 170-6. Bibcode:1988Sci...241..170R. ...
Caspase Substrates. *Cathepsin Substrates. *Chymotrypsin Substrates. *Dipeptidyl Peptidase (DPP) Subtrates. *Elastase ...
Caspase Substrates. *Cathepsin Substrates. *Chymotrypsin Substrates. *Dipeptidyl Peptidase (DPP) Subtrates. *Elastase ...
Caspase Substrates. *Cathepsin Substrates. *Chymotrypsin Substrates. *Dipeptidyl Peptidase (DPP) Subtrates. *Elastase ...
Caspase Substrates. *Cathepsin Substrates. *Chymotrypsin Substrates. *Dipeptidyl Peptidase (DPP) Subtrates. *Elastase ...
Caspase Substrates. *Cathepsin Substrates. *Chymotrypsin Substrates. *Dipeptidyl Peptidase (DPP) Subtrates. *Elastase ...
  • 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)
  • It is caused by mutations in the CASP8 gene that encodes the protein caspase-8. (wikipedia.org)
  • Mice with a conditional deletion of caspase-8 in the intestinal epithelium (Casp8(ΔIEC)) spontaneously developed inflammatory lesions in the terminal ileum and were highly susceptible to colitis. (nih.gov)
  • Defects in CASP8 are the cause of caspase-8 deficiency (CASP8D) [MIM:607271]. (abcam.com)
  • 213 Caspase 8 (CASP8) Antikörper von 27 Herstellern verfügbar auf www.antikoerper-online.de. (antikoerper-online.de)
  • Caspase 8 (Casp8) is essential for death-receptor-mediated apoptosis activity and therefore its modulation might be critical for the pathogenesis of NASH. (wur.nl)
  • On www.antibodies-online.com are 406 Caspase 8, Apoptosis-Related Cysteine Peptidase (CASP8) Antibodies from 37 different suppliers available. (antibodies-online.com)
  • Plays a role in the inhibition of apoptosis by interacting with the pro-domain of pro-caspase-8/CASP8 and thus preventing its activation. (uniprot.org)
  • Caspase-8 (Casp8)-mediated signaling triggers extrinsic apoptosis while suppressing receptor-interacting protein kinase (RIPK) 3-dependent necroptosis. (jimmunol.org)
  • Background/Aim: Recently, mounting evidence has shown that caspase-8 (CASP8) rs3834129 (-652, 6N insertion/deletion) polymorphism may serve as a genetic biomarker for personal risk of various cancer types. (iiarjournals.org)
  • In the literature, mounting evidence has shown loss of homeostasis of the apoptosis pathway to be associated with the development of oral cancer ( 15 ), and genomic polymorphisms of caspase-8 (CASP8), one of the most important components of this family of proteins in extrinsic apoptosis signaling ( 16 , 17 ), may serve as a biomarker for oral cancer. (iiarjournals.org)
  • Boster Bio Anti-Caspase-8 CASP8 Antibody catalog # A00042. (bosterbio.com)
  • The minor allele of two caspase 8 polymorphisms, namely CASP8 -652 6N InsDel (rs3834129) and CASP8 Asp302His (rs1045485), were repeatedly associated with reduced breast cancer susceptibility. (biomedcentral.com)
  • We observed an allele-dose dependent association between CASP8 -652 6N InsDel and caspase 8 mRNA expression in breast cancer tissue, with homozygous deletion carriers showing lowest relative caspase 8 expression ( p = 0.0131). (biomedcentral.com)
  • The non-coding CASP8 -652 6N InsDel polymorphism, a functional 6-bp deletion located in the promoter region of the CASP8 gene, has been associated with reduced CASP8 mRNA expression and concomitantly impaired caspase-8 activity and reduced "activation induced cell death" (AICD) in stimulated T-lymphocytes [ 3 ]. (biomedcentral.com)
  • The second polymorphism, CASP8 Asp302His, is located in the coding region of caspase 8 and results in aspartic acid to histidine substitution (Fig. 1a ). (biomedcentral.com)
  • Biochemically, caspase-8 was found to enter the complex of the inhibitor of NF-κB kinase (IKK) with the upstream Bcl10-MALT1 (mucosa-associated lymphatic tissue) adapter complex which were crucial for the induction of nuclear translocation of NF-κB. (wikipedia.org)
  • The UL36 gene product inhibits a more proximal event in Fas-mediated apoptosis by complexing with pro-caspase-8 in a way that suppresses its proteolytic activation, prompting its designation as viral inhibitor of caspase-8-induced apoptosis (vICA). (pnas.org)
  • The caspase-8 inhibitor FLIP promotes act. (mendeley.com)
  • Results: Under conditions in which proliferation of CD3-activated human T lymphocytes is increased by recombinant FasL, there was activation of the transcription factors NF-κB and AP-1 and recruitment of the caspase-8 inhibitor and FADD-interacting protein FLIP (FLICE-like inhibitory protein). (mendeley.com)
  • In the present study, we used SB203580, a p38MAPK inhibitor, and Z-LETD-FMK, a caspase-8 inhibitor, to determine the relation of p38MAPK and caspase-8 in the apoptosis process induced by DATS. (scielo.br)
  • Z-IETD-FMK is a potent small-molecule inhibitor of Caspase-8 (CASP-8) [1,2]. (invivogen.com)
  • CASP-8 plays a key role in regulated cell death, acting as an initiator of apoptosis but an inhibitor of necroptosis [2-4]. (invivogen.com)
  • THP1-HMGB1-Lucia™ cells were incubated with recombinant human TNF-α (100 ng/ml), BV6 (cIAP inhibitor, 5 µM), and increasing concentrations of Z-IETD-FMK (caspase-8 inhibitor). (invivogen.com)
  • Fluorescein (FITC)-conjugated IETD-FMK, a specific inhibitor of caspase-8, is utilized in this assay for detection. (thermofisher.com)
  • When detecting caspase-8, we utilize a specific FITC-conjugated caspase-8 inhibitor, IETD-FMK. (nexcelom.com)
  • Besides a general caspase inhibitor, caspase-2 and 8- specific inhibitors largely abrogated HOXA5-induced apoptosis whereas caspase-1, 3, 6 and 9-specific inhibitors had no significant effects. (aacrjournals.org)
  • Our inhibitor studies further implicated CaMKII g in the activation of extracellular signal-regulated kinases 1 and 2 (ERK 1/2) culminating in caspase-8/caspase-3 mediated apoptosis of HKM cells. (fluoridealert.org)
  • A potent, cell-permeable, and irreversible inhibitor of caspase-8 and granzyme B. Effectively inhibits influenza virus-induced apoptosis in HeLa cells. (alfa.com)
  • This in vitro assay employs the fluorescent inhibitor probe FAM-LETD-FMK to label active caspase-8 enzyme in living cells. (immunochemistry.com)
  • In the present study, we first treated a number of breast cancer cell lines with the proteasome inhibitor MG132 and observed that caspase-8 activation plays an important role in MG132-induced apoptosis. (asm.org)
  • The caspase 8 inhibitor c-FLIP L can act in vitro as a molecular switch between cell death and growth signals transmitted by the death receptor Fas (CD95). (asm.org)
  • Expression of death receptor pathway inhibitor cellular FLICE inhibitory protein (cFLIP), initiator caspase-8, and granzyme B inhibitor protease inhibitor-9 (PI-9) have been reported to determine susceptibility to cell- and chemotherapy-mediated killing in several tumor types. (aacrjournals.org)
  • The apoptosis was blocked completely by caspase-8 or caspase-3 inhibitor, but inhibited partly by caspase-9 inhibitor. (lu.se)
  • Moreover, treatment of HeLa cells with fisetin induced a sustained activation of the phosphorylation of ERK1/2, and inhibition of ERK1/2 by PD98059 (MEK1/2 inhibitor) or transfection with the mutant ERK1/2 expression vector significantly abolished the fisetin-induced apoptosis through the activation of caspase-8/-3 pathway. (springer.com)
  • Interferon-gamma-induced sensitization of colon carcinomas to ZD9331 targets caspases, downstream of Fas, independent of mitochondrial signaling and the inhibitor of apoptosis survivin. (semanticscholar.org)
  • Once inside the cell, the inhibitor binds covalently to the active caspase (10). (celltechnology.com)
  • Per usual in non-apoptotic growing cells caspase activated dnase is held in check inactivated in the cytoplasm thanks to the association with its inhibitor, inhibitor of caspase-activated DNase (ICAD) also known as DNA fragmentation factor 45 kDa (DFF45). (wikipedia.org)
  • Recently, the function of apoptotic caspase-8 has been extended to the negative regulation of necroptosis, the cleavage of inflammatory interleukin-1β (IL-1β) to its mature bioactive form, either directly or via the NLRP3 inflammasome, and the regulation of cytokine transcriptional responses. (nih.gov)
  • Here, we demonstrate that cleavage of the intersubunit linker of c-FLIP(L) by procaspase-8 potentiates the activation process by enhancing heterodimerization between the two proteins and vastly improving the proteolytic activity of unprocessed caspase-(C)8. (rcsb.org)
  • Cleavage of pNA peptides by caspases generates pNA that is monitored colorimetrically at ~405 nm. (anaspec.com)
  • The caspases constitute a family of aspartate-specific cysteine proteases that mediate a sequence of cleavage events. (thermofisher.com)
  • Recruitment of the inactive proenzyme to oligomerized receptors leads to caspase activation and autoproteolytic cleavage. (thermofisher.com)
  • Subsequent dimerization leads to caspase-8 activation via autocatalytic cleavage, which leads to the formation of a 12-kDa prodomain and a 43-kDa intermediate fragment that is further cleaved to produce 26-kDa and 18-kDa active enzymes. (thermofisher.com)
  • Abeta 17-42 activated caspase-8 and caspase-3, induced poly(ADP-ribose) polymerase cleavage, but did not activate caspase-9. (sigmaaldrich.com)
  • Apoptosis in response to the ligand CD95L (also known as Fas ligand) is initiated by caspase-8, which is activated by dimerization and self-cleavage at death-inducing signaling complexes (DISCs). (sciencemag.org)
  • Previous work indicated that the degree of substrate cleavage by caspase-8 determines whether a cell dies or survives in response to a death stimulus. (sciencemag.org)
  • We derived and experimentally validated a minimal model in which cleavage of caspase-8 in the enzymatic domain occurs in an interdimeric manner through interaction between DISCs, whereas prodomain cleavage sites are cleaved in an intradimeric manner within DISCs. (sciencemag.org)
  • The activation of caspase-8 by combined intra- and interdimeric cleavage ensures weak signaling at low concentrations of CD95L and strongly accelerated activation at higher ligand concentrations, thereby contributing to precise control of apoptosis. (sciencemag.org)
  • For a caspase-9-specific test, 5 μg of pcWNV-Cp-DJY or pcWNV-CpWT was cotransfected with a dominant negative caspase-9 (DN caspase-9) construct, and cleavage of procaspase-9 protein was determined by Western blot analysis with antihuman caspase-9 antibody (MBL, Nagoya, Japan). (cdc.gov)
  • DMPS treatment led to the activation of caspase-9 and caspase-3, accompanied by the cleavage of poly(ADP-ribose) polymerase (PARP) and led to cytochrome c release, depolarization of the mitochondrial membrane potential, and downregulation of the anti-apoptotic members of the bcl-2 family. (unboundmedicine.com)
  • We also observed that DMPS activated the caspase-8-Bid-Bax pathway and that the inhibition of caspase-8 by z-IETD-fmk or small interfering RNA suppressed the cleavage of Bid, cytochrome c release, caspase-3 activation, and apoptotic cell death. (unboundmedicine.com)
  • Activation of caspases during apoptosis results in the cleavage of critical cellular substrates so precipitating the dramatic morphological changes of apoptosis. (biovendor.com)
  • Apart from being activated by CD95 cleavage of caspase-8 by granzymeB during T-lymphocyte induced apoptosis has been shown. (biovendor.com)
  • In apoptotic cells, caspase-8 undergoes two sequential autoproteolytic cleavage reactions that separate the large and small catalytic subunits as well as deleting a small linker peptide sequence (amino acids 374-384) and the prodomain (amino acids 1-216), releasing the mature tetramer form into the cytoplasm ( 10 ). (aacrjournals.org)
  • Recruitment of procaspase-8 into the death signaling complex leads to its dimerization, autoproteolytic cleavage and formation of a highly active heterotetramer. (haematologica.org)
  • The retention of Spi-2 proteins' caspase-8 specificity during chordopoxvirus evolution, despite this function being readily lost through cleavage site mutagenesis, suggests that caspase-8 inhibition is crucial for poxviral pathogenesis and spread. (portlandpress.com)
  • Further downstream, caspase-8 triggers the proteolytic activation of other caspases and cleavage of cellular substrates. (rupress.org)
  • The radiation induced cleavage pattern of procaspase-8 into mature caspase-8 resembled that following CD95 crosslinking and resulted in cleavage of the proapoptotic substrate BID. (diva-portal.org)
  • A high local concentration of caspase 8 zymogens is thought to facilitate self-processing and cleavage to the active enzyme ( 34 ). (asm.org)
  • Activated caspase 8 then initiates apoptosis by cleavage of the downstream effector caspases 3, 6, and 7 ( 10 ). (asm.org)
  • At this membrane-bound complex, called the death-inducing signaling complex, autolytic cleavage of pro-caspase-8 into active caspase-8 occurs ( 5 ). (aacrjournals.org)
  • During apoptosis, pro-caspases 1 - 3 and 6 - 10 are processed at aspartate residues by self-proteolysis and/or cleavage by another caspase. (vwr.com)
  • We show that A20-mediated ubiquitination inhibits caspase-8 cleavage and TRAIL-induced apoptosis in glioblastoma through 2 signaling complexes. (aacrjournals.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)
  • The dimerization and cleavage of caspase-8 in the DISC are the critical upstream events in TNF family ligand-induced apoptosis ( 9 - 12 ), and ubiquitination of proteins in the DISC regulates these biochemical processes ( 13 ). (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)
  • Cullin 3 (CUL3), an E3 ligase, adds K48- and K63-linked polyubiquitin chains to caspase-8 and facilitates its dimerization and cleavage in the DISC, where A20 deubiquitinating enzyme removes the polyubiquitin chains from caspase-8 ( 23 ). (aacrjournals.org)
  • Caspase-8-mediated cleavage inhibits IRF-3 protein by facilitating its proteasome-mediated degradation. (bio-protocol.org)
  • Our studies indicate that IRF3 can be proteolytically processed by caspase-8-dependent cleavage (Sears et al . (bio-protocol.org)
  • 2011). The direct involvement of caspase-8 was confirmed by in vitro cleavage assay using recombinant proteins and in vivo by virus activated caspase-8. (bio-protocol.org)
  • The proteolytic cleavage of IRF3 can be inhibited by chemical inhibition or genetic ablation of caspase-8. (bio-protocol.org)
  • Caspases can be detected via immunoprecipitation, immuno-blotting techniques using caspase specific antibodies, or by employing fluorogenic substrates which become fluorescent upon cleavage by the caspase. (celltechnology.com)
  • Activation of caspase-8 involves a two-step proteolysis: the cleavage of caspase-8 to generate a 43 and a 12 kDa fragment which is further processed to 10 kDa. (antibody-antibodies.com)
  • During apoptosis procaspase-8 is processed at aspartate residues by selfproteolysis and/or cleavage by another caspase. (antibody-antibodies.com)
  • CAD release from ICAD inhibition is achieved by cleavage of ICAD at these Asp residues by the caspase-3. (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)
  • Background: Activation of Fas (CD95) by its ligand (FasL) rapidly induces cell death through recruitment and activation of caspase-8 via the adaptor protein Fas-associated death domain protein (FADD). (mendeley.com)
  • Caspase-8 is a 51 kb gene with 13 exons encoding for a 496 amino acid protein that maps to 2q33.1. (wikipedia.org)
  • The mutations lead to functional caspase-8 deficiency by destabilizing the caspase-8 protein and inactivating its enzymatic capacity. (wikipedia.org)
  • Instead, the loss of Casp-8 caused hyperactivation of p38 MAPK downstream of receptor-interacting serine/threonine protein kinase 3 (RIPK3) and destabilization of vascular endothelial cadherin (VE-cadherin) at EC junctions. (jci.org)
  • Each Caspase-8 Peptide and Caspase-8 Protein is fully covered by our Guarantee+, to give you complete peace of mind and the support when you need it. (novusbio.com)
  • The CED-4-homologous protein FLASH is involved in Fas-mediated activation of caspase-8 during apoptosis [see comments] [published erratum appears in Nature 1999 Jul 1;400(6739):89]. (jax.org)
  • The N-terminal FADD-like death effector domain of Caspase 8 suggests that it may interact with Fas-interacting protein FADD. (thermofisher.com)
  • Caspase 8 binds to the death effector domain (DED) of FADD through an analogous DED domain present in tandem in the pro-form of the Caspase 8 protein. (thermofisher.com)
  • Additionally we are shipping Caspase 8 Kits (72) and Caspase 8 Proteins (26) and many more products for this protein. (antibodies-online.com)
  • In this study, we investigated the function of p38 mitogen-activated protein kinase (MAPK) and caspase-8 in DATS-induced apoptosis of human CNE2 cells using MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide], flow cytometry assay, and Western blotting. (scielo.br)
  • The CARD8 gene encodes different CARD8 isoforms that contain the caspase-associated recruitment domain (CARD) in their carboxy-termini that acts as a protein-protein interaction interface. (atlasgeneticsoncology.org)
  • The human caspase-3 gene encodes a cytoplasmic protein that is highly expressed in lung, spleen, heart, liver, kidney and cells of the immune system. (scbt.com)
  • m-IgG Fc BP-HRP (mouse IgG Fc binding protein-HRP) is the preferred secondary detection reagent for caspase-3 Antibody (E-8) for WB and IHC(P) applications. (scbt.com)
  • caspase-3 Antibody (E-8) is a high quality monoclonal caspase-3 antibody (also designated CASP3 antibody or CPP32 antibody) suitable for the detection of the caspase-3 protein of human origin. (scbt.com)
  • We observed that the WNV-Cp protein is a pathogenic protein, which drives apoptosis in vitro through the mitochodrial/caspase-9 pathway. (cdc.gov)
  • I found that caspase-8 and receptor-interacting protein kinase-3 (RIPK3), RIPK1 and FADD are required for Yersinia-induced cell death. (upenn.edu)
  • This enhanced caspase-8 oligomerization and activation are promoted through its interaction with the ubiquitin-binding protein SQSTM1/p62 and the microtubule-associated protein light chain 3 (LC3), which are enriched at intracellular membranes in response to proteotoxic stress. (asm.org)
  • Our results unveiled a previously unknown mechanism through which disruption of protein homeostasis induces caspase-8 oligomerization, activation, and apoptosis. (asm.org)
  • Upon activation of Fas by its ligand, the DD undergoes homotypic interaction with a DD in the adaptor protein FADD, which then recruits the initiator caspase 8 via their mutual N-terminal death effector domains (DED) ( 3 ). (asm.org)
  • This event leads to the recruitment and activation of an adapter protein, FADD (Fas-associated death domain-containing protein), and to the subsequent activation of caspases, a family of cysteine proteases that exist as inactive zymogens in normal cells ( 5 , 34 ). (asm.org)
  • Protein level changes of procaspase 8, procaspase 9 and cleaved caspase 9 were determined by Western blot. (arvojournals.org)
  • A gene on chromosome 2q33-q34 that encodes a protein belonging to the cysteine-aspartic acid protease (caspase) family which, once activated by proteolytic processing, plays a central role in the execution phase of cell apoptosis, as well as various stages of embryological development. (thefreedictionary.com)
  • Chen YC, Shen SC, Lee WR, Lin HY, Ko CH, Shih CM, Yang LL (2002) Wogonin and fisetin induction of apoptosis through activation of caspase 3 cascade and alternative expression of p21 protein in hepatocellular carcinoma cells SK-HEP-1. (springer.com)
  • In this study, we show that sphingosine induces death receptor-independent caspase-8 activation and apoptotic cell death via p38 mitogen-activated protein kinase (MAPK) activation and that suppression of the MAPK/extracellular signal-regulated kinase (ERK) kinase/ERK pathway by protein phosphatase 2A (PP2A) is required for p38 MAPK activation. (aacrjournals.org)
  • Caspase (CASP)8 is an autoactivating aspartate-specific cysteine protease that initiates extrinsic apoptosis and prevents receptor interacting protein (RIP) kinase (RIPK)1-RIPK3-driven necroptosis. (escholarship.org)
  • Caspase-8 is a 55 kDa cytosolic protein that is synthesized as an inactive pro-enzyme. (antibody-antibodies.com)
  • Fas-AssociatedDeathDomain (FADD) and receptor interacting protein 1 (RIP1) are death domain containing molecules that interact with the C-terminal portion of IPS-1 and induce NF-kB through interaction and activation of initiator caspases (caspase-8 and -10). (reactome.org)
  • Among the extrinsic pathway, caspase-8 cleaves the Bcl-2 related protein Bid, which in turn induces cytochrome c release from mitochondria and caspase-3 activation, likewise resulting in apoptosis [ 1 , 2 ]. (biomedcentral.com)
  • Caspase-activated DNase (CAD) or DNA fragmentation factor subunit beta is a protein that in humans is encoded by the DFFB gene. (wikipedia.org)
  • Caspase 3 is responsible for cellular differentiation, although it is unclear how this kind of protein can promote the cell apoptosis. (wikipedia.org)
  • Although ScA initiates apoptosis via both the intrinsic and extrinsic pathways, the more sensitive pathway involves activation of caspase 8, which requires concentrations in the low nanomolar range and below, to initiate alterations in the cell membrane and apoptosis. (pnas.org)
  • The selective activation of the caspase 8 pathway by a small molecule is promising, because few currently used anticancer agents have this property. (pnas.org)
  • Caspase-8 (Casp-8), a key protease in the extrinsic cell death-signaling pathway, regulates cell death via both apoptosis and necroptosis. (jci.org)
  • In Pcys-treated gut cell lines, caspase 8 (apoptosis extrinsic pathway) but not caspase 9 (apoptosis intrinsic pathway) is activated after 3 hours through P38 phosphorylation (90 min), emphasizing the potency of lowbush blueberry Pcys to eradicate gut TRAIL-resistant cancer cells. (hindawi.com)
  • The extrinsic pathway is activated by the binding of ligands (including TNFα, FasL, and TRAIL) to cell-surface receptors and the conversion of procaspase-8 to the active caspase-8 protease. (nexcelom.com)
  • Because Caspase-8 activation is such an early step in the extrinsic apoptosis pathway, measurement of Caspase-8 is an interesting alternative to measurement of apoptosis via Annexin V-FITC / PI, which involves binding to phosphatidylserine (PS) on the surface of apoptotic cells. (nexcelom.com)
  • These results demonstrate that Abeta 17-42 induced neuronal apoptosis via a Fas-like/caspase-8 activation pathway. (sigmaaldrich.com)
  • Furthermore, we demonstrate that caspase-1-independent apoptosis requires the activation of caspase-9 and of the intrinsic pathway in a typical type II cell manner. (archives-ouvertes.fr)
  • Finally, we identify the AIM2/ASC-dependent caspase-1-independent pathway as an innate immune mechanism able to restrict bacterial replication in vitro and control IFN-γ levels in vivo in Casp1(KO) mice. (archives-ouvertes.fr)
  • In this work, we identified that the caspase-1/11-independent pathway is composed of Naip5/NLRC4/ASC/Caspase-8 and it is essential for the control of flagellated Legionella spp. (usp.br)
  • Apoptosis is induced through the mitochondrial pathway resulting in caspase-9 activation and downstream caspase-3 activation. (cdc.gov)
  • Taken together, these results indicate that caspase-8 acts upstream of caspase-3, and that the caspase-8-mediated mitochondrial pathway is important in DMPS-induced apoptosis. (unboundmedicine.com)
  • Caspase-3, caspase-7, and caspase-8 are important caspases in the apoptosis pathway and play an important role in the development and progression of cancer. (aacrjournals.org)
  • The most studied are the steroid metabolism pathway genes ( 2 - 4 ), cell-cycle control pathway genes ( 5 - 7 ), and DNA repair pathway genes ( 8 , 9 ). (aacrjournals.org)
  • EG also activated the death receptor-dependent pathway of apoptosis by enhancing the expression of caspases-8, -9, and -3 and the Bcl-2 interacting domain (Bid). (mdpi.com)
  • Caspase-8 subsequently activates caspase-3, thereby initiating the proteolytic pathway, and ultimately resulting in the apoptotic disassembly of the cell. (haematologica.org)
  • These results suggest that chemotherapeutic drug-induced caspase activation is entirely controlled by a receptor-independent mitochondrial pathway, whereas CD95-induced apoptosis can be regulated by a separate pathway not requiring Apaf-1 function. (rupress.org)
  • We conclude that radiation activates caspase-8 via an Lck-controlled pathway independently of CD95 ligand expression, This is a novel signaling event required for radiation induced apoptosis in T lymphoma cells. (diva-portal.org)
  • The expression patterns of cFLIP, caspase-8, and the absence of PI-9 provide a rationale to preferentially exploit the perforin/granzyme pathway in cytotoxic therapies against Ewing sarcoma. (aacrjournals.org)
  • Keto- and acetyl-keto-boswellic acids inhibit proliferation and induce apoptosis in Hep G2 cells via a caspase-8 dependent pathway. (lu.se)
  • To explore the apoptotic pathway, specific caspase inhibitors were employed. (lu.se)
  • The apoptotic effect is mediated by a pathway dependent on caspase-8 activation. (lu.se)
  • In clinical trials, however, investigators have proven that cancers are resistant to TRAIL pathway-targeted therapies ( 6 - 8 ), thus suggesting that cancers escape from TRAIL-mediated immunosurveillance and are resistant to TRAIL-targeted therapies. (aacrjournals.org)
  • A close relationship exists between the ERK pathway and the p38 MAPK or JNK pathway in a variety of eukaryotic cells ( 8 - 11 ). (aacrjournals.org)
  • Furthermore, up-regulation of caspase-3 and caspase-8 activities substantiated the induction of apoptosis through caspase-dependent pathway. (nottingham.ac.uk)
  • Among the death receptor signaling pathway, the initiator Caspase 8, a 55 kDa cysteine protease, plays an important role in intrinsic and extrinsic apoptosis induction. (biomedcentral.com)
  • In terms of the intrinsic apoptosis pathway, caspase-8 activates the death inducing signaling complex (DISC), which in turn induces downstream effector caspase-3, finally resulting in apoptosis [ 1 , 2 ]. (biomedcentral.com)
  • The following product was used in this experiment: Caspase 8 Polyclonal Antibody from Thermo Fisher Scientific, catalog # 13423-1-AP. (thermofisher.com)
  • This antibody can recognize the pro- and cleaved-caspase 8. (thermofisher.com)
  • Caspase-8 antibody was raised against a 15 amino acid synthetic peptide from near the carboxy terminus human caspase-8 isoform E.The immunogen is located within the last 50 amino acids of Caspase-8. (genetex.com)
  • WB analysis of HT-29 cell lysate in (A) the presence or (B) the absence of blocking peptide using GTX31285 Caspase 8 antibody. (genetex.com)
  • This reagent is now offered in a bundle with caspase-3 Antibody (E-8) ( see ordering information below ). (scbt.com)
  • caspase-3 Antibody (E-8) is available as both the non-conjugated anti-caspase-3 antibody form, as well as multiple conjugated forms of anti-caspase-3 antibody, including agarose, HRP, PE, FITC and multiple Alexa Fluor ® conjugates. (scbt.com)
  • Caspase-8 Antibody antibody storage GENTAUR recommends for long therm storage to freeze at -24 C. For short time storage up to 30 days we suggest fridge storage at 1 to 10 C. Prevent multiple freeze taw cycles of Caspase-8 Antibody. (antibody-antibodies.com)
  • 100 µg (0.5 mg/ml) affinity purified rabbit anti-caspase-8 polyclonal antibody in phosphate buffered saline (PBS), pH 7.2, containing 30% glycerol, 0.5% BSA, 0.01% thimerosal. (antibody-antibodies.com)
  • The affinity purified antibody mainly detects the 26 kDa fully cleaved fragment and the 35-43 kDa intermediate of caspase-8 in apoptotic samples. (antibody-antibodies.com)
  • Caspase-8 Antibody is supplied in PBS containing 0.02% sodium azide. (bosterbio.com)
  • Caspase-8 antibody can be used for the detection of caspase-8 by Western blot at 0.5 to 2 μg/mL. (bosterbio.com)
  • Western blot analysis of caspase-8 in Jurkat cell lysate with caspase-8 antibody at 1 μg/mL in (A) the absence and (B) the presence of blocking peptide. (bosterbio.com)
  • Immunohistochemistry of Caspase-8 in human spleen tissue with Caspase-8 antibody at 5 μg/mL. (bosterbio.com)
  • Immunofluorescence of Caspase-8 in Jurkat cells with Caspase-8 antibody at 20 μg/mL. (bosterbio.com)
  • Caspases exist as inactive proenzymes composed of a prodomain , a large protease subunit , and a small protease subunit. (wikipedia.org)
  • The clinical phenotype of CEDS patients represented a paradox since caspase-8 was considered to be chiefly a proapoptotic protease , that was mainly involved in signal transduction from Tumor necrosis factor receptor family death receptors such as Fas. (wikipedia.org)
  • The clinical phenotype of CEDS patients represented a paradox because caspase-8 was considered to be chiefly a pro-apoptotic protease, that was mainly involved in signal transduction. (wikipedia.org)
  • The crystal structures of the protease-like domain of c-FLIP(L) alone and in complex with zymogen C8 identify the unique determinants that favor heterodimerization over procaspase-8 homodimerization, and induce the latent active site of zymogen C8 into a productive conformation. (rcsb.org)
  • Most upstream protease of the activation cascade of caspases responsible for the TNFRSF6/FAS mediated and TNFRSF1A induced cell death. (abcam.com)
  • Caspase-8 is a cysteine protease best known for mediating signals downstream of death receptors leading to apoptosis. (sciencemag.org)
  • Knockout of caspase-8 , a cysteine protease that participates in the signaling for cell death by receptors of the TNF/nerve growth factor family, is lethal to mice in utero. (jimmunol.org)
  • The caspase cysteine protease family is known mainly for the participation of some of its members in programmed cell death in eukaryotes ( 2 ). (jimmunol.org)
  • Caspases exist as inactive proenzymes composed of a pro-domain, a large protease subunit, and a small protease subunit. (thermofisher.com)
  • Caspase-3, also known as apopain, SCA-1, Yama and CPP32, is an aspartate-specific cysteine protease that belongs to the ICE subfamily of caspases. (scbt.com)
  • Caspase-8 is a cysteine protease, which cleaves downstream substrates such as effector caspases, to initiate the apoptotic cascade and transmit apoptotic signals downstream of death receptors ( 16 ). (aacrjournals.org)
  • Caspase-8 is a member of the aspartate-specific cysteine protease family that is typically synthetized as an inactive zymogen and activated upon an appropriate stimulus. (haematologica.org)
  • A synthetic peptide that irreversibly inhibits FLICE and related protease/caspase activity and blocks apoptosis. (creative-enzymes.com)
  • In all cases, apoptosis is mediated by caspases, although it is unclear how these diverse apoptotic stimuli cause protease activation. (rupress.org)
  • Caspase-8, which is also known as FLICE, MACHalpha1, and Mch5, cleaves its substrates at the C-terminal aspartic acid residue of the motif Asp-X-X-Asp. (thermofisher.com)
  • Caspase-8 (also know as FLICE, MASH, Mch5) is a member of the caspase-family of cysteine proteases. (antibody-antibodies.com)
  • pNA (4-nitroaniline)-derived caspase substrates are widely used for the colorimetric detection of various caspase activities. (anaspec.com)
  • Substrates of caspase-8 include caspases-3 and -7, as well as the pro-apoptotic Bcl-2 family member Bid. (thermofisher.com)
  • In that scenario, pro-caspase-8 could potentially cleave key substrates for motility-remaining to be identified-or could function noncatalytically as an interaction partner for a motility factor. (aacrjournals.org)
  • Caspases lead to the proteolysis of a number of cellular substrates, a process which finally results in the apoptotic collapse of the cell. (rupress.org)
  • The active caspase-8 is routinely tested at BioVision for its ability to enzymatically cleave these two substrates Ac-IETD-pNA (Cat. (antibody-antibodies.com)
  • Active caspase-8 is useful in studying enzyme regulation, determining target substrates, screening caspase inhibitors, or as a positive control in caspase activity assays. (antibody-antibodies.com)
  • Activated Caspase 8 then activates other downstream caspases including Caspase 9, thereby committing the cell to undergo apoptosis. (thermofisher.com)
  • The results indicated that DATS activates p38MAPK and caspase-8, but both inhibitors have an effect on P38MAPK and caspase-8 activity. (scielo.br)
  • Caspase-3 cleaves and activates SREBPs between the basic helix-loop-helix leucine zipper domain and the membrane attachment domain. (scbt.com)
  • Caspase-3 also cleaves and activates caspase-6, -7 and -9. (scbt.com)
  • Abeta 17-42 in Alzheimer's disease activates JNK and caspase-8 leading to neuronal apoptosis. (sigmaaldrich.com)
  • Cytochrome c then complexes with Apaf-1 to activate procaspase-9, which in turn targets and activates caspase-3 ( 22 , 42 ). (asm.org)
  • Caspase-8, also called FLICE, has an N-terminal domain with sequence homology to the death effector domain of FADD that allows association of caspase-8 with the TNF/Fas family of receptors. (ihcworld.com)
  • Caspase-8 is activated by association with the Fas/FADD death-inducing signaling complex to release two active subunits, p18 and p10, into the cytosol where they activate other caspases amplifying the apoptotic signal. (ihcworld.com)
  • FADD, in addition, contains an NH 2 -terminal so-called death effector domain (DED), which binds to one of the DEDs of caspase-8. (rupress.org)
  • As such, v-FLIP can be recruited into the death-inducing signaling complex (DISC) of Fas, thereby competing with recruitment of caspase 8 to FADD. (asm.org)
  • We determined that the mechanism of influenza virus-induced apoptosis involved death signaling through FADD/caspase-8 activation, while other viruses such as vesicular stomatitis virus (VSV) and Sindbis virus (SNV) did not significantly provoke PKR-mediated apoptosis but did induce cytolysis of fibroblasts via activation of caspase-9. (asm.org)
  • The apical target of FADD is caspase-8/FLICE ( 30 ). (asm.org)
  • The anticancer activity of TRAIL is attributable to its ability to induce apoptosis through the binding of death receptors 4 and 5 (DR4, DR5) and the recruitment of intracellular apoptosis-initiating caspase-8 through Fas-associated death domain (FADD) for the assembly of a death-inducing signaling complex (DISC) ( 4 ). (aacrjournals.org)
  • In contrast to TNFR1, DR4 and DR5 recruit FADD and caspase-8 in the assembly of a plasma membrane-bound DISC, where caspase-8 becomes dimerized and cleaved, initiating apoptosis ( 21 , 22 ). (aacrjournals.org)
  • Cagnol S, Van Obberghen-Schilling E, Chambard JC (2006) Prolonged activation of ERK1, 2 induces FADD-independent caspase 8 activation and cell death. (springer.com)
  • By interfering with caspase-8 activation, vICA functions in a manner similar to the viral and cellular FLIPs ( 8 ), but lack of any sequence homology suggests that this CMV death suppressor may represent a new class of viral and potentially cellular antiapoptotic proteins. (pnas.org)
  • We offer Caspase-8 Peptides and Caspase-8 Proteins for use in common research applications: Blocking/Neutralizing, Control, Functional, SDS-Page. (novusbio.com)
  • Our Caspase-8 Peptides and Caspase-8 Proteins can be used in a variety of model species: Human, Mouse. (novusbio.com)
  • Choose from our Caspase-8 Peptides and Proteins. (novusbio.com)
  • Within this family of proteins is caspase-8, which is unusual as it can promote both cell death, and inflammatory gene expression induced by Toll-like Receptors. (upenn.edu)
  • In principle, it could also facilitate the interactions of caspase-8 promigratory proteins containing phosphotyrosine binding domains. (aacrjournals.org)
  • Spi-2 proteins like CrmA potently inhibit caspases-1, -4 and -5, which produce proinflammatory cytokines, and caspase-8, which facilitates cytotoxic lymphocyte-mediated target cell death. (portlandpress.com)
  • For example, active caspase-8 is also known to activate Bid, a proapoptotic member of the Bcl-2 family of proteins that can trigger a loss in mitochondrial transmembrane potential and cause an efflux of cytochrome c into the cytoplasm ( 26 ). (asm.org)
  • Subsequently, the intracellular death domains of these death receptors attract adaptor proteins that, in turn, recruit the proform of caspase-8. (aacrjournals.org)
  • Moreover, we used recombinant proteins in vitro to conclude that IRF3 is a substrate of caspase-8 (Sears et al . (bio-protocol.org)
  • Caspase_8, mouse recombinant recombinant proteins Most stable storage is at - 81 C or lower but some lyophilised proteins can be stored at +4C. (antibody-antibodies.com)
  • Caspase_8, mouse recombinant mus musculus murine Caspase_8, mouse recombinant detects proteins from variouse species most likely human. (antibody-antibodies.com)
  • Active caspase-8 has been shown to activate caspase-3 leading to degradation of a variety of cellular target proteins during apoptosis. (antibody-antibodies.com)
  • Systemic treatment of zebrafish or local treatment of the chick chorioallantoic membrane with ScA resulted in dose-dependent inhibition of angiogenesis, whereas topical treatment blocked tumor growth among caspase-8-expressing tumors. (pnas.org)
  • Controlling apoptosis by inhibition of caspases. (invivogen.com)
  • We further show that AIM2 engagement leads to ASC-dependent, caspase-1-independent activation of caspase-8 and caspase-9 and that caspase-1-independent death is reverted upon caspase-8 inhibition. (archives-ouvertes.fr)
  • IAPs block apoptotic events induced by caspase-8 and cytochrome c by direct inhibition of distinct caspases. (alfa.com)
  • All potently blocked caspases-1, -4, -5 and -8 activity but exhibited negligible inhibition of caspases-2, -3 and -6. (portlandpress.com)
  • In contrast, inhibition of ATP production did not affect caspase activation after triggering of CD95. (rupress.org)
  • We show here that inhibition of proteasomal degradation results in an increased oligomerization and activation of caspase-8 on the cytosolic side of intracellular membranes. (asm.org)
  • We went on to study the molecular mechanism and significance of caspase-8 activation in response to proteasome inhibition. (asm.org)
  • The above results indicate that MUC1 gene silencing induces growth inhibition in SMMC‑7721 cells through Bax‑mediated mitochondrial and caspase-8-mediated death receptor apoptotic pathways. (spandidos-publications.com)
  • Inhibition of p38 MAPK led to the marked suppression of death receptor-independent caspase-8 activation and subsequent cell death induced by sphingosine. (aacrjournals.org)
  • ScA Induces Apoptosis Selectively via Caspase 8. (pnas.org)
  • Overexpression of Caspase 8 induces apoptosis, which can be blocked by inhibitors specific for the ICE family. (thermofisher.com)
  • We conclude that fluoride -induced apoptosis is largely dependent on Ca 2+ induced superoxide generation leading to elevation in CaMKII g which in turn induces the phosphorylation of ERK 1/2 and downstream activation of extrinsic caspase cascade in HKM cells. (fluoridealert.org)
  • Kim W-H, Song H-O, Choi H-J, Bang H-I, Choi D-Y, Park H. Ethyl Gallate Induces Apoptosis of HL-60 Cells by Promoting the Expression of Caspases-8, -9, -3, Apoptosis-Inducing Factor and Endonuclease G. International Journal of Molecular Sciences . (mdpi.com)
  • We provide evidence that ionizing radiation induces a rapid activation of caspase-8 (FLICE) followed by apoptosis independently of CD95 ligand/receptor interaction. (diva-portal.org)
  • After human CNE2 cells were treated with 100 μM DATS and inhibitors (10 μM SB203580 and Z-LETD-FMK for p38MAPK and caspase-8, respectively), changes in cell viability and apoptosis and in p38MAPK and caspase-8 activity were detected. (scielo.br)
  • Selective caspase-8 and caspase-3 inhibitors completely blocked Abeta 17-42-induced neuronal death. (sigmaaldrich.com)
  • However, these caspase inhibitors did not show any effect on the alternations of cell viability caused by boswellic acids. (lu.se)
  • The methodology is based on carboxyfluorescein (FAM) labeled fluoromethyl ketone (FMK)-peptide inhibitors of caspases. (celltechnology.com)
  • Activation of caspases requires proteolytic processing at conserved internal aspartic residues to generate a heterodimeric enzyme consisting of the large and small subunits. (wikipedia.org)
  • Homology between the sense portion of the siRNA sequence and the mRNA enables the nuclease enzyme to bind and cleave the caspase transcript into small pieces, which are degraded by the cell's machinery. (abcam.com)
  • 1998). Enzymatic activity of two caspases related to interleukin-1beta-converting enzyme. (anaspec.com)
  • 2000). Caspase 8: an efficient method for large-scale autoactivation of recombinant procaspase 8 by matrix adsorption and characterization of the active enzyme. (anaspec.com)
  • However, application of the conditional knockout approach to investigate the cause of death of caspase-8 knockout embryos revealed that this enzyme also serves cellular functions that are nonapoptotic. (jimmunol.org)
  • Caspase is an inactive enzyme zymogen under normal circumstances, but once activated it will trigger the caspase cascade, eventually leading to apoptosis. (scielo.br)
  • As an initiator caspase, this enzyme initiates a caspase signaling cascade that results in apoptosis. (thermofisher.com)
  • The active caspase-3 enzyme is a heterodimer composed of two p17 and two p11 subunits. (scbt.com)
  • The remaining green fluorescent signal is a direct measure of the active caspase-8 enzyme activity present in the cell at the time the reagent was added. (immunochemistry.com)
  • The recombinant human caspases 1 - 3 and 6 - 10 are members of the ICE (interleukin-1 β converting enzyme) family of cysteine proteases. (vwr.com)
  • The matured (processed) form of these caspases consists of large and small subunits, which associate to form a heterotetramer active enzyme. (vwr.com)
  • One unit of the recombinant caspase-8 is the enzyme activity that cleaves 1 nmol of the caspase substrate IETD-pNA (pNA: pnitroanaline) per hour at 37°C in a reaction solution containing 50 mM Hepes, pH 7.2, 50 mM NaCl, 0.1% Chaps, 10 mM EDTA, 5% Glycerol, and 10 mM DTT. (antibody-antibodies.com)
  • The lyophilized caspase-8 is stable for 1 year at -70°C. Following reconstitution in PBS, the enzyme should be aliquoted and immediately stored at -70°C. Avoid multiple freeze/thaw cycles as activity might decrease. (antibody-antibodies.com)
  • Some reports mention an apoptosis inhibitory function of CARD8 involving its CARD-dependent binding to procaspase-9, whereas others did not find an association between CARD8 and caspase-9 and instead found either pro-apoptotic activity of CARD8 and associations with the inflammatory caspase-1 or the regulatory subunit of IkB kinase (NEMO) thereby suppressing NF-kB activation. (atlasgeneticsoncology.org)
  • The caspase-3 precursor is first cleaved at Asp175-Ser176 to produce the p11 subunit and the p20 peptide. (scbt.com)
  • Stimulation of motility with epidermal growth factor induced the phosphorylation of caspase-8 on tyrosine-380 and the interaction of caspase-8 with the p85α subunit of phosphatidylinositol 3-kinase. (aacrjournals.org)
  • ref. 5 ), as well as through direct interactions of Rac, cdc42, and Rac-GEFs with the p85 regulatory subunit ( 6 , 7 ), which are involved in cdc42-mediated c-Jun-NH 2 -kinase activation ( 8 ). (aacrjournals.org)
  • In this report, we show that Y380-phosphorylated pro-caspase-8 interacts with the p85 subunit of PI3K, promoting cell adhesion and motility. (aacrjournals.org)
  • Caspase 8 plays a role in APOPTOSIS by cleaving and activating EFFECTOR CASPASES. (curehunter.com)
  • During apoptosis in humans, initiator caspases integrate molecular signals into proteolytic activity ( 11 ) and subsequently activate the downstream effector caspases, thus transmitting and amplifying the apoptotic signal ( 12 ). (aacrjournals.org)
  • Consequently, the activated caspase-8 might lead to either activation of effector caspases such as caspase-3 or loss in DeltaPsi(m). (unboundmedicine.com)
  • In apoptosis, caspases are responsible for proteolytic cleavages that lead to cell disassembly (effector caspases), and are involved in upstream regulatory events (initiator caspases). (celltechnology.com)
  • During the execution of the apoptotic cascade, activated caspase-3 releases SREBP from the membrane of the ER in a proteolytic reaction that is distinct from their normal sterol-dependent activation. (scbt.com)
  • The central component of this process is a cascade of proteolytic enzymes called caspases. (celltechnology.com)
  • As is common with other proteases, caspases are synthesized as precursors that undergo proteolytic maturation, either autocatalytically or in a cascade by enzymes with similar specificity (5). (celltechnology.com)
  • Caspase-8 belongs to a family of evolutionally conserved cysteine proteases that play a key role in regulating programmed cell death or apoptosis. (nexcelom.com)
  • Caspase family of cysteine proteases has been shown to play a key role in apoptosis. (antibody-antibodies.com)
  • In this study, we report the establishment of conditional knockout of the caspase-8 gene using the Cre/ loxP recombination system, and its use for exploring these other functions. (jimmunol.org)
  • Mutations in the caspase-8 gene not only affect apoptosis but also affect host defense. (aappublications.org)
  • Since uncleaved caspase-8 functions together with its homolog, cFLIP, our findings implicate the activity of a caspase-8/cFLIP heterodimer in control of inflammatory cytokines during microbial infection, and provide new mechanistic insight into how caspase-8 regulates gene expression. (upenn.edu)
  • Of 35 selected single-nucleotide polymorphisms, four in the caspase-7 gene were in high linkage disequilibrium (rs11593766, rs3124740, rs11196445, and rs11196418) and associated with the risk for endometrial cancer. (aacrjournals.org)
  • No association was observed between polymorphisms of the caspase-8 gene and risk for endometrial cancer. (aacrjournals.org)
  • Further investigation using western blotting revealed that cytochrome c was released from the mitochondria into the cytoplasm, and caspase‑8 and caspase‑9 were activated in MUC1 gene‑silenced SMMC‑7721 cells. (spandidos-publications.com)
  • In addition, results from the co‑immunoprecipitation experiments demonstrated that the MUC1 cytoplasmic tail can bind directly to Bax or caspase‑8 and these interactions were reduced upon MUC1 gene silencing in SMMC‑7721 cells. (spandidos-publications.com)
  • The purpose of this study was to use laser capture microdissection (LCM) to isolate RGC coupled with real-time PCR to test the hypothesis that gene expression of initiator caspases would be elevated during RGC death in experimental glaucoma. (arvojournals.org)
  • There was no fold change in caspase-9 gene expression level suggesting that HK-1 cellular apoptosis occurred independent of caspase-9. (nottingham.ac.uk)
  • a Schematic overview of the caspase-8 gene and localization of the caspase 8 polymorphisms of interest. (biomedcentral.com)
  • The CDDP-pretreated cells indeed demonstrated more increased TRAIL-mediated caspase-8 activation, loss of mitochondrial membrane potential (DeltaPsi(m)), and apoptosis than untreated cells. (unboundmedicine.com)
  • Both the increased caspase activation and mitochondrial dysfunction induced by combination of CDDP and TRAIL would contribute to enhanced apoptotic cell death. (unboundmedicine.com)
  • MitoCasp A simultaneous dual parameter Assay For: Mitochondrial Membrane Potential Detection & Caspase (poly, 3/7, 8, 9, 1) Activity. (celltechnology.com)
  • Simultaneous detection of mitochondrial membrane potential and caspase activity. (celltechnology.com)
  • Utilizing these two reagents in combination Caspase activity and mitochondrial membrane potential can be analyzed simultaneously. (celltechnology.com)
  • The translocation of PS to the surface of the cell membrane occurs downstream in the apoptotic process and identifies cells committed to death through either the extrinsic or intrinsic apoptosis pathways following activation of Caspase-3 2 . (nexcelom.com)
  • This is similar to the situation observed in patients with a mutation in caspase-8, who have decreased concentrations of circulating antibodies after antigenic stimulation. (sciencemag.org)
  • Antibodies to p38, phospho-p38 (p-p38), and caspase-8 were purchased from Cell Signaling (USA). (scielo.br)
  • The extent of apoptosis was assessed by the TUNEL method and caspase 3, 6 and 8 expression by immunohistochemistry with specific antibodies. (semanticscholar.org)
  • 1997). Substrate specificities of caspase family proteases. (anaspec.com)
  • Caspase enzymes specifically recognize a 4 amino acid sequence (on their substrate) which necessarily includes an aspartic acid residue. (celltechnology.com)
  • DFFA is the substrate for caspase-3 and triggers DNA fragmentation during apoptosis. (wikipedia.org)
  • The CaspGLOW™ Fluorescein Active Caspase-8 Staining Kit contains all the reagents necessary to detect active caspase-8 in cells with high sensitivity. (thermofisher.com)
  • Although the genesis of certain tumor types such as neuroblastoma and small-cell lung cancer involves the loss of caspase-8 expression, which suppresses anoikis in neuroblastomas ( 4 ), expression is maintained or increased in most tumor types (Supplementary Fig. S1). (aacrjournals.org)
  • Furthermore, TUCAN/CARD8-54 was found to inhibit chemotherapy-induced caspase-9 activation and Fas ligand-induced caspase-8 activation. (atlasgeneticsoncology.org)
  • Caspase-8 is involved in the initiation of the cell death signal cascade. (wikipedia.org)
  • These active enzymes can then cleave other caspases, thereby generating a caspase signaling cascade that leads to a form of programmed cell death termed apoptosis. (thermofisher.com)
  • 2009). Simultaneous Quantitative Monitoring of Drug-induced Caspase Cascade Pathways in Carcinoma Cells. (nexcelom.com)
  • DN caspase-9 (provided courtesy of Emad S. Alnmeri, Thomas Jefferson University, Philadelphia, PA) has been reported to inhibit the caspase cascade ( 5 ). (cdc.gov)
  • Fluoride-induced headkidney macrophage cell apoptosis involves activation of the CaMKIIg-ERK 1/2-caspase-8 axis: the role of superoxide in initiating the apoptotic cascade. (fluoridealert.org)
  • Active caspase-8 can cleave and activate "executioner" caspases (primarily caspase-3, caspase-6, and caspase-7) starting an amplifying cascade of caspase activation. (aacrjournals.org)
  • Further work revealed that caspase-8 was essential for the induction of the transcription factor "nuclear factor κB" ( NF-κB ) after stimulation through antigen receptors, Fc receptors, or Toll-like receptor 4 in T, B, and natural killer cells . (wikipedia.org)
  • Consistent with the induction of apoptosis via the lipid compartment, we noted accumulation and aggregation of ceramide in treated cells and subsequent colocalization with caspase 8. (pnas.org)
  • Consistent with its role in cell death induction, deletion of caspase-8 in hepatocytes protected them from Fas-induced caspase activation and death. (jimmunol.org)
  • Thus, besides participating in cell death induction by receptors of the TNF/nerve growth factor family, caspase-8, apparently independently of these receptors, also mediates nonapoptotic and perhaps even antiapoptotic activities. (jimmunol.org)
  • Thus, blockade of CASP-8 is necessary for the induction of necroptosis upon engagement of death receptors. (invivogen.com)
  • Using mice that specifically ablate caspase-8 auto-processing, I have demonstrated that caspase-8 enzymatic, but not autoprocessing activity, mediates induction of inflammatory cytokines by a wide variety of TLR stimuli. (upenn.edu)
  • Western blot analysis further confirmed that caspase-2 and -8 were activated after induction of HOXA5 expression. (aacrjournals.org)
  • Overexpression of dominant-negative caspase-8 interfered with radiation-induced apoptosis, Caspase-8 activation by ionizing radiation was not observed in cells genetically defective for the Src-like tyrosine kinase Lck, Cells lacking Lck also displayed a marked resistance towards apoptosis induction upon ionizing radiation. (diva-portal.org)
  • In addition, fisetin triggered the activations of caspases-3 and -8 and the cleavages of poly (ADP-ribose) polymerase, resulting in apoptosis induction. (springer.com)
  • These results indicate that expression of HOXA5 can induce apoptosis through an apoptotic mechanism mediated by caspase-2 and -8. (aacrjournals.org)
  • Silencing LC3 by shRNA, or the LC3 mutants defective in membrane localization or p62 interaction fail to induce caspase-8 activation and apoptosis. (asm.org)
  • Anticancer drugs induce caspase-8/FLICE activation and apoptosis in the absence of CD95 receptor/ligand interaction. (semanticscholar.org)
  • article{Wesselborg1999AnticancerDI, title={Anticancer drugs induce caspase-8/FLICE activation and apoptosis in the absence of CD95 receptor/ligand interaction. (semanticscholar.org)
  • Deletion of caspase-8 inhibited the increase in B cell numbers elicited by agonists for the Toll-like receptors (TLRs), TLR2, -3, and -4. (sciencemag.org)
  • Studies of caspase-8 have focused on the ability of this caspase to interact with receptors of the TNF/nerve growth factor (NGF) 5 family and to signal for their cell death-inducing effect ( 10 , 11 , 12 ). (jimmunol.org)
  • Upon stimulation of death receptors such as CD95/APO-1/Fas, TRAIL-R1, TRAIL-R2, TNFR1, and TRAMP, caspase-8 is recruited to the death-inducing signaling complex (DISC). (thermofisher.com)
  • This association with the cell surface death receptors has shown caspase-8 to be a proximal regulator of apoptosis. (ihcworld.com)
  • Interestingly, caspase-8, whose function appeared to be restricted to death receptors, was also activated by these drugs under normal conditions, but not after ATP depletion. (rupress.org)
  • Their activation has been mainly studied upon triggering of death receptors, such as CD95 (Fas/APO-1) and tumor necrosis factor-R1, which recruit caspase-8/FLICE as the most proximal effector to the receptor complex. (semanticscholar.org)
  • Activated caspase-8 is able to cleave additional downstream caspases, which include caspase-3, to ultimately elicit the morphological hallmarks of apoptosis, including DNA fragmentation and cell shrinkage. (asm.org)
  • Prevention of ATP production completely inhibited caspase activation and apoptosis in response to chemotherapeutic drugs and staurosporine. (rupress.org)
  • Isoform 5, isoform 6, isoform 7 and isoform 8 lack the catalytic site and may interfere with the pro-apoptotic activity of the complex. (abcam.com)
  • ICT's FLICA assay kits are used by researchers seeking to quantitate apoptosis via caspase activity in cultured cells and tissues. (immunochemistry.com)
  • The FAM FLICA Caspase-8 assay probe allows researchers to assess caspase-8 activation. (immunochemistry.com)
  • We recommend using 1 unit/assay for analyzing caspase activity. (antibody-antibodies.com)
  • For a complete caspase-8 assay protocol, please refer to BioVision's Caspase-8 Fluorometric or Colorimetric Assay Kits (Cat. (antibody-antibodies.com)
  • In contrast, lytic forms of cell death, such as RIPK3- and MLKL-driven necroptosis, and caspase-1/11-dependent pyroptosis, are postulated to be inflammatory via the release of damage associated molecular patterns (DAMPs). (nih.gov)
  • Together, these findings provide molecular insights into a key aspect of c-FLIP(L) function that modulates procaspase-8 activation to elicit diverse responses in different cellular contexts. (rcsb.org)
  • Modeling indicated that sustained membrane-bound caspase-8 activity is followed by transient cytosolic activity, which can be interpreted as a molecular timer mechanism reflected by a limited lifetime of active caspase-8. (sciencemag.org)
  • The tetrapeptide IETD binds preferentially to the active site of CASP-8 [1,2]. (invivogen.com)
  • IETD-FMK is cell-permeable and binds irreversibly to active caspase-8 within the cell. (nexcelom.com)
  • The FLICA reagent FAM-LETD-FMK enters each cell and irreversibly binds to activated caspase-8. (immunochemistry.com)
  • Clinical data have suggested both apoptotic and nonapoptotic roles for caspase-8 in human disease. (sciencemag.org)
  • Two papers in the September issue of Structure with Folding & Design have for the first time revealed the structure of the key apoptotic initiator, caspase 8. (nih.gov)
  • Sensitivity to ScA was significantly increased among cells expressing caspase 8, whereas siRNA knockdown of caspase 8 increased survival after exposure to ScA. (pnas.org)
  • Although vICA is dispensable for viral replication in vitro , the common targeting of caspase-8 activation by diverse herpesviruses argues for an important role for this antiapoptotic mechanism in the pathogenesis of viral infection in the host, most likely in avoiding immune clearance by cytotoxic lymphocytes and natural killer cells. (pnas.org)
  • Here we demonstrate a critical role for caspase-8 in regulating necroptosis of intestinal epithelial cells (IECs) and terminal ileitis. (nih.gov)
  • Here, we show that expression of Casp-8 in endothelial cells (ECs) is required for proper postnatal retina angiogenesis. (jci.org)
  • F ) Quantification of cCasp-3 + IsoB4 + cells per vessel area revealing fewer apoptotic ECs in Casp-8 ECKO retinas compared with Casp-8 WT ( n = 6 WT, n = 7 ECKO). (jci.org)
  • Caspase-8 is known to be important in regulating T cells. (sciencemag.org)
  • Although caspase-8 was not necessary for B cell development, B cells from bcasp8 −/− mice were more resistant to apoptosis stimulated by the death receptor CD95 than were cells from wild-type mice. (sciencemag.org)
  • Although bcasp8 −/− B cells were resistant to apoptosis induced by CD95, the lack of bcasp8 −/− B cell expansion in response to the TLR4 agonist lipopolysaccharide (LPS) was due to increased cell death mediated by caspase-3. (sciencemag.org)
  • Although perhaps best known for its apoptotic functions, caspase-8 acts to mediate TLR signaling and NF-κB activation in B cells. (sciencemag.org)
  • Caspase-8 deletion in bone-marrow cells resulted in arrest of hemopoietic progenitor functioning, and in cells of the myelomonocytic lineage, its deletion led to arrest of differentiation into macrophages and to cell death. (jimmunol.org)
  • However, increasing evidence suggests that the death-inducing caspases, beside their apoptotic role, also have functions that contribute to activities of living cells (see, e.g. (jimmunol.org)
  • f Annexin-V/PI flow cytometry analysis of PC3 empty vector(EV) and procaspase-8(C8) CRISPR cells following pre-treatment for 24 h with 2.5 µM Entinostat(Ent) and a further 24 h with 1 µM TL32711 and 10 ng/mL TNFα combination. (nature.com)
  • In addition, Caspase 8 also reacts with Jurkat cells and Tonsil. (thermofisher.com)
  • In conclusion, our data indicate that p38MAPK and caspase-8 are involved in the process of DATS-induced apoptosis in human CNE2 cells and interact with each other. (scielo.br)
  • In the central control and effective stage of apoptosis, activated caspase-8 can lead directly to the appearance of apoptotic structural characteristics in cells, and play a key role in the process of apoptosis (6,7). (scielo.br)
  • Caspase-3 is expressed in cells as an inactive precursor from which the p17 and p11 subunits of the mature caspase-3 are proteolytically generated during apoptosis. (scbt.com)
  • 3,4 Some cancer therapies in development include molecules that trigger activation of Caspase-8-mediated apoptosis, specifically in cancer cells. (nexcelom.com)
  • The CaspGLOW™Fluorescein Active Caspase-8 Staining Kit offers a simple, sensitive method for detection of active Caspase-8 in living cells. (nexcelom.com)
  • The fluorescent marker (FITC) on the IETD-FMK allows for the detection of cells undergoing apoptosis via Caspase-8 activation using the Vision CBA Analysis System . (nexcelom.com)
  • To determine how a death ligand stimulus is effectively translated into caspase-8 activity, we assessed this activity over time in single cells with compartmentalized probes that are cleaved by caspase-8 and used multiscale modeling to simultaneously describe single-cell and population data with an ensemble of single-cell models. (sciencemag.org)
  • RD cells transfected with pcWNV-Cp-DJY or pcDNA3.1 plasmid DNA were processed for transmission electron microscope analysis as described ( 7 , 8 ). (cdc.gov)
  • In addition, cells subjected to DMPS exhibited significantly increased reactive oxygen species (ROS) generation, and ROS scavengers, such as quercetin and Tiron, but not N-acetylcysteine (NAC), inhibited DMPS-induced activations of caspase-8, -3 and subsequent apoptotic cell death, indicating the role of ROS in caspase-8-mediated apoptosis. (unboundmedicine.com)
  • Our results also suggest that ROS are critical regulators of caspase-8-mediated apoptosis in DMPS-treated leukemia cells. (unboundmedicine.com)
  • Caspase-3 and caspase-7 have been identified as key executors of apoptosis in mammalian cells and play a central role in the execution phase of apoptosis ( 14 , 15 ). (aacrjournals.org)
  • Herein, we report that pro-caspase-8 is capable of restoring cell migration/adhesion to caspase-8-null cells, establishing the first biological function of a pro-caspase. (aacrjournals.org)
  • Tyrosine-380 was required for the restoration of cell motility and cell adhesion in caspase-8-null cells, demonstrating the importance of the caspase-8-p85 interaction for these nonapoptotic functions. (aacrjournals.org)
  • Caspase-8 has also been implicated in the proinvasive effects of FASL in tumor cells ( 3 ). (aacrjournals.org)
  • However, the pro-caspase-8 form predominates in nonapoptotic cells. (aacrjournals.org)
  • ICT's Caspase-8 FLICA kit was used to detect apoptosis in U937 cells, a histiocytic lymphoma cell line. (immunochemistry.com)
  • FLICA revealed that 41.9% of cells treated with CHX had caspase-8 activity, compared with 19.1% of cells treated with TNF, and only 1.9% of the control cells (Ms. Jennifer Mitchell, Scripps). (immunochemistry.com)
  • In contrast, activation-induced cell death of T cells in c-FLIP L Tg mice was unaffected, suggesting that this deletion process can proceed in the absence of active caspase 8. (asm.org)
  • Results: The TF signaling complexes were shown to prevent apoptosis induced by serum starvation and TRAIL in cancer cells by reduced activation of caspase-8 in a PI3k/AKT-dependent manner. (diva-portal.org)
  • 2011). A specific site in IRF3 is targeted by caspase-8, activated in RNA or DNA virus-infected and dsRNA-stimulated cells (Sears et al . (bio-protocol.org)
  • 2011). In the current protocol, we have outlined a simple and detailed procedure to biochemically analyze the proteolysis of IRF3 in virus-infected cells and the specific role of caspase-8 in this process. (bio-protocol.org)
  • In virus-infected cells, IRF3 can be proteolytically cleaved by caspase-8, which gets activated during infection. (bio-protocol.org)
  • Erucylphosphocholine-induced apoptosis in glioma cells: involvement of death receptor signalling and caspase activation. (semanticscholar.org)
  • Similar to other caspases, caspase-8 also exists in cells as an inactive proenzyme. (antibody-antibodies.com)
  • Apoptosis is a caspase-dependent programmed form of cell death, which is commonly believed to be an immunologically silent process, required for mammalian development and maintenance of cellular homoeostasis. (nih.gov)
  • 1 Caspase-8 quickly converts procaspase-3 to active Caspase-3, facilitating many of the cellular and biochemical events of apoptosis. (nexcelom.com)
  • Our findings clearly imply that activation of p38 MAPK promotes death receptor-independent activation of caspase-8 and apoptotic cell death pathways, thus providing a novel cellular mechanism for the anticancer activity of sphingolipid metabolites. (aacrjournals.org)
  • AIM2/ASC triggers caspase-8-dependent apoptosis in Francisella-infected caspase-1-deficient macrophages. (archives-ouvertes.fr)
  • Francisella tularensis, the agent of tularaemia, triggers AIM2/ASC-dependent caspase-3-mediated apoptosis in caspase-1-deficient macrophages. (archives-ouvertes.fr)
  • This disease, called CEDS, stands for "Caspase eight deficiency state. (wikipedia.org)
  • Caspase-8 deficiency (CEDS) is a very rare genetic disorder of the immune system. (wikipedia.org)
  • However, deletion of caspase-8 in mice resulted in death in utero, which was associated with cardiac deformations, neural tube defects, and hemopoietic progenitor deficiency ( 13 , 14 ). (jimmunol.org)
  • The 3 known defects of lymphocyte apoptosis, Fas deficiency, FasL deficiency, and caspase 10 deficiency all have a similar phenotype: the early presentation of significant adenopathy, splenomegaly, and autoimmune disease. (aappublications.org)
  • Caspase-8 is now known to have an undefined but integral function in lymphocyte activation and the phenotype of patients with caspase-8 deficiency reflects this, with both lymphoid expansion and immunodeficiency. (aappublications.org)
  • This means affected individuals have a mutation on each of their two caspase-8 alleles. (wikipedia.org)
  • These data may provide a mechanism to explain the immunodeficiency in patients with a mutation in caspase-8. (sciencemag.org)
  • Sequencing revealed a homozygous caspase-8 mutation. (aappublications.org)
  • Moreover, the biochemical form of caspase-8 differed in the two pathways. (wikipedia.org)
  • Intense research into the signaling pathways of apoptosis has revealed a dominant role for proteases belonging to the caspase family, which in humans has 11 members at present. (nih.gov)
  • MUC1-CT is involved in numerous signaling pathways, including Wnt/β-catenin ( 4 ), c-Src ( 5 ), Grb2/Sos ( 6 ), glycogen synthase kinase 3 β ( 4 ), epidermal growth factor receptor ( 7 , 8 ) and nuclear factor-κB ( 9 , 10 ), which regulate the processes of cell survival and proliferation. (spandidos-publications.com)
  • Genetic polymorphisms in the caspase genes may affect cancer risk through altering expression levels and functions of these genes. (aacrjournals.org)
  • Caspase-8 single nucleotide polymorphisms are reported to be genomic markers for the prediction of the personal risk for several types of cancers such as that of the digestive tract ( 19 , 20 ), breast ( 21 - 23 ), prostate ( 24 ), lung ( 25 ) and bladder ( 26 ), and neuroblastoma ( 27 ). (iiarjournals.org)
  • Analysis of caspase-8 polymorphisms in breast cancer patients. (biomedcentral.com)
  • The defect in lymphocyte activation and protective immunity suggested that caspase-8 had additional signaling roles in lymphocytes . (wikipedia.org)
  • To study B cell-specific roles for caspase-8, Lemmers et al . (sciencemag.org)
  • Because no such phenotype results from targeting of any of the known TNF/NGF family members that use caspase-8 in their signaling, these findings suggested that caspase-8 serves other functional roles as well. (jimmunol.org)
  • The caspases represent a family of sulphydryl proteases which play important regulatory roles within the cell. (ihcworld.com)
  • Caspases play important roles in apoptosis and inflammation. (immunochemistry.com)
  • The mammalian caspases play distinct roles in apoptosis and inflammation. (celltechnology.com)
  • Caspases are usually involved in apoptosis and inflammation but they also exhibit nonapoptotic functions. (reactome.org)
  • Western blots suggested that the Fas signal was intact up to recruitment of Fas-associated death domain, but that subsequent recruitment of caspase-8 was defective. (aappublications.org)
  • Treatment with TRAIL leads to the recruitment of caspase-8 to the plasma membrane-bound preligand assembly complex for the assembly of a death-inducing signaling complex. (aacrjournals.org)
  • v-FLIP resembles caspase 8 in containing two DED but lacks the enzymatic C-terminal portion. (asm.org)
  • Many malignant tumors maintain expression of caspase 8, suggesting it may be an attractive target for tumor suppression ( 10 ). (pnas.org)
  • Previously, we reported that caspase-8 promotes cell migration, cell adhesion, and Rac activation in normal and tumor cell lines ( 2 ). (aacrjournals.org)
  • Thus, caspase-8 may contribute to metastasis in the more typical anoikis-resistant tumor cell context. (aacrjournals.org)
  • A combinatorial approach defines specificities of members of the caspase family and granzyme B. Functional relationships established for key mediators of apoptosis. (invivogen.com)
  • In this review, we discuss the emerging crosstalk between cell death and innate immune cell inflammatory signalling, particularly focusing on novel non-apoptotic functions of caspase-8. (nih.gov)
  • Together, our data demonstrate a critical function of caspase-8 in regulating intestinal homeostasis and in protecting IECs from TNF-α-induced necroptotic cell death. (nih.gov)
  • EC-specific Casp-8-KO pups (Casp-8ECKO) showed reduced retina angiogenesis, as the loss of Casp-8 reduced EC proliferation, sprouting, and migration independently of its cell death function. (jci.org)
  • Taking these data together, we show that Casp-8 acts in a cell death-independent manner in ECs to regulate the formation of the retina vasculature and that Casp-8 in ECs is mechanistically involved in the pathophysiology of ROP. (jci.org)
  • Caspases: key players in programmed cell death. (anaspec.com)
  • Caspase 8 is involved in the programmed cell death induced by Fas and various apoptotic stimuli. (thermofisher.com)
  • Lavrik, Golks, Krammer: Caspases: pharmacological manipulation of cell death. (antibodies-online.com)
  • A long pro-domain caspase that contains a death effector domain in its pro-domain region. (curehunter.com)
  • In addition to its role in cell death, caspase-8 has been linked to cell adhesion and motility. (thermofisher.com)
  • Caspase-1 causes pyroptosis, a necrotic-like cell death. (archives-ouvertes.fr)
  • Caspases are proteases that are best characterized for their abilities to regulate apoptotic or pyroptotic cell death programs, both of which are critical for the proper operation of the mammalian immune system. (upenn.edu)
  • Caspase-8 plays an essential role in apoptotic signal transduction from the death receptor. (haematologica.org)
  • One is mediated by recruitment of the proximal regulator caspase-8 to the death receptor complex. (rupress.org)
  • The Recruitment of Fas-associated Death Domain/Caspase-8 in Ras-induced Apoptosis -- Chen et al. (aacrjournals.org)
  • Processed caspases (caspase-8/10) encoding the DED (death effector domain) strongly activate NF-kB. (reactome.org)
  • Consistent with these findings, real-time polymerase chain reaction (PCR) analysis of the abundance of transcripts of NF-κB target genes showed that deletion of caspase-8 decreased the LPS-induced expression of these genes. (sciencemag.org)
  • These results suggest that caspase-8 phosphorylation converts it from a proapoptotic factor to a cell motility factor that, through tyrosine-380, interacts with p85, an established cell migration component. (aacrjournals.org)
  • CEDS is caused by homozygous mutations in caspase-8. (wikipedia.org)
  • Caspase-8 mutations lead to a disorder characterized by expansion of lymphocytes in secondary lymphoid organs and abnormal lymphocyte activation. (aappublications.org)