Apoptotic Protease-Activating Factor 1: A CARD signaling adaptor protein that plays a role in the mitochondria-stimulated apoptosis (APOPTOSIS, INTRINSIC PATHWAY). It binds to CYTOCHROME C in the CYTOSOL to form an APOPTOSOMAL PROTEIN COMPLEX and activates INITIATOR CASPASES such as CASPASE 9.Caspases: A family of intracellular CYSTEINE ENDOPEPTIDASES that play a role in regulating INFLAMMATION and APOPTOSIS. They specifically cleave peptides at a CYSTEINE amino acid that follows an ASPARTIC ACID residue. Caspases are activated by proteolytic cleavage of a precursor form to yield large and small subunits that form the enzyme. Since the cleavage site within precursors matches the specificity of caspases, sequential activation of precursors by activated caspases can occur.Apoptosis: One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.Caspase 3: A short pro-domain caspase that plays an effector role in APOPTOSIS. It is activated by INITIATOR CASPASES such as CASPASE 9. Isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.Caspase 9: A long pro-domain caspase that contains a caspase recruitment domain in its pro-domain region. Caspase 9 is activated during cell stress by mitochondria-derived proapoptotic factors and by CARD SIGNALING ADAPTOR PROTEINS such as APOPTOTIC PROTEASE-ACTIVATING FACTOR 1. It activates APOPTOSIS by cleaving and activating EFFECTOR CASPASES.Cysteine Endopeptidases: ENDOPEPTIDASES which have a cysteine involved in the catalytic process. This group of enzymes is inactivated by CYSTEINE PROTEINASE INHIBITORS such as CYSTATINS and SULFHYDRYL REAGENTS.Cysteine Proteinase Inhibitors: Exogenous and endogenous compounds which inhibit CYSTEINE ENDOPEPTIDASES.Enzyme Activation: Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.Proto-Oncogene Proteins c-bcl-2: Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma.Cytochrome c Group: A group of cytochromes with covalent thioether linkages between either or both of the vinyl side chains of protoheme and the protein. (Enzyme Nomenclature, 1992, p539)Proteins: Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.Protease Inhibitors: Compounds which inhibit or antagonize biosynthesis or actions of proteases (ENDOPEPTIDASES).HIV Protease: Enzyme of the human immunodeficiency virus that is required for post-translational cleavage of gag and gag-pol precursor polyproteins into functional products needed for viral assembly. HIV protease is an aspartic protease encoded by the amino terminus of the pol gene.Serine Endopeptidases: Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.Peptide Hydrolases: Hydrolases that specifically cleave the peptide bonds found in PROTEINS and PEPTIDES. Examples of sub-subclasses for this group include EXOPEPTIDASES and ENDOPEPTIDASES.Endopeptidases: A subclass of PEPTIDE HYDROLASES that catalyze the internal cleavage of PEPTIDES or PROTEINS.Cysteine Proteases: A subclass of peptide hydrolases that depend on a CYSTEINE residue for their activity.Protease La: A prokaryotic ATP-dependent protease that plays a role in the degradation of many abnormal proteins. It is a tetramer of 87-kDa subunits, each of which contains a proteolytic site and a ATP-binding site.ATP-Dependent Proteases: Proteases that contain proteolytic core domains and ATPase-containing regulatory domains. They are usually comprised of large multi-subunit assemblies. The domains can occur within a single peptide chain or on distinct subunits.Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Protease Nexins: Extracellular protease inhibitors that are secreted from FIBROBLASTS. They form a covalent complex with SERINE PROTEASES and can mediate their cellular internalization and degradation.Serine Proteinase Inhibitors: Exogenous or endogenous compounds which inhibit SERINE ENDOPEPTIDASES.DNA Fragmentation: Splitting the DNA into shorter pieces by endonucleolytic DNA CLEAVAGE at multiple sites. It includes the internucleosomal DNA fragmentation, which along with chromatin condensation, are considered to be the hallmarks of APOPTOSIS.In Situ Nick-End Labeling: An in situ method for detecting areas of DNA which are nicked during APOPTOSIS. Terminal deoxynucleotidyl transferase is used to add labeled dUTP, in a template-independent manner, to the 3 prime OH ends of either single- or double-stranded DNA. The terminal deoxynucleotidyl transferase nick end labeling, or TUNEL, assay labels apoptosis on a single-cell level, making it more sensitive than agarose gel electrophoresis for analysis of DNA FRAGMENTATION.Substrate Specificity: A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts.bcl-2-Associated X Protein: A member of the Bcl-2 protein family and homologous partner of C-BCL-2 PROTO-ONCOGENE PROTEIN. It regulates the release of CYTOCHROME C and APOPTOSIS INDUCING FACTOR from the MITOCHONDRIA. Several isoforms of BCL2-associated X protein occur due to ALTERNATIVE SPLICING of the mRNA for this protein.Caspase Inhibitors: Endogenous and exogenous compounds and that either inhibit CASPASES or prevent their activation.Antigens, CD95: 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.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Mitochondria: Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)Signal Transduction: The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.Phagocytosis: The engulfing and degradation of microorganisms; other cells that are dead, dying, or pathogenic; and foreign particles by phagocytic cells (PHAGOCYTES).Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.Cell Line, Tumor: A cell line derived from cultured tumor cells.Cathepsins: A group of lysosomal proteinases or endopeptidases found in aqueous extracts of a variety of animal tissues. They function optimally within an acidic pH range. The cathepsins occur as a variety of enzyme subtypes including SERINE PROTEASES; ASPARTIC PROTEINASES; and CYSTEINE PROTEASES.Jurkat Cells: A CELL LINE derived from human T-CELL LEUKEMIA and used to determine the mechanism of differential susceptibility to anti-cancer drugs and radiation.Amino Acid Chloromethyl Ketones: Inhibitors of SERINE ENDOPEPTIDASES and sulfhydryl group-containing enzymes. They act as alkylating agents and are known to interfere in the translation process.Caspase 8: A long pro-domain caspase that contains a death effector domain in its pro-domain region. Caspase 8 plays a role in APOPTOSIS by cleaving and activating EFFECTOR CASPASES. Activation of this enzyme can occur via the interaction of its N-terminal death effector domain with DEATH DOMAIN RECEPTOR SIGNALING ADAPTOR PROTEINS.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Oligopeptides: Peptides composed of between two and twelve amino acids.Calpain: 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 3.4.22.4.Necrosis: The pathological process occurring in cells that are dying from irreparable injuries. It is caused by the progressive, uncontrolled action of degradative ENZYMES, leading to MITOCHONDRIAL SWELLING, nuclear flocculation, and cell lysis. It is distinct it from APOPTOSIS, which is a normal, regulated cellular process.Blotting, Western: Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Annexin A5: A protein of the annexin family isolated from human PLACENTA and other tissues. It inhibits cytosolic PHOSPHOLIPASE A2, and displays anticoagulant activity.Mutation: Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.Apoptosis Regulatory Proteins: A large group of proteins that control APOPTOSIS. This family of proteins includes many ONCOGENE PROTEINS as well as a wide variety of classes of INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS such as CASPASES.Ubiquitin-Specific Proteases: Members of the peptidase C19 family which regulate signal transduction by removing UBIQUITIN from specific protein substrates via a process known as deubiquitination or deubiquitylation.Cytochromes c: Cytochromes of the c type that are found in eukaryotic MITOCHONDRIA. They serve as redox intermediates that accept electrons from MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III and transfer them to MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX IV.Tumor Cells, Cultured: Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.Phosphatidylserines: Derivatives of phosphatidic acids in which the phosphoric acid is bound in ester linkage to a serine moiety. Complete hydrolysis yields 1 mole of glycerol, phosphoric acid and serine and 2 moles of fatty acids.Kinetics: The rate dynamics in chemical or physical systems.Endopeptidase Clp: An ATP-dependent protease found in prokaryotes, CHLOROPLASTS, and MITOCHONDRIA. It is a soluble multisubunit complex that plays a role in the degradation of many abnormal proteins.Metalloendopeptidases: ENDOPEPTIDASES which use a metal such as ZINC in the catalytic mechanism.Enzyme Precursors: Physiologically inactive substances that can be converted to active enzymes.Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water.Subtilisins: A family of SERINE ENDOPEPTIDASES isolated from Bacillus subtilis. EC 3.4.21.-Aspartic Acid Endopeptidases: A sub-subclass of endopeptidases that depend on an ASPARTIC ACID residue for their activity.Serpins: A family of serine proteinase inhibitors which are similar in amino acid sequence and mechanism of inhibition, but differ in their specificity toward proteolytic enzymes. This family includes alpha 1-antitrypsin, angiotensinogen, ovalbumin, antiplasmin, alpha 1-antichymotrypsin, thyroxine-binding protein, complement 1 inactivators, antithrombin III, heparin cofactor II, plasminogen inactivators, gene Y protein, placental plasminogen activator inhibitor, and barley Z protein. Some members of the serpin family may be substrates rather than inhibitors of SERINE ENDOPEPTIDASES, and some serpins occur in plants where their function is not known.Protein Processing, Post-Translational: 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.Caspase 1: A long pro-domain caspase that has specificity for the precursor form of INTERLEUKIN-1BETA. It plays a role in INFLAMMATION by catalytically converting the inactive forms of CYTOKINES such as interleukin-1beta to their active, secreted form. Caspase 1 is referred as interleukin-1beta converting enzyme and is frequently abbreviated ICE.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Pepstatins: N-acylated oligopeptides isolated from culture filtrates of Actinomycetes, which act specifically to inhibit acid proteases such as pepsin and renin.Protein Binding: The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.Chymotrypsin: A serine endopeptidase secreted by the pancreas as its zymogen, CHYMOTRYPSINOGEN and carried in the pancreatic juice to the duodenum where it is activated by TRYPSIN. It selectively cleaves aromatic amino acids on the carboxyl side.Protein Structure, Tertiary: The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.Membrane Proteins: Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.Trypsin: A serine endopeptidase that is formed from TRYPSINOGEN in the pancreas. It is converted into its active form by ENTEROPEPTIDASE in the small intestine. It catalyzes hydrolysis of the carboxyl group of either arginine or lysine. EC 3.4.21.4.Flow Cytometry: Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.Fas Ligand Protein: A transmembrane protein belonging to the tumor necrosis factor superfamily that was originally discovered on cells of the lymphoid-myeloid lineage, including activated T-LYMPHOCYTES and NATURAL KILLER CELLS. It plays an important role in immune homeostasis and cell-mediated toxicity by binding to the FAS RECEPTOR and triggering APOPTOSIS.Sequence Homology, Amino Acid: The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.Proteolysis: Cleavage of proteins into smaller peptides or amino acids either by PROTEASES or non-enzymatically (e.g., Hydrolysis). It does not include Protein Processing, Post-Translational.Tumor Suppressor Protein p53: Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. A mutant or absent p53 protein has been found in LEUKEMIA; OSTEOSARCOMA; LUNG CANCER; and COLORECTAL CANCER.Poly(ADP-ribose) Polymerases: Enzymes that catalyze the transfer of multiple ADP-RIBOSE groups from nicotinamide-adenine dinucleotide (NAD) onto protein targets, thus building up a linear or branched homopolymer of repeating ADP-ribose units i.e., POLY ADENOSINE DIPHOSPHATE RIBOSE.bcl-X Protein: A member of the bcl-2 protein family that plays a role in the regulation of APOPTOSIS. Two major isoforms of the protein exist due to ALTERNATIVE SPLICING of the BCL2L1 mRNA and are referred to as Bcl-XS and Bcl-XL.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Mice, Inbred C57BLCloning, Molecular: The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.Caspase 6: A short pro-domain caspase that plays an effector role in APOPTOSIS. It is activated by INITIATOR CASPASES such as CASPASE 7; CASPASE 8; and CASPASE 10. Isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.Models, Molecular: Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.Electrophoresis, Polyacrylamide Gel: Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.Caspase 7: A short pro-domain caspase that plays an effector role in APOPTOSIS. It is activated by INITIATOR CASPASES such as CASPASE 3 and CASPASE 10. Several isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.Molecular Weight: The sum of the weight of all the atoms in a molecule.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Cathepsin L: A ubiquitously-expressed cysteine protease that plays an enzymatic role in POST-TRANSLATIONAL PROTEIN PROCESSING of proteins within SECRETORY GRANULES.Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.Macrophages: 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.)HeLa Cells: The first continuously cultured human malignant CELL LINE, derived from the cervical carcinoma of Henrietta Lacks. These cells are used for VIRUS CULTIVATION and antitumor drug screening assays.Bacterial Proteins: Proteins found in any species of bacterium.Caspase 2: A long pro-domain caspase that contains a caspase recruitment domain in its pro-domain region. Activation of this enzyme can occur via the interaction of its caspase recruitment domain with CARD SIGNALING ADAPTOR PROTEINS. Caspase 2 plays a role in APOPTOSIS by cleaving and activating effector pro-caspases. Several isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.Pancreatic Elastase: A protease of broad specificity, obtained from dried pancreas. Molecular weight is approximately 25,000. The enzyme breaks down elastin, the specific protein of elastic fibers, and digests other proteins such as fibrin, hemoglobin, and albumin. EC 3.4.21.36.Trypsin Inhibitors: Serine proteinase inhibitors which inhibit trypsin. They may be endogenous or exogenous compounds.Escherichia coli: A species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.Transfection: The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Proto-Oncogene Proteins: Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.

C. elegans MAC-1, an essential member of the AAA family of ATPases, can bind CED-4 and prevent cell death. (1/406)

In the nematode Caenorhabditis elegans, CED-4 plays a central role in the regulation of programmed cell death. To identify proteins with essential or pleiotropic activities that might also regulate cell death, we used the yeast two-hybrid system to screen for CED-4-binding proteins. We identified MAC-1, a member of the AAA family of ATPases that is similar to Smallminded of Drosophila. Immunoprecipitation studies confirm that MAC-1 interacts with CED-4, and also with Apaf-1, the mammalian homologue of CED-4. Furthermore, MAC-1 can form a multi-protein complex that also includes CED-3 or CED-9. A MAC-1 transgene under the control of a heat shock promoter prevents some natural cell deaths in C. elegans, and this protection is enhanced in a ced-9(n1950sd)/+ genetic background. We observe a similar effect in mammalian cells, where expression of MAC-1 can prevent CED-4 and CED-3 from inducing apoptosis. Finally, mac-1 is an essential gene, since inactivation by RNA-mediated interference causes worms to arrest early in larval development. This arrest is similar to that observed in Smallminded mutants, but is not related to the ability of MAC-1 to bind CED-4, since it still occurs in ced-3 or ced-4 null mutants. These results suggest that MAC-1 identifies a new class of proteins that are essential for development, and which might regulate cell death in specific circumstances.  (+info)

Apaf-1 and caspase-9 in p53-dependent apoptosis and tumor inhibition. (2/406)

The ability of p53 to promote apoptosis in response to mitogenic oncogenes appears to be critical for its tumor suppressor function. Caspase-9 and its cofactor Apaf-1 were found to be essential downstream components of p53 in Myc-induced apoptosis. Like p53 null cells, mouse embryo fibroblast cells deficient in Apaf-1 and caspase-9, and expressing c-Myc, were resistant to apoptotic stimuli that mimic conditions in developing tumors. Inactivation of Apaf-1 or caspase-9 substituted for p53 loss in promoting the oncogenic transformation of Myc-expressing cells. These results imply a role for Apaf-1 and caspase-9 in controlling tumor development.  (+info)

CIPER, a novel NF kappaB-activating protein containing a caspase recruitment domain with homology to Herpesvirus-2 protein E10. (3/406)

We have identified and characterized CIPER, a novel protein containing a caspase recruitment domain (CARD) in its N terminus and a C-terminal region rich in serine and threonine residues. The CARD of CIPER showed striking similarity to E10, a product of the equine herpesvirus-2. CIPER formed homodimers via its CARD and interacted with viral E10 but not with several apoptosis regulators containing CARDs including ARC, RAIDD, RICK, caspase-2, caspase-9, or Apaf-1. Expression of CIPER induced NF-kappaB activation, which was inhibited by dominant-negative NIK and a nonphosphorylable IkappaB-alpha mutant but not by dominant-negative RIP. Mutational analysis revealed that the N-terminal region of CIPER containing the CARD was sufficient and necessary for NF-kappaB-inducing activity. Point mutations in highly conserved residues in the CARD of CIPER disrupted the ability of CIPER to activate NF-kappaB and to form homodimers, indicating that the CARD is essential for NF-kappaB activation and dimerization. We propose that CIPER acts in a NIK-dependent pathway of NF-kappaB activation.  (+info)

mE10, a novel caspase recruitment domain-containing proapoptotic molecule. (4/406)

Apoptotic signaling is mediated by homophilic interactions between conserved domains present in components of the death pathway. The death domain, death effector domain, and caspase recruitment domain (CARD) are examples of such interaction motifs. We have identified a novel mammalian CARD-containing adaptor molecule termed mE10 (mammalian E10). The N-terminal CARD of mE10 exhibits significant homology (47% identity and 64% similarity) to the CARD of a gene from Equine Herpesvirus type 2. The C-terminal region is unique. Overexpression of mE10 in MCF-7 human breast carcinoma cells induces apoptosis. Mutational analysis indicates that CARD-mediated mE10 oligomerization is essential for killing activity. The C terminus of mE10 bound to the zymogen form of caspase-9 and promoted its processing to the active dimeric species. Taken together, these data suggest a model where autoproteolytic activation of pro-caspase-9 is mediated by mE10-induced oligomerization.  (+info)

Human skeletal muscle cytosols are refractory to cytochrome c-dependent activation of type-II caspases and lack APAF-1. (5/406)

Apoptotic regulatory mechanisms in skeletal muscle have not been revealed. This is despite indications that remnant apoptotic events are detected following exercise, muscle injury and the progression of dystrophinopathies. The recent elicitation of a cytochrome c-mediated induction of caspases has led to speculation regarding a cytochrome c mechanism in muscle. We demonstrate that cytosols from skeletal muscle biopsies from healthy human volunteers lack the ability to activate type-II caspases by a cytochrome c-mediated pathway despite the confirmed presence of both procaspase-3 and -9. This was not due to the presence of an endogenous inhibitor, as the muscle cytosols enhanced caspase activity when added to a control cytosol, subsequently activated by cytochrome c and dATP. In addition, we demonstrate that muscle cytosols lack the apoptosis protease activator protein-1 (APAF-1), both at the protein and mRNA levels. These data indicate that human skeletal muscle cells will be refractory to mitochondrial-mediated events leading to apoptosis and thus can escape a major pro-apoptotic regulatory mechanism. This may reflect an evolutionary adaptation of cell survival in the presence of the profusion of mitochondria required for energy generation in motility.  (+info)

An APAF-1.cytochrome c multimeric complex is a functional apoptosome that activates procaspase-9. (6/406)

We report here the reconstitution of the de novo procaspase-9 activation pathway using highly purified cytochrome c, recombinant APAF-1, and recombinant procaspase-9. APAF-1 binds and hydrolyzes ATP or dATP to ADP or dADP, respectively. The hydrolysis of ATP/dATP and the binding of cytochrome c promote APAF-1 oligomerization, forming a large multimeric APAF-1.cytochrome c complex. Such a complex can be isolated using gel filtration chromatography and is by itself sufficient to recruit and activate procaspase-9. The stoichiometric ratio of procaspase-9 to APAF-1 is approximately 1 to 1 in the complex. Once activated, caspase-9 disassociates from the complex and becomes available to cleave and activate downstream caspases such as caspase-3.  (+info)

Human CARD4 protein is a novel CED-4/Apaf-1 cell death family member that activates NF-kappaB. (7/406)

The nematode CED-4 protein and its human homolog Apaf-1 play a central role in apoptosis by functioning as direct activators of death-inducing caspases. A novel human CED-4/Apaf-1 family member called CARD4 was identified that has a domain structure strikingly similar to the cytoplasmic, receptor-like proteins that mediate disease resistance in plants. CARD4 interacted with the serine-threonine kinase RICK and potently induced NF-kappaB activity through TRAF-6 and NIK signaling molecules. In addition, coexpression of CARD4 augmented caspase-9-induced apoptosis. Thus, CARD4 coordinates downstream NF-kappaB and apoptotic signaling pathways and may be a component of the host innate immune response.  (+info)

Mistletoe lectin activates caspase-8/FLICE independently of death receptor signaling and enhances anticancer drug-induced apoptosis. (8/406)

Mistletoe lectin I (ML-I) is a major active component in plant extracts of Viscum album that is increasingly used in adjuvant cancer therapy. ML-I exerts potent immunomodulating and cytotoxic effects, although its mechanism of action is largely unknown. We show that treatment of leukemic T- and B-cell lines with ML-I induced apoptosis, which required the prior activation of proteases of the caspase family. The involvement of caspases is demonstrated because (a) a peptide caspase inhibitor almost completely prevented ML-I-induced cell death and (b) proteolytic activation of caspase-8, caspase-9, and caspase-3 was observed. Because caspase-8 has been implicated as a regulator of apoptosis mediated by death receptors, we further investigated a potential receptor involvement in ML-I-induced effects. Cell death triggered by ML-I was neither attenuated in cell clones resistant to CD95 nor in cells that were rendered refractory to other death receptors by overexpressing a dominant-negative FADD mutant. In contrast, ML-I triggered a receptor-independent mitochondria-controlled apoptotic pathway because it rapidly induced the release of cytochrome c into the cytosol. Because ML-I was also observed to enhance the cytotoxic effect of chemotherapeutic drugs, these data may provide a molecular basis for clinical trials using MLs in anticancer therapy.  (+info)

*Cytochrome c

Upon release of cytochrome c to the cytoplasm, the protein binds apoptotic protease activating factor-1 (Apaf-1).[5] ... This release of cytochrome c in turn activates caspase 9, a cysteine protease. Caspase 9 can then go on to activate caspase 3 ... Pro-apoptotic:. BAX. BAK1/Bcl-2 homologous antagonist killer. Bcl-2-associated death promoter. Anti-apoptotic:. Bcl-2. Bcl-xL. ... intrinsic apoptotic signaling pathway. • activation of cysteine-type endopeptidase activity involved in apoptotic process by ...

*Programmed cell death

Knockout or inhibition of apoptotic protease activating factor 1 (APAF1), also results in malformations and increased embryonic ... An atrophic factor is a force that causes a cell to die. Only natural forces on the cell are considered to be atrophic factors ... Anoikis Apoptosis-inducing factor Apoptosis versus Pseudoapoptosis Apoptosome Apoptotic DNA fragmentation Autolysis (biology) ... Solomon M, Belenghi B, Delledonne M, Menachem E, Levine A (1999). "The involvement of cysteine proteases and protease inhibitor ...

*APAF1

Apoptotic protease activating factor 1, also known as APAF1, is a human homolog of C. elegans CED-4 gene. This gene encodes a ... Riedl SJ, Li W, Chao Y, Schwarzenbacher R, Shi Y (Apr 2005). "Structure of the apoptotic protease-activating factor 1 bound to ... Kim H, Jung YK, Kwon YK, Park SH (1999). "Assignment of apoptotic protease activating factor-1 gene (APAF1) to human chromosome ... "Structural basis of procaspase-9 recruitment by the apoptotic protease-activating factor 1". Nature. 399 (6736): 549-57. doi: ...

*History of apoptosis research

... apoptotic protease activating factor). The team published their results in an article entitled "Apaf-1, a human protein ... Landmark research by David L. Vaux and colleagues described the anti-apoptotic and tumorigenic (tumor-causing) role of the ... Zou H, Henzel WJ, Liu X, Lutschg A, Wang X (August 1997). "Apaf-1, a human protein homologous to C. elegans CED-4, participates ... 39: 1-10. doi:10.1042/bse0390001. Diamantis, Aristidis; Magiorkinis, Emmanouil; Sakorafas, George H.; Androutsos, George (2008 ...

*Reactive oxygen species

... or apoptotic protease activating factor-1, which is free-floating in the cell's cytoplasm. Using energy from the ATPs in the ... ROS then activate various transcription factors such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB ... The production of ROS is strongly influenced by stress factor responses in the plant, these factors that increase ROS ... After growth factor stimulation of RTKs, ROS can trigger activation of signaling pathways involved in cell migration and ...

*Xiaodong Wang (biochemist)

Caspase-9 and the Apoptotic Protease Activating factor-1 (APAF1). These components are essential for forming a ternary complex ... 103 (1): 7-9. doi:10.1073/pnas.0509187103. PMC 1324996 . PMID 16380419. Zou, H.; Henzel, W. J.; Liu, X.; Lutschg, A.; Wang, X ... called the apoptosome that activates Caspase-3 downstream of the intracellular or mitochondrial pathway of apoptosis. He was ... 1997-08-08). "Apaf-1, a human protein homologous to C. elegans CED-4, participates in cytochrome c-dependent activation of ...

*Apoptosome

... apoptotic protease activating factor 1) upon mitochondria-mediated apoptosis which must be stimulated by some type of stress ... c-dependent Caspase Activation in Ovarian Cancer Cell Lines Due to Diminished or Absent Apoptotic Protease Activating Factor-1 ... Once activated, this initiator caspase can then activate effector caspases and trigger a cascade of events leading to apoptosis ... By activating the apoptosome by an outside stimulus apoptosis can occur and get rid of the mutated cells. Numerous approaches ...

*Apoptosis

Once cytochrome c is released it binds with Apoptotic protease activating factor - 1 (Apaf-1) and ATP, which then bind to pro- ... which are proteases, or enzymes that degrade proteins. The two pathways both activate initiator caspases, which then activate ... Pro-apoptotic:. BAX. BAK1/Bcl-2 homologous antagonist killer. Bcl-2-associated death promoter. Anti-apoptotic:. Bcl-2. Bcl-xL. ... Some apoptotic factors are vital during mitochondrial respiration e.g. cytochrome C.[72] Pathological inactivation of apoptosis ...

*Apoptosis

Once cytochrome c is released it binds with Apoptotic protease activating factor - 1 (Apaf-1) and ATP, which then bind to pro- ... which are proteases, or enzymes that degrade proteins. The two pathways both activate initiator caspases, which then activate ... Some apoptotic factors are vital during mitochondrial respiration e.g. cytochrome C.[80] Pathological inactivation of apoptosis ... There also exists a caspase-independent apoptotic pathway that is mediated by AIF (apoptosis-inducing factor).[43] ...

*Purpura fulminans

Activated protein C binds to endothelial protein C receptor and subsequently cleaves the endothelial cell protease activated ... with increased synthesis of prothrombotic proteins Factor VIII, von Willebrand factor, and fibrinogen. ... not only altering coagulation profiles but down-regulating pro-inflammatory and pro-apoptotic mediators, up-regulation of anti- ... Kondaveeti S, Hibberd ML, Booy R, Nadel S, Levin M (1999). "Effect of the Factor V Leiden mutation on the severity of ...

*CARD domain

Ice protease-activating factor, also known as NLR family, card domain containing 4 (NLRC4), CARD, LRR, and NACHT-containing ... apoptotic peptidase activating factor 1 (also called CED4) [26] GLAVA1: glavaris peptidase activating factor 1 (also called ... Activating mutations in at least two related PYD-containing proteins, cryopyrin/CIAS-1 and pyrin/MEFV, have been linked to ... Hofmann K, Bucher P, Tschopp J (1997). "The CARD domain: a new apoptotic signalling motif". Trends Biochem Sci. 22 (5): 155-6. ...

*Apoptosis

Once cytochrome c is released it binds with Apoptotic protease activating factor - 1 (Apaf-1) and ATP, which then bind to pro- ... which are proteases, or enzymes that degrade proteins. The two pathways both activate initiator caspases, which then activate ... Some apoptotic factors are vital during mitochondrial respiration e.g. cytochrome C. Pathological inactivation of apoptosis in ... Before the apoptotic cell is disposed of, there is a process of disassembly. There are three recognized steps in apoptotic cell ...

*Caspase-activated DNase

The factor that seems to induce more cell differentiation is caspase-3 protease. This was identified as the penultimate stage ... Cell apoptotic death is a process executed by cysteine proteases that allows the animals to keep their homeostasis, also ... "The Contribution of Apoptosis-inducing Factor, Caspase-activated DNase, and Inhibitor of Caspase-activated DNase to the Nuclear ... Caspase-activated DNase (CAD) or DNA fragmentation factor subunit beta is a protein that in humans is encoded by the DFFB gene ...

*SHC1

regulation of epidermal growth factor-activated receptor activity. • regulation of growth. • Ras protein signal transduction. • ... When the coagulated protease-activated protein C inhibits p66SHC a cytoprotective effect on diabetic nephropathy is placed on ... negative regulation of apoptotic process. • positive regulation of MAPK cascade. • negative regulation of transcription, DNA- ... epidermal growth factor receptor signaling pathway. • cellular response to growth factor stimulus. • MAPK cascade. • Fc-epsilon ...

*Tumor necrosis factor alpha

... which then activates JNK. JNK translocates to the nucleus and activates transcription factors such as c-Jun and ATF2. The JNK ... and anti-apoptotic factors. Activation of the MAPK pathways: Of the three major MAPK cascades, TNF induces a strong activation ... Nevertheless, TRADD binds FADD, which then recruits the cysteine protease caspase-8. A high concentration of caspase-8 induces ... reported another cytotoxic factor produced by macrophages and named it tumor necrosis factor (TNF). Both factors were described ...

*Picornain 3C

Caspase stands for cysteine-aspartic acid protease and play an essential role in the apoptotic pathway of the cell. Protease 2A ... protein and other transcription factors at glutamine-glycine sites This inhibition of transcription is caused by Protease 3C, ... which leads to the release of cytochrome C from mitochondria and activating caspase- 9 (Chau). 3C is responsible for the ... Chau, DH (2007). "Coxsackievirus B3 proteases 2A and 3C induce apoptotic cell death through mitochondrial injury and cleavage ...

*Caspase 8

TRAIL-activated apoptotic signaling pathway. • proteolysis. • macrophage differentiation. • TRIF-dependent toll-like receptor ... cysteine-type endopeptidase activity involved in apoptotic process. • tumor necrosis factor receptor binding. • cysteine-type ... Caspases exist as inactive proenzymes composed of a prodomain, a large protease subunit, and a small protease subunit. ... apoptotic process. • extrinsic apoptotic signaling pathway. • negative regulation of extrinsic apoptotic signaling pathway via ...

*Death-inducing signaling complex

This apoptotic activity is critical for tissue homeostasis and immune function. APO-1-mediated apoptosis can be inhibited by a ... In order to do this, downstream targets such as FLICE must be activated. In its inactive state, FLICE's two death domains are ... CAP4 is also called FLICE, a cysteine protease with two death effector domains. CAP3 is the prodomain of FLICE generated during ... In glioma cells, the effects of TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) have been shown to induce DISC- ...

*Caspase 3

Caspase-3 is activated in the apoptotic cell both by extrinsic (death ligand) and intrinsic (mitochondrial) pathways. The ... a member of the NF-E2 family of transcription factors, as a substrate for caspase-3(-like) proteases". Cell Death and ... In intrinsic activation, cytochrome c from the mitochondria works in combination with caspase-9, apoptosis-activating factor 1 ... This protein cleaves and activates caspases 6 and 7; and the protein itself is processed and activated by caspases 8, 9, and 10 ...

*Mannan-binding lectin

... intact apoptotic cells, as well as cell debris by phagocytes. The complement system can be activated through three pathways: ... which have protease domains. There are also sMAP (also called MAp19) and MAp44, which do not have protease domains and are ... It is produced in the liver as a response to infection, and is part of many other factors termed acute phase proteins. ... a serine protease called MASP (MBL-associated serine protease). There are three MASPs: MASP-1, MASP-2 and MASP-3, ...

*Stress granule

... granule formation is often downstream of the stress-activated phosphorylation of eukaryotic translation initiation factor eIF2α ... and the pro-apoptotic kinase ROCK1. Stress granules and processing bodies share RNA and protein components, both appear under ... and because the aggregates are resistant to proteases. It has also been proposed that microtubules play a role in the formation ... Delestienne N, Wauquier C, Soin R, Dierick JF, Gueydan C, Kruys V (June 2010). "The splicing factor ASF/SF2 is associated with ...

*Biochemical cascade

... of a serine protease and its glycoprotein co-factors are activated to become active components that then catalyze the next ... Recruitment of FAK by integrin leads to Akt activation and this inhibits pro-apoptotic factors like BAD and Bax. When adhesion ... The transcriptional factors are activated by the primary messengers, in most cases, due to their function as nuclear receptors ... FGF (Fibroblast Growth Factor) ligands bind to receptors tyrosine kinase, FGFR (Fibroblast Growth Factor Receptors), and form a ...

*STAT5

Activated STAT5 dimers are, however, short-lived and the dimers are made to undergo rapid deactivation. Deactivation may be ... For example, mutations may lead to increased expression of anti-apoptotic genes, the products of which actively prevent cell ... Indirect inhibition targets kinases associated with STAT5, or targets proteases that carry out terminal truncation of proteins ... Cytokine Growth Factor Rev. 10 (2): 131-57. doi:10.1016/S1359-6101(99)00011-8. PMID 10743504. Nosaka T, Kawashima T, Misawa K, ...

*Rho-associated protein kinase

The pro-apoptotic protease, caspase 3, activates ROCK kinase activity by cleaving the C-terminal PH domain. As a result, the ... elongation factor, translation co-factor), MARCKS (myristylated alanine-rich C kinase substrate), Caponin (unknown function), ... Active ROCK in these cells seems to stimulate the disruption of E-Cadherin-mediated cell-cell contacts by activating actomyosin ... ROCKs contribute to neurite retraction by inducing growth cone collapse by activating actomyosin contractility. It is also ...

*Collectin

"A second serine protease associated with mannan-binding lectin that activates complement". Nature. 386 (6624): 506-510. doi: ... SP-A can also bind to TLR2 (toll-like receptor 2). This interaction causes decrease of TNF-α (tumor necrosis factor-α) ... Collectins SP-A and SP-D enhance clearance of apoptotic cells by macrophages. Collectins are linked with activation of lectin ... SP-A and SP-D can suppress activated T-lymphocytes and IL-2 (interleukin-2) production. SP-D increases bacterial antigen ...

*Geoffrey M. Cooper

Identification of the MDM2 oncoproteinas a substrate for CPP32-like apoptotic proteases. J. Biol. Chem. 272:15049-15052. Lopes ... apoptotic transcriptional program mediated by inhibition of FOXO and non-canonical activation of NFkappaB transcription factors ... B-Raf inhibits programmed cell death downstream of cytochrome c release from mitochondria by activating the MEK/Erk pathway. ... Mammalian transcription factor LSF is a target of ERK signaling. J. Cell. Biochem. 89:733-746. Hartley, D. and Cooper, G.M. ...

*PSEN1

regulation of epidermal growth factor-activated receptor activity. • regulation of resting membrane potential. • regulation of ... apoptotic process. • activation of MAPKK activity. • thymus development. • positive regulation of coagulation. • negative ... such that they either directly regulate gamma secretase activity or themselves are protease enzymes. Multiple alternatively ... negative regulation of epidermal growth factor-activated receptor activity. • cell adhesion. • hematopoietic progenitor cell ...

*Caspase 8

"TRAF1 is a substrate of caspases activated during tumor necrosis factor receptor-alpha-induced apoptosis". J. Biol. Chem. 276 ( ... Caspases exist as inactive proenzymes composed of a prodomain, a large protease subunit, and a small protease subunit. ... This protein is involved in the programmed cell death induced by Fas and various apoptotic stimuli. The N-terminal FADD-like ... Further work revealed that caspase-8 was essential for the induction of the transcription factor "nuclear factor κB" (NF-κB) ...
According to biochemical assays, the Bcl-2 protein Diva from mouse regulates programmed cell death by heterodimerizing with other members of the family and by interacting with the apoptotic protease-activating factor Apaf-1. In typical Bcl-2 heterodimers, peptide fragments comprising the Bcl-2 homology domain 3 (BH3 domain) of proapoptotic members are capable of forming functional complexes with prosurvival proteins. High-resolution structural studies have revealed that the BH3 peptide forms an α-helix positioned in a canonical hydrophobic cleft of the antiapoptotic protein. Because Diva shows mutations in conserved residues within this area, it has been proposed to have a different interacting surface. However, we showed previously that Diva binds through the canonical groove the BH3 peptide of the human Bcl-2 killing member Harakiri. To further test Divas binding capabilities, here we show Nuclear Magnetic Resonance (NMR) data, indicating that Diva binds peptides derived from the BH3 domain ...
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Apoptosis is a controlled form of cellular demolition, catalyzed by a family of cysteine proteases called caspases. In response to diverse proapoptotic stimuli, caspase-9 is recruited and activated within an oligomeric complex called the apoptosome. The apoptosome drives autocatalytic processing of caspase-9, triggering a proteolytic caspase cascade that results in the biochemical and morphological changes characteristic of cell death. It is unclear why caspase-9 undergoes autocatalytic processing following apoptosome recruitment, because interdomain processing is dispensable for caspase-9 activity. A study has shed light on this issue by demonstrating that caspase-9 processing within the apoptosome promotes its displacement from the complex, leading to inactivation of this protease. Thus, autoprocessing of caspase-9 within the apoptosome serves as a "molecular timer" that limits the proteolytic activity of this complex through displacement of bound caspase-9 molecules. This timer mechanism may ...
Because neither E2F1 overexpression nor derepression with the addition of TSA alone was able to induce Apaf-1 up-regulation in mature neurons (Figs. 4 c and 5 a), we hypothesized that this region of chromatin may be highly repressed in mature neurons. Indeed, expression of E2F1 in the presence of TSA induced a marked transcriptional increase in Apaf-1 (Fig. 5 c) and rendered mature P28 neurons sensitive to cytochrome c (Fig. 5 d). This sensitivity of P28 neurons was dependent on the up-regulation of Apaf-1, as neurons isolated from Apaf-1-deficient mice failed to undergo cytochrome c-induced apoptosis after TSA and E2F1 treatment (Fig. 5 e). These data support the model that neuronal maturation is accompanied by increased repression of Apaf-1 at the level of chromatin structure.. We tested this model directly with a chromatin immunoprecipitation (ChIP) assay using antibodies to acetylated histone 3 (AcH3), which is indicative of active chromatin, and histone 3 trimethylated on lysine 9 (MeH3K9), ...
... ; Caspase-9 precursor (EC 3.4.22.-) (CASP-9) (ICE-like apoptotic protease 6) (ICE-LAP6) (Apoptotic protease Mch-6) (Apoptotic protease activating factor 3) (APAF-3). [Source:Uniprot/SWISSPROT;Acc:P55211 ...
Expression of APAF1 (APAF-1, CED4) in cancer tissue. The cancer tissue page shows antibody staining of the protein in 20 different cancers.
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The invention relates to an isolated nucleic acid molecule encoding a caspase-14 polypeptide or functional fragment thereof, a vector that contains the nucleic acid molecule and a host cell that contains the vector. The invention also relates to an isolated gene encoding caspase-14, as well as functional fragments thereof. The gene or nucleic acid molecule can include single or double stranded nucleic acids corresponding to coding or non-coding strands of the caspase-14 nucleotide sequence. Isolated caspase-14 polypeptides or functional fragments thereof are also provided, as are antibodies that specifically bind thereto. In addition, the invention relates to methods of identifying compounds that modulate caspase-14 activity.
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 ...
... , Authors: Frank A. Kruyt. Published in: Atlas Genet Cytogenet Oncol Haematol.
Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.
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Apoptotic signaling is altered at many loci in cancer cells. Although many tumors develop resistance to cytochrome c-induced apoptosis, we have discovered that breast cancer cells exhibit a unique hypersensitivity to cytochrome c-induced apoptosis. Interestingly, this sensitivity is not due to changes in core apoptosomal proteins ( 44) but is due to a PHAPI-mediated posttranslational event that enhances the recruitment of caspase-9 to the Apaf-1 CARD. These findings have the potential to affect breast cancer chemotherapy through the development of apoptosome activators or cytochrome c mimetics as shown, in principle, by the fact that malignant mammary epithelial cells could be more easily killed by cytosolic cytochrome c than their normal counterparts.. PHAPI-mediated increase in caspase activation in breast cancer. Whereas many inhibitory signaling pathways converge on the apoptosome, there are very few physiologic/pathologic examples of enhanced apoptosome activation. Our data suggest that ...
The effect was found to be associated with increased expression of E2F-1 in cervical cancer cells as there is no CAPE-mediated induction of E2F-1 in the precancerous cervical Z172 cells. CAPE also upregulated the E2F-1 target genes cyclin A, cyclin E, and apoptotic protease activation of factor 1 (Apaf-1) but down regulated cyclin B and myeloid leukemia cell differentiation protein (Mcl-1). These results suggested the involvement of E2F-1 in CAPE-mediated growth inhibition and cell cycle arrest. Transient transfection studies with luciferase reporters revealed that CAPE altered transcriptional activity of the apaf-1 and mcl-1 promoters. Further studies using chromatin immunoprecipitation (ChIP) assays demonstrated that in CAPE-treated cells, E2F-1 binding to the apaf-1 and cyclin B promoters was increased and decreased, respectively. Furthermore, E2F-1 silencing abolished CAPE-mediated effects on cell cycle arrest, apoptosis, and related gene expression ...
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The present study examined levels of various components of the cell death machinery and drug sensitivity of 60 human cancer cell lines to anticancer drugs. With the exception of procaspase-3, which was undetectable in MCF-7 cells, caspases-2, -3, -6, -7, -8, and -9, as well as Apaf-1, were detectable in all 60 cell lines. Although these components of the cell death machinery varied widely in abundance, strong correlations between levels of Apaf-1 or procaspase-2, -3, -6, -8, or -9 and sensitivity to any class of antineoplastic agent were not observed. These results, although negative, have several important implications.. The attempt to correlate drug sensitivity with levels of various components of the cell death machinery was prompted by previous studies indicating that drug-induced apoptosis is markedly diminished when certain key components of the core cell-death machinery, particularly Apaf-1, procaspase-9, or procaspase-3, are genetically or functionally deleted (36, 37, 38 , 58 , 88 , 99) ...
Diva (death inducer binding to vBcl-2 and Apaf-1) is a Bcl-2 family member, and has been reported to play roles in apoptosis and oocyte maturation. Diva has also been shown to interact with Nm23-H2/NDPK B, which is involved in cellular differentiation. The main aim of this study was to elucidate the function and possible mechanisms for Diva in cellular differentiation in the brain. In the present study, in PC-12 cells, Diva expression was decreased after differentiation and reciprocally, NDPK B expression was increased and it translocated into the nucleus. Endogenous Diva was also shown to interact with both ß-tubulin and NDPK B. Overexpression of Diva in PC-12 cells did not change the expression level of NDPK B, but inhibited its nuclear localization. Diva-overexpressing cells had a decreased percentage of differentiated cells and average neurite length was shortened. This was due to the formation of more Diva/NDPK B and Diva/ß-tubulin complexes, at the expense of NDPK B/ß-tubulin complexes. ...
Chris Cory is currently on a nationwide tour with DIVA DOG, partnering with animal rescue groups and pit bull advocacy organizations. So far, we have brought DIVA DOGs message to LA, Philadelphia, Portland (OR), Kansas City, Fredericksburg (VA) and now Toronto. We are starting to go international! Hoping to bring DIVA DOG to the UK by Labor Day.. The next stops on the DIVA DOG tour are Montclair (NJ), NYC and Birmingham(AL). Woo-hoo! All upcoming events info is in our Monthly Newsletter/E-Zine. Keep on the lookout for some new and exciting DIVA DOG events in July and August to commemorate Coral the Diva Dogs birthday July 23. We will be working with a wonderful rescue called Mariahs Promise in Colorado and bringing DIVA DOG right to the Denver area, where BSL (breed-specific legislation) is really destroying homes and families, as pit bulls are ripped from their families based soley upon their breed. To learn more about the seriousness of this issue and how BSL is something that MUST be ...
Chris Cory is currently on a nationwide tour with DIVA DOG, partnering with animal rescue groups and pit bull advocacy organizations. So far, we have brought DIVA DOGs message to LA, Philadelphia, Portland (OR), Kansas City, Fredericksburg (VA) and now Toronto. We are starting to go international! Hoping to bring DIVA DOG to the UK by Labor Day.. The next stops on the DIVA DOG tour are Montclair (NJ), NYC and Birmingham(AL). Woo-hoo! All upcoming events info is in our Monthly Newsletter/E-Zine. Keep on the lookout for some new and exciting DIVA DOG events in July and August to commemorate Coral the Diva Dogs birthday July 23. We will be working with a wonderful rescue called Mariahs Promise in Colorado and bringing DIVA DOG right to the Denver area, where BSL (breed-specific legislation) is really destroying homes and families, as pit bulls are ripped from their families based soley upon their breed. To learn more about the seriousness of this issue and how BSL is something that MUST be ...
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Curators comment: (updated: 22 Mar 2007 23:30:25 GMT). The simulation image shown corresponds to active caspase-3 temporal evolution for Apaf-1 concentration of 20nM as depicted in Fig-2A of the paper. Result obtained from MathSBML.. ...
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The apoptosome is the cellular structure that facilitates programmed cell death. A new 3D map of it lays groundwork for future drug development.
14-3-3 tau mediates E2F1 stabilization. 14-3-3 tau interacts with ATM-phosphorylated E2F1 during DNA damage and inhibits E2F1 ubiquitination. 14-3-3 tau is also required for expression and induction of E2F1 apoptotic targets, such as p73, Apaf-1, and caspases, during DNA damage ...
Expression of CASP9 (APAF-3, ICE-LAP6, MCH6, PPP1R56) in vagina tissue. Antibody staining with HPA001473, HPA046488 and CAB004348 in immunohistochemistry.
Apoptosis or programmed cell death is a process with typical morphological characteristics including plasma membrane blebbing, cell shrinkage, chromatin condensation and fragmentation. A family of cystein-dependent aspartate-directed proteases, called caspases, is responsible for the proteolytic cleavage of cellular proteins leading to the characteristic apoptotic features, e.g. cleavage of caspase-activated DNase resulting in internucleosomal DNA fragmentation. Currently, two pathways for activating caspases have been studied in detail. One starts with ligation of a death ligand to its transmembrane death receptor, followed by recruitment and activation of caspases in the death-inducing signalling complex. The second pathway involves the participation of mitochondria, which release caspase-activating proteins into the cytosol, thereby forming the apoptosome where caspases will bind and become activated. In addition, two other apoptotic pathways are emerging: endoplasmic reticulum stress-induced ...
Proteasome inhibitors including bortezomib have attracted considerable attention as potential anticancer agents, but the mechanism(s) by which proteasome inhibitors induce apoptosis is poorly understood. In the present study, we provided evidence using the human Jurkat T-cell leukemic cell line with or without stable silencing of the key adaptor protein, Apaf-1, that bortezomib-induced apoptosis but not Fas (death receptor)-mediated apoptosis is dependent on Apaf-1 expression. Furthermore, we noted that expression of Apaf-1 was variable in a panel of pediatric ALL patient samples, and Apaf-1 expression was absent altogether in one patient. The primary cells presented with a high degree of spontaneous apoptosis upon ex vivo culture; however, the Apaf-1-deficient sample presented the lowest sensitivity toward bortezomib-induced apoptosis, thus providing correlative evidence for a role of Apaf-1 in bortezomib-induced cell killing (defects in other apoptosis signaling pathways may also come into ...
As previously reported, recombinant xEIAP/XLX is rapidly degraded by at least two distinct, consecutively acting proteolytic systems [11, 14]. Within 2 h incubation, xEIAP/XLX is significantly degraded in both CSF-arrested and interphase egg extracts in a C-terminal RING finger-dependent manner. Subsequently, spontaneous cytochrome c-induced caspase activation begins after 4 h incubation in interphase egg extracts (apoptotic egg extracts), and the remaining xEIAP/XLX is cleaved by the activated caspases at yet unidentified site(s). This caspase activation is delayed or suppressed in CSF-arrested egg extracts by a p42MAPK-dependent pathway [7-11]. We found that the electrophoretic mobilities of recombinant 6XHis-tagged (6XHis-FL) and MBP-tagged (MBP-FL) xEIAP/XLX slightly decreased during incubation in CSF-arrested but not interphase egg extracts (Fig. 1B), whereas those of other BIR family proteins (xSurvivin1/xBIR1, xSurvivin2/SIX, and xXIAP) did not (data not shown). However, the rapid ...
Complete information for CARD10 gene (Protein Coding), Caspase Recruitment Domain Family Member 10, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Induction of apoptosis and NF-kB activation by Apaf-1/Nod1 family members and DD proteins (Inohara et al., 2000). The more recent study suggested that IKKgamma binds to the site in C-terminal regulatory region of IKKbeta which is located after the HLH motif. Images ...
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Most drug discovery efforts focus on generating inhibitors leading to loss-of-function phenotypes. My lab has been focusing on discovering ways to activate enzymes leading to gain-of-function phenotypes. Many enzymes such as proteases and kinases are stored in dormant "off" forms that are subsequently activated through post-translational modification. Work will be presented for discovery of small molecule activators for the apoptotic proteases known as caspases, as well a Ser-Thr kinase PDK-1. Our group is also developing split-proteins that can be activated by orthogonal small molecule dimerizers to phenocopy the effects seen from the small molecule activators. Such protein activators allow one to ignite signaling from specific nodes and thus probe the sufficiency of enzyme activity to drive a cellular response. Protein activation, as opposed to inhibition, expands the landscape for drug discovery.. Citation Format: James A. Wells, Dennis Wolan, Julie Zorn, Debajyoti Datta, Daniel Gray, Jack ...
Units: umol/l. Method: spatial interpolation produced with DIVA (Data-Interpolating Variational Analysis). URL: http://modb.oce.ulg.ac.be/DIVA. Comment: Every year of the time dimension corresponds to a 10-year centred average for the autumn season (Sep-Nov). Diva settings: Snr=1.0, CL=0.7 ...
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... by heterodimerizing with other members of the family and by interacting with the apoptotic protease-activating factor Apaf-1. ... The structure of transcription termination factor Nrd1 reveals an original mode for GUAA recognition. ... Altogether, our results shed light on important factors governing Diva-BH3 peptide molecular recognition mode. ... Cyclic amino acid linkers stabilizing key loops of brain derived neurotrophic factor. ...
more infohttps://pesquisa.bvsalud.org/portal/?lang=pt&q=au:%22Santiveri,%20Clara%20M%22

DNA and factor VII-activating protease protect against the cytotoxicity of histones | Blood AdvancesDNA and factor VII-activating protease protect against the cytotoxicity of histones | Blood Advances

18 or apoptotic or (secondary) necrotic cells.12,26⇓⇓⇓-30 For apoptotic and necrotic cells, both passive and active mechanisms ... Factor seven activating protease (FSAP): does it activate factor VII? J Thromb Haemost. 2012;10(5):859-866. ... We previously established that the serine protease factor VII-activating protease (FSAP) is activated in serum upon incubation ... Nucleosome-releasing factor: a new role for factor VII-activating protease (FSAP). FASEB J. 2008;22(12):4077-4084. ...
more infohttp://www.bloodadvances.org/content/1/26/2491?sso-checked=true

Apaf1 - Apoptotic protease-activating factor 1 - Mus musculus (Mouse) - Apaf1 gene & proteinApaf1 - Apoptotic protease-activating factor 1 - Mus musculus (Mouse) - Apaf1 gene & protein

Oligomeric Apaf-1 mediates the cytochrome c-dependent autocatalytic activation of pro-caspase-9 (Apaf-3), leading to the ... Apoptotic protease-activating factor 1UniRule annotation. ,p>Information which has been generated by the UniProtKB automatic ... tr,G3XA09,G3XA09_MOUSE Apoptotic protease-activating factor 1 OS=Mus musculus OX=10090 GN=Apaf1 PE=1 SV=1 ... IPR017251. Apaf-1. IPR037963. APAF1_CARD_dom. IPR024977. Apc4_WD40_dom. IPR001315. CARD. IPR011029. DEATH-like_dom_sf. ...
more infohttp://www.uniprot.org/uniprot/G3XA09

Requirement of Apoptotic Protease-Activating Factor-1 for Bortezomib-Induced Apoptosis but Not for Fas-Mediated Apoptosis in...Requirement of Apoptotic Protease-Activating Factor-1 for Bortezomib-Induced Apoptosis but Not for Fas-Mediated Apoptosis in...

apoptotic protease-activating factor 1. B-CLL. B-cell chronic lymphoblastic leukemia. BH3. Bcl-2 homology domain 3. DEVD-AMC. ... Requirement of Apoptotic Protease-Activating Factor-1 for Bortezomib-Induced Apoptosis but Not for Fas-Mediated Apoptosis in ... Requirement of Apoptotic Protease-Activating Factor-1 for Bortezomib-Induced Apoptosis but Not for Fas-Mediated Apoptosis in ... 2005) Plasma membrane sequestration of apoptotic protease-activating factor-1 in human B-lymphoma cells: a novel mechanism of ...
more infohttp://molpharm.aspetjournals.org/content/83/1/245

Apoptotic protease-activating factor 1Apoptotic protease-activating factor 1

positive regulation of apoptotic signaling pathway 23 intrinsic apoptotic signaling pathway in response to endoplasmic ... The apoptosome binds and cleaves caspase 9 preproprotein, releasing its mature, activated form. Activated caspase 9 stimulates ... cellular response to transforming growth factor beta stimulus 54 activation of cysteine-type endopeptidase activity involved in ... activation of cysteine-type endopeptidase activity involved in apoptotic process 80 ...
more infohttps://pharos.nih.gov/idg/targets/O14727

Mitochondrial-Shaping Proteins in Cardiac Health and Disease - the Long and the Short of It! | SpringerLinkMitochondrial-Shaping Proteins in Cardiac Health and Disease - the Long and the Short of It! | SpringerLink

BAK and Apoptotic protease activating factor 1 (APAF1) to amplify cell death caused by certain factors such as BID and ... cytosolic calcium overload which occurs during acute IRI may activate calcineurin thereby dephosphorylating and activating Drp1 ... as well as mitochondrial transcription factor A (TFAM) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha ... The apoptotic protein tBid promotes leakage by altering membrane curvature. J Biol Chem. 2002;277:32632-9.PubMedCrossRefGoogle ...
more infohttps://link.springer.com/article/10.1007%2Fs10557-016-6710-1

p53- and Bax-Mediated Apoptosis in Injured Rat Spinal Cord | SpringerLinkp53- and Bax-Mediated Apoptosis in Injured Rat Spinal Cord | SpringerLink

Apoptotic protease activating factor 1. ATM. Ataxia telangiectasia mutated. ATR. Ataxia telangiectasia and Rad3 related ... Expression of APAF1, caspase 9 and caspase 3 activities confirmed the intrinsic apoptotic pathway after SCI. Activated p53 and ... Apoptotic cytosol facilitates Bax translocation to mitochondria that involves cytosolic factor regulated by Bcl-2. Cancer Res ... Eve DJ, Dennis JS, Citron BA (2007) Transcription factor p53 in degenerating spinal cords. Brain Res 1150:174-181PubMedCrossRef ...
more infohttps://link.springer.com/article/10.1007%2Fs11064-011-0530-2

Polyphenols in Colorectal Cancer: Current State of Knowledge including Clinical Trials and Molecular Mechanism of ActionPolyphenols in Colorectal Cancer: Current State of Knowledge including Clinical Trials and Molecular Mechanism of Action

Apoptotic protease activating factor 1. APC:. Activated protein C. Bax:. Bcl-2-associated X protein. ... EGFR: epidermal growth factor receptor, TGFβ R1/2: transforming growth factor, beta receptor 1/2, EMT: epithelial-mesenchymal ... Transforming growth factor-β (TGF-β) is a multifunctional polypeptide that binds to specific TGF-β receptors for paracrine and ... Caffeic acid showed apoptotic cell death against HCT 15 cell lines although IC50 value was very high (800 μM). Similar findings ...
more infohttps://www.hindawi.com/journals/bmri/2018/4154185/

Molecules  | Free Full-Text | Astaxanthin Protects PC12 Cells against Homocysteine- and Glutamate-Induced Neurotoxicity | HTMLMolecules | Free Full-Text | Astaxanthin Protects PC12 Cells against Homocysteine- and Glutamate-Induced Neurotoxicity | HTML

... activating cascade of caspases involving caspases 12 and 3. Conclusively, the damages caused by Glu and Hcy to PC12 cells can ... The mechanisms of action include: (1) increasing calcium influx; (2) producing ROS; (3) initiating lipid peroxidation; (4) ... apoptotic protease activating factor 1). ... Figure 7. Summary of the apoptotic pathways induced by ... Chang, C.H.; Chen, C.Y.; Chiou, J.Y.; Peng, R.Y.; Peng, C.H. Astaxanthine secured apoptotic death of PC12 cells induced by beta ...
more infohttps://www.mdpi.com/1420-3049/25/1/214/htm

APAF1 peptide (ab7873) | AbcamAPAF1 peptide (ab7873) | Abcam

Apoptotic protease activating factor. *Apoptotic protease activating factor 1. *Apoptotic protease-activating factor 1 ... Oligomeric Apaf-1 mediates the cytochrome c-dependent autocatalytic activation of pro-caspase-9 (Apaf-3), leading to the ... Contains 1 CARD domain.. Contains 1 NB-ARC domain.. Contains 13 WD repeats. ... Apoptotic peptidase activating factor 1. * ...
more infohttp://www.abcam.com/apaf1-peptide-ab7873.html

Autophagic and Apoptotic Effects of HDAC Inhibitors on Cancer CellsAutophagic and Apoptotic Effects of HDAC Inhibitors on Cancer Cells

Apoptotic protease-activating factor 1. Atg:. Autophagy-related gene. BAPTA:. 1,2-bis(o-aminophenoxy)ethane-N,N,. -tetraacetic ... In both pathways, activated caspases (cysteine aspartic acid-specific proteases) cleave their substrates and activate other ... the p53 tumor-suppressor protein is stabilized and activated as a transcription factor, capable of inducing apoptosis. Nuclear ... At that time, ERK was specifically activated at a lower concentration but not at a higher concentration of retinamide [57].(11) ...
more infohttps://www.hindawi.com/journals/bmri/2011/830260/

Anti-Caspase-9 antibody [10-1-87] (ab115792) | AbcamAnti-Caspase-9 antibody [10-1-87] (ab115792) | Abcam

10-1-87] validated for WB and tested in Human. Immunogen corresponding to recombinant full length protein ... Apoptotic protease Mch-6 antibody. *Apoptotic protease-activating factor 3 antibody. *CASP-9 antibody ... All lanes : Anti-Caspase-9 antibody [10-1-87] (ab115792) at 1 µg/ml. Lane 1 : Jurkat cell lysate. Lane 2 : Jurkat cell lysate, ... Binding of caspase-9 to Apaf-1 leads to activation of the protease which then cleaves and activates caspase-3. Proteolytically ...
more infohttp://www.abcam.com/caspase-9-antibody-10-1-87-ab115792.html

Expanded functions for a family of plant intracellular immune receptors beyond specific recognition of pathogen effectors | PNASExpanded functions for a family of plant intracellular immune receptors beyond specific recognition of pathogen effectors | PNAS

2005) Structure of the apoptotic protease-activating factor 1 bound to ADP. Nature 434:926-933. ... 2F). Hence, recognition of one or more MAMPs expressed by Pto DC3000ΔhrpL activates MTI responses that result in SA ... Hence, ADR1-L2 is not activated via the canonical mechanism used by NB-LRR and NLR receptors as microbial sensors, at least for ... STAND proteins are molecular switches that toggle from an ADP-bound "off" position to an ATP-bound "on" state that activates ...
more infohttps://www.pnas.org/content/108/39/16463

Growth Factor Signaling in Cell Survival: Implications for Cancer Treatment | Journal of Pharmacology and Experimental...Growth Factor Signaling in Cell Survival: Implications for Cancer Treatment | Journal of Pharmacology and Experimental...

Once in the cytoplasm, cytochrome c binds to apoptotic protease-activating factor-1, which binds and activates caspase-9 ... apoptotic protease-activating factor 1; PKA, cAMP-dependent protein kinase; ANT, adenine nucleotide transporter. ... nerve growth factor), brain-derived neurotrophic factor, and growth factors (insulin-like growth factor-1, platelet-derived ... Protection from growth factor withdrawal-induced cell death through enforced expression of anti-apoptotic Bcl-2 family members ...
more infohttp://jpet.aspetjournals.org/content/298/3/873

Expression of APAF1 in cancer - Summary - The Human Protein AtlasExpression of APAF1 in cancer - Summary - The Human Protein Atlas

APAF-1, CED4) in cancer tissue. The cancer tissue page shows antibody staining of the protein in 20 different cancers. ... Apoptotic protease-activating factor 1 Show all. Predicted intracellular proteins. Plasma proteins. Cancer-related genes. ... Apoptotic peptidase activating factor 1. Protein classi. Protein class the gene product belongs to according to selected gene ... Apoptotic peptidase activating factor 1 (HGNC Symbol). Entrez gene summary. This gene encodes a cytoplasmic protein that ...
more infohttp://www.proteinatlas.org/ENSG00000120868-APAF1/pathology

Luteolin inhibits multi-heavy metal mixture-induced HL7702 cell apoptosis through downregulation of ROS-activated mitochondrial...Luteolin inhibits multi-heavy metal mixture-induced HL7702 cell apoptosis through downregulation of ROS-activated mitochondrial...

2772), apoptotic protease activating factor 1 (Apaf1; cat. no. 8969), cleaved caspase-9 (cat. no. 7237), caspase-3 (cat. no. ... Apoptotic analysis. Multi-heavy metal mixture induced HL7702 cell apoptosis in a dose-dependent manner, while 20 μM luteolin ... Apoptotic assays revealed that the multi-heavy metal mixture induced HL7702 cell apoptosis in a dose-dependent manner, which ... Certain harmful extracellular factors may break this balance, resulting in excessive ROS generation beyond the cell scavenging ...
more infohttps://www.spandidos-publications.com/ijmm/41/1/233

Harte MT[au] - PubMed - NCBIHarte MT[au] - PubMed - NCBI

Regulation of apoptotic protease activating factor-1 oligomerization and apoptosis by the WD-40 repeat region. ... Mutations within subdomain II of the extracellular region of epidermal growth factor receptor selectively alter TGF alpha ... 2016 Oct 5;109(1). doi: 10.1093/jnci/djw199. Print 2017 Jan. ... 1.. Activation of STING-Dependent Innate Immune Signaling By S- ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed?cmd=search&term=Harte+MT%5Bau%5D&dispmax=50

Cytochrome c - WikipediaCytochrome c - Wikipedia

Upon release of cytochrome c to the cytoplasm, the protein binds apoptotic protease activating factor-1 (Apaf-1).[5] ... This release of cytochrome c in turn activates caspase 9, a cysteine protease. Caspase 9 can then go on to activate caspase 3 ... Pro-apoptotic:. BAX. BAK1/Bcl-2 homologous antagonist killer. Bcl-2-associated death promoter. Anti-apoptotic:. Bcl-2. Bcl-xL. ... intrinsic apoptotic signaling pathway. • activation of cysteine-type endopeptidase activity involved in apoptotic process by ...
more infohttps://en.wikipedia.org/wiki/Cytochrome_C

Programmed cell death - WikipediaProgrammed cell death - Wikipedia

Knockout or inhibition of apoptotic protease activating factor 1 (APAF1), also results in malformations and increased embryonic ... An atrophic factor is a force that causes a cell to die. Only natural forces on the cell are considered to be atrophic factors ... Anoikis Apoptosis-inducing factor Apoptosis versus Pseudoapoptosis Apoptosome Apoptotic DNA fragmentation Autolysis (biology) ... Solomon M, Belenghi B, Delledonne M, Menachem E, Levine A (1999). "The involvement of cysteine proteases and protease inhibitor ...
more infohttps://en.wikipedia.org/wiki/Programmed_cell_death

IJERPH  | Free Full-Text | Cellular and Mitochondrial Effects of Alcohol Consumption | HTMLIJERPH | Free Full-Text | Cellular and Mitochondrial Effects of Alcohol Consumption | HTML

Apoptotic protease activating factor-1; ATP, adenosine triphosphate; ADP, adenosine diphosphate. ... Apoptotic protease activating factor-1; ATP, adenosine triphosphate; ADP, adenosine diphosphate. ... favoring the translocation to the mitochondria of the pro-apoptotic factor Bax that forms a complex with a voltage-dependent ... favoring the translocation of the pro-apoptotic factor bax, which forms a complex with voltage-dependent anion channel (VDAV). ...
more infohttps://www.mdpi.com/1660-4601/7/12/4281/htm

Anti-Mouse (Murine) APAF1 antibody for Immunohistochemistry (Paraffin-embedded Sections) (IHC (p))Anti-Mouse (Murine) APAF1 antibody for Immunohistochemistry (Paraffin-embedded Sections) (IHC (p))

Apoptotic protease-activating factor 1, KIAA0413 Gene ID 317 NCBI Accession NP_001151 ... Apoptotic peptidase activating factor 1, also known as APAF1, is a protein which in humans is encoded by the APAF1 gene. This ... Apoptotic Peptidase Activating Factor 1 (APAF1) Antibodies show synonyms for this antigen * APAF1 ... Images for product: anti-Apoptotic Peptidase Activating Factor 1 (APAF1) (N-Term) antibody ...
more infohttp://www.antibodies-online.com/p53-signaling-pathway-2/apaf1-antibody-180/mouse-ihc-p-2157/

anti-APAF1 antibody (Apoptotic Peptidase Activating Factor 1) (AA 12-28)</span...anti-APAF1 antibody (Apoptotic Peptidase Activating Factor 1) (AA 12-28)</span...

... for Apoptosis Protease Activating Factor-1). Cytochrome c associates with APAF-1 in the presence of dATP or ATP and induces an ... anti-APAF1 antibody (Apoptotic Peptidase Activating Factor 1) (AA 12-28) APAF1 antibody (Apoptotic Peptidase Activating Factor ... Apoptotic Peptidase Activating Factor 1 (APAF1) show synonyms for this antigen * APAF1 ... anti-Apoptotic Peptidase Activating Factor 1 (APAF1) (AA 12-28) antibody (Image 2) Read product details ...
more infohttp://www.antibodies-online.com/antibody/967648/anti-Apoptotic+Peptidase+Activating+Factor+1+APAF1+AA+12-28+antibody/

Polarized Scorpion Venom Solution and a Method for Making Polarized Scorpion Venom Solution - Mikaelian, ArthurPolarized Scorpion Venom Solution and a Method for Making Polarized Scorpion Venom Solution - Mikaelian, Arthur

... "apoptotic protease activating factor-1"). Using the energy provided by ATP, these complexes aggregate to form apoptosomes. The ... Some examples of positive signals: growth factors for neurons; and Interleukin-2 (IL-2), an essential factor for the mitosis of ... Cell survival is maintained by a balance between pro-apoptotic and anti-apoptotic stimuli. Dysregulation of apoptosis can ... They are all proteases. They get their name because they cleave proteins, mostly each other, at aspartic acid (Asp) residues. ...
more infohttp://www.freepatentsonline.com/y2009/0123558.html

Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade.  - PubMed - NCBICytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade. - PubMed - NCBI

Apoptotic Protease-Activating Factor 1. *Cytochrome c Group. *Deoxyadenine Nucleotides. *Multienzyme Complexes ... Activated caspase-9 in turn cleaves and activates caspase-3. Depletion of caspase-9 from S-100 extracts diminished caspase-3 ... indicating that caspase-9 is the most upstream member of the apoptotic protease cascade that is triggered by cytochrome c and ... We report here the purification of the third protein factor, Apaf-3, that participates in caspase-3 activation in vitro. Apaf-3 ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/9390557?dopt=Abstract
  • It is also becoming clear that mitosis and apoptosis are toggled or linked in some way and that the balance achieved depends on signals received from appropriate growth or survival factors. (wikipedia.org)
  • The extrinsic pathway of apoptosis is triggered by external signals that activate cell surface death receptors, including Fas. (thefreelibrary.com)
  • Under physiological conditions plasmin activates growth factors resulting in the generation of survival signals, as required during wound healing ( 8 ). (mcponline.org)
  • Cellular conditions experienced during energy-limited states - elevated calcium, shifts in cellular adenylate status, compromised mitochondrial membrane potential - are precisely those that trigger, at least in mammals, the mitochondrion to initiate opening of the permeability transition pore, to assemble additional protein release channels, and to release pro-apoptotic factors. (biologists.org)
  • The report 'Proprotein Convertase SubtilisinKexin Type 9 - Pipeline Review, H1 2018' outlays comprehensive information on the Proprotein Convertase Subtilisin/Kexin Type 9 (Proprotein Convertase 9 or Neural Apoptosis Regulated Convertase 1 or Subtilisin/Kexin Like Protease PC9 or PCSK9 or EC 3.4.21. (researchandmarkets.com)
  • These proteases are synthesized as inactive proenzymes which, upon proteolytic cleavage at aspartate residues, form an active complex composed of two heterodimeric subunits. (rupress.org)
  • In addition, the induction of autophagy has been also observed in malignant cells following treatment with histone deacetylase (HDAC) inhibitors [ 1 ]. (hindawi.com)
  • Class III PI3K complex, containing hVps34, Beclin-1, p150 and Atg14-like protein or ultraviolet irradiation resistance-associated gene (UVRAG), is required for the induction of autophagy. (wikipedia.org)
  • Therefore, permeabilization of the outer mitochondrial membrane (OMM) is considered a crucial event during the early phase of the apoptotic process. (rsc.org)