A CARD signaling adaptor protein that plays a role in the mitochondria-stimulated apoptosis (APOPTOSIS, INTRINSIC PATHWAY). It binds to CYTOCHROME C in the CYTOSOL to form an APOPTOSOMAL PROTEIN COMPLEX and activates INITIATOR CASPASES such as CASPASE 9.
A 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.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
A 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.
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.
Exogenous and endogenous compounds which inhibit CYSTEINE ENDOPEPTIDASES.
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.
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.
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)
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.
Compounds which inhibit or antagonize biosynthesis or actions of proteases (ENDOPEPTIDASES).
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.
Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.
Hydrolases that specifically cleave the peptide bonds found in PROTEINS and PEPTIDES. Examples of sub-subclasses for this group include EXOPEPTIDASES and ENDOPEPTIDASES.
A subclass of PEPTIDE HYDROLASES that catalyze the internal cleavage of PEPTIDES or PROTEINS.
A subclass of peptide hydrolases that depend on a CYSTEINE residue for their activity.
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.
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.
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.
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.
Extracellular protease inhibitors that are secreted from FIBROBLASTS. They form a covalent complex with SERINE PROTEASES and can mediate their cellular internalization and degradation.
Exogenous or endogenous compounds which inhibit SERINE ENDOPEPTIDASES.
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.
An in situ method for detecting areas of DNA which are nicked during APOPTOSIS. Terminal deoxynucleotidyl transferase is used to add labeled dUTP, in a template-independent manner, to the 3 prime OH ends of either single- or double-stranded DNA. The terminal deoxynucleotidyl transferase nick end labeling, or TUNEL, assay labels apoptosis on a single-cell level, making it more sensitive than agarose gel electrophoresis for analysis of DNA FRAGMENTATION.
A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts.
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.
Endogenous and exogenous compounds and that either inhibit CASPASES or prevent their activation.
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.
Established cell cultures that have the potential to propagate 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.
Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)
The 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.
The engulfing and degradation of microorganisms; other cells that are dead, dying, or pathogenic; and foreign particles by phagocytic cells (PHAGOCYTES).
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 cell line derived from cultured tumor cells.
A group of lysosomal proteinases or endopeptidases found in aqueous extracts of a variety of animal tissues. They function optimally within an acidic pH range. The cathepsins occur as a variety of enzyme subtypes including SERINE PROTEASES; ASPARTIC PROTEINASES; and CYSTEINE PROTEASES.
A CELL LINE derived from human T-CELL LEUKEMIA and used to determine the mechanism of differential susceptibility to anti-cancer drugs and radiation.
Inhibitors of SERINE ENDOPEPTIDASES and sulfhydryl group-containing enzymes. They act as alkylating agents and are known to interfere in the translation process.
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.
Proteins prepared by recombinant DNA technology.
Peptides composed of between two and twelve amino acids.
Cysteine proteinase found in many tissues. Hydrolyzes a variety of endogenous proteins including NEUROPEPTIDES; CYTOSKELETAL PROTEINS; proteins from SMOOTH MUSCLE; CARDIAC MUSCLE; liver; platelets; and erythrocytes. Two subclasses having high and low calcium sensitivity are known. Removes Z-discs and M-lines from myofibrils. Activates phosphorylase kinase and cyclic nucleotide-independent protein kinase. This enzyme was formerly listed as EC
The 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.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A protein of the annexin family isolated from human PLACENTA and other tissues. It inhibits cytosolic PHOSPHOLIPASE A2, and displays anticoagulant activity.
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 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.
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 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.
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.
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
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.
The rate dynamics in chemical or physical systems.
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.
ENDOPEPTIDASES which use a metal such as ZINC in the catalytic mechanism.
Physiologically inactive substances that can be converted to active enzymes.
The process of cleaving a chemical compound by the addition of a molecule of water.
A family of SERINE ENDOPEPTIDASES isolated from Bacillus subtilis. EC 3.4.21.-
A sub-subclass of endopeptidases that depend on an ASPARTIC ACID residue for their activity.
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.
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 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.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
N-acylated oligopeptides isolated from culture filtrates of Actinomycetes, which act specifically to inhibit acid proteases such as pepsin and renin.
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.
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.
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.
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 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
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.
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.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
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.
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.
Enzymes that catalyze the transfer of multiple ADP-RIBOSE groups from nicotinamide-adenine dinucleotide (NAD) onto protein targets, thus building up a linear or branched homopolymer of repeating ADP-ribose units i.e., POLY ADENOSINE DIPHOSPHATE RIBOSE.
A 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.
Elements of limited time intervals, contributing to particular results or situations.
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.
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 used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
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.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
The sum of the weight of all the atoms in a molecule.
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.
A ubiquitously-expressed cysteine protease that plays an enzymatic role in POST-TRANSLATIONAL PROTEIN PROCESSING of proteins within SECRETORY GRANULES.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
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.)
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.
Proteins found in any species of bacterium.
A long pro-domain caspase that contains a caspase recruitment domain in its pro-domain region. Activation of this enzyme can occur via the interaction of its caspase recruitment domain with CARD SIGNALING ADAPTOR PROTEINS. Caspase 2 plays a role in APOPTOSIS by cleaving and activating effector pro-caspases. Several isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.
A 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
Serine proteinase inhibitors which inhibit trypsin. They may be endogenous or exogenous compounds.
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.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
The relationship between the dose of an administered drug and the response of the organism to the drug.
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.
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)

The apoptotic protease-activating factor 1 (Apaf-1) split luciferase biosensor continues to be used like a biological tool for the detection of early stage of apoptosis. and in human being diseases, the systems involved in this technique and the advancement of assays to recognize drug-like molecules that could be therapeutically useful possess drawn a whole lot of interest in the field. To day, many assays ideal for high-throughput testing have already been used and made for the detection of apoptosis. Each one uses particular feature of apoptosis pathway (whether intrinsic or extrinsic). Nevertheless, until the advancement of the Apaf-1 break up luciferase complementary assay, non-e could be utilized to monitor apoptosome development inside the cell loss of life signaling pathway [7,8,9]. With this novel split luciferase reporter, Nluc/Apaf-1 and Cluc/Apaf-1, the N-terminal and C-terminal fragments of luciferase, are genetically fused to the N-terminal site of Apaf-1 [10,11]. Here, we extended ...
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 ...
TY - JOUR. T1 - Negative regulation of the Apaf-1 apoptosome by Hsp70. AU - Saleh, Ayman. AU - Srinivasula, Srinivasa M.. AU - Balkir, Levent. AU - Robbins, Paul D.. AU - Alnemri, Emad S.. N1 - Funding Information: ACKNOWLEDGEMENTS We thank the members of Robbins laboratory, especially M. Serrano, B. Baldwin, T. Kenniston and J. Mai, for technical support. We also thank Y. Lazebnik and S. H. Kaufmann for Apaf-1 and caspase-9 antibodies, respectively, and R. Morimoto for hsp70 cDNA. This work was supported by NIH grants AG14357 and AG13487 (to E.S.A.) and CA55227 (to P.D.R.). Correspondence and requests for materials should be addressed to E.S.A.. PY - 2000/8. Y1 - 2000/8. N2 - Release of cytochrome c from mitochondria by apoptotic signals induces ATP/dATP-dependent formation of the oligomeric Apaf-1-caspase-9 apoptosome. Here we show that the documented anti-apoptotic effect of the principal heat-shock protein, Hsp70, is mediated through its direct association with the caspase-recruitment ...
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), ...
Detailed annotation info for ENST00000348549; 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 ...
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 ...
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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Release of cytochrome c from mitochondria by apoptotic signals induces ATP/dATP-dependent formation of the oligomeric Apaf-1-caspase-9 apoptosome. Here we show that the documented anti-apoptotic effect of the principal heat-shock protein, Hsp70, is mediated through its direct association with the ca …
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 ...
CARD8 (caspase recruitment domain family, member 8), 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. ...
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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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Apoptotic protease activating factor 1, also known as APAF1, is a human homolog of C. elegans CED-4 gene. The protein was ... 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 ... Overview of all the structural information available in the PDB for UniProt: O14727 (Apoptotic protease-activating factor 1) at ...
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 ...
Upon release of cytochrome c to the cytoplasm, the protein binds apoptotic protease activating factor-1 (Apaf-1). Cytochrome c ... This release of cytochrome c in turn activates caspase 9, a cysteine protease. Caspase 9 can then go on to activate caspase 3 ... The release of cytochrome c from mitochondria to the cytosol, where it activates the caspase family of proteases, is believed ... One of the ways cell apoptosis is activated is by release of cytochrome c from the mitochondria into cytosol. A study has shown ...
... 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. PMID 14585070. Diamantis, Aristidis; Magiorkinis, Emmanouil; Sakorafas, George H.; Androutsos ...
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 ...
... 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 ...
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 ... There also exists a caspase-independent apoptotic pathway that is mediated by AIF (apoptosis-inducing factor). Amphibian frog ...
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 ...
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][permanent dead link] GLAVA1: glavaris peptidase activating ... The adaptor protein VISA further activates the inhibitor of nuclear factor kappa-B kinase (IKK)-protein-kinase family members. ... Activating mutations in at least two related PYD-containing proteins, cryopyrin/CIAS-1 and pyrin/MEFV, have been linked to ...
Re-release of the cytokine can occur due to the proteolytic activity of the pro-apoptotic serine protease - granzyme B. Plasmin ... a serine protease present in the blood, activated as part of inflammatory reactions, then participates in the definitive ... Due to high affinity to its ligand, free betaglycan is an important factor in the deposition and neutralization of this ... Johnson DW, Qumsiyeh M, Benkhalifa M, Marchuk DA (1996). "Assignment of human transforming growth factor-beta type I and type ...
... and interferon regulatory factor 3 (IRF3). NFkB, IRF1, and IRF3 are transcription factors and play critical roles in the ... This is significant because the CARD domain is where two cytosolic proteins bind to activate MAVS, signaling that there is a ... Li XD, Sun L, Seth RB, Pineda G, Chen ZJ (December 2005). "Hepatitis C virus protease NS3/4A cleaves mitochondrial antiviral ... Activation of apoptosis by caspase 8 is independent of the Bax/Bak apoptotic pathway, the main pathway of apoptosis in cells. ...
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 ... October 2005). "The contribution of apoptosis-inducing factor, caspase-activated DNase, and inhibitor of caspase-activated ... Caspase-activated DNase (CAD) or DNA fragmentation factor subunit beta is a protein that in humans is encoded by the DFFB gene ...
SPI-2 expression also inhibits the apoptotic pathway activated by Fas-ligand and TNFα. Deletion of SPI-2 leads to virus ... SPI-2 is one of these immunomodulatory factors. SPI-2 is a nonglycosylated peptide with size of 38,5 kDa. It is expressed in an ... SPI-2 belongs in superfamily of the inhibitors of serine proteases (serpins). Serpins are the most broadly distributed family ... In mammals serpins are secreted in plasma where they serve as inhibitors of proteases involved in blood coagulation, ...
AMP-activated protein kinase (AMPK), the O-GlcNAc transferase enzyme (OGT), and the pro-apoptotic kinase ROCK1. RNA phase ... Delestienne N, Wauquier C, Soin R, Dierick JF, Gueydan C, Kruys V (June 2010). "The splicing factor ASF/SF2 is associated with ... and because the aggregates are resistant to proteases. It has also been proposed that microtubules play a role in the formation ... Upon incubating the cells in biotin and treating the cells with hydrogen peroxide, the APEX enzyme will be briefly activated to ...
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- ...
When the coagulated protease-activated protein C inhibits p66SHC a cytoprotective effect on diabetic nephropathy is placed on ... SHC1 has been found to act in signaling information after epidermal growth factor (EGF) stimulation. Activated tyrosine kinase ... p66SHC operates as a redox enzyme linked to apoptotic cell death. p66SHC has been related to the sirtuin-1 system and has been ... p52SHC and p46SHC activate the Ras-ERK pathway. p66SHC inhibits ERK1/2 activity and antagonize mitogenic and survival abilities ...
... 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, ...
... 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 ...
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 ... Therefore, protease 3C depends on poliovirus 3CD protein for the translocation of 3C protease to carry out transcription ...
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 ...
"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 ...
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. ...
"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) ...
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, ...
... 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 ...
... proteases, and thus the apoptotic cascade. Additional sources of neuronal cell death related to excitotoxicity involve energy ... including activating and inactivating certain K+ channels. Epinephrine is found in the lateral tegmental system, medulla, ... Diagnosis of the disease often stems from clinical observation as well as analysis of family history and other risk factors, ... ions into the postsynaptic cell through ion channels activated by neurotransmitter binding. There are two different kinds of ...
Apoptotic stimuli, such as Bax and Bak, as well as other factors can trigger OMA1 activation and OPA1 processing, which are ... Zhang K, Li H, Song Z (May 2014). "Membrane depolarization activates the mitochondrial protease OMA1 by stimulating self- ... Two controversial models describe OMA1 either as membrane-anchored protease or as integral membrane protease. Google's ... Anand R, Wai T, Baker MJ, Kladt N, Schauss AC, Rugarli E, Langer T (March 2014). "The i-AAA protease YME1L and OMA1 cleave OPA1 ...
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 ...
1996). "Mch3, a novel human apoptotic cysteine protease highly related to CPP32". Cancer Res. 55 (24): 6045-52. PMID 8521391. ... This protein cleaves and activates caspases 3 and 7, and the protein itself is processed by caspase 8. Mutations in this gene ... Zheng, L; Schickling O; Peter M E; Lenardo M J (August 2001). "The death effector domain-associated factor plays distinct ... a novel human apoptotic cysteine protease containing two FADD-like domains". Proc Natl Acad Sci USA. 93 (15): 7464-9. Bibcode: ...
... proteins are transcription factors that activate expression of many pro-proliferative genes through binding enhancer box ... In B cells, Myc acts as a classical oncogene by regulating a number of pro-proliferative and anti-apoptotic pathways, this also ... Myc cleavage is mediated by the calpain family of calcium-dependent cytosolic proteases. The cleavage of Myc by calpains is a ... Myc is activated upon various mitogenic signals such as serum stimulation or by Wnt, Shh and EGF (via the MAPK/ERK pathway). By ...
Activated CD8+ T cells induce keratinocyte apoptosis through various mechanisms such as secretion of tumor necrosis factor (TNF ... the release of proinflammatory mediators and proteases by mast cells, and perturbations in the innate immune response that may ... degeneration of the basal layer with apoptotic keratinocytes (referred to as Civatte, colloid, hyaline, or cytoid bodies) An ... activates CD8+ T cells on keratinocytes or by encounters with activated CD4+ helper T cells or cytokines produced by activated ...
Specifically, mannose binding triggers recruitment of MBL-associated serine proteases (MASPs). The serine proteases activate ... and single stranded RNA which recruit factors via twin N-terminal CARD domains to activate antiviral gene programs, which may ... Ting JP, Williams KL (April 2005). "The CATERPILLER family: an ancient family of immune/apoptotic proteins". Clinical ... NLRP3 can be activated and give rise to NLRP3 inflammasome by ATP, bacterial pore-forming toxins, alum and crystals. Alongside ...
... while c-Jun-ER activated cells have been shown to be apoptotic. Increased AP-1 levels lead to increased transactivation of ... "Serratia marcescens serralysin induces inflammatory responses through protease-activated receptor 2". Infection and Immunity. ... Navas TA, Baldwin DT, Stewart TA (November 1999). "RIP2 is a Raf1-activated mitogen-activated protein kinase kinase". The ... The growth factors TGF alpha, TGF beta, and IL2 have all been shown to stimulate c-Fos, and thereby stimulate cellular ...
... activating transcription factor 4) and uniquely responsive to ER stress. CHOP causes downregulation of the anti-apoptotic ... where it is cleaved by proteases to form an active 50kDa transcription factor that translocates to the nucleus. It binds to ... The activated domain is able to activate the transcription factor XBP1(Xbox binding protein) mRNA (the mammalian equivalent of ... ATF6 (activating transcription factor 6) is a basic leucine zipper transcription factor. Upon Grp78 dissociation, the entire ...
... a novel cell surface receptor for the protease factor Xa". J. Biol. Chem. 269 (5): 3139-42. doi:10.1016/S0021-9258(17)41838-2. ... 7 are effector proteases whereas caspase-8 is an initiator caspase that sits more upstream in the apoptotic pathway. These ... Activated CTLs specific for a particular antigen kill their target cells by first recognizing parts of the survivin protein ... a novel cell surface receptor for the protease factor Xa". J. Biol. Chem. 269 (5): 3139-42. doi:10.1016/S0021-9258(17)41838-2. ...
Arginine starvation is known to be a cause of programmed cell death, and local removal is a strong apoptotic agent. Host ... On an immunological level, activated host T lymphocytes attack endothelial cells that have been injured in order to remove the ... Natural barriers consist of mucus layers, bile salt, proteases, and lipases. Additionally, peristalsis and the renewal of ... CDC (July 15, 2015). "Sources of Infection & Risk Factors". Parasites - Giardia. Archived from the original on September 7, ...
Once activated, they change shape and become more amorphous or amoeba-like and can extend pseudopods as they hunt for antigens ... These neutrophil extracellular traps (NETs) comprise a web of fibers composed of chromatin and serine proteases that trap and ... Chen A, Seifert HS (November 2011). "Neisseria gonorrhoeae-mediated inhibition of apoptotic signalling in polymorphonuclear ... "ITAM signaling by Vav family Rho guanine nucleotide exchange factors regulates interstitial transit rates of neutrophils in ...
Chai J, Du C, Wu JW, Kyin S, Wang X, Shi Y (2000). "Structural and biochemical basis of apoptotic activation by Smac/DIABLO". ... While cytochrome c directly activates APAF1 and caspase 9, SMAC binds IAPs, such as XIAP and cIAP proteins, to inhibit their ... "The polypeptide chain-releasing factor GSPT1/eRF3 is proteolytically processed into an IAP-binding protein". The Journal of ... "HtrA2 promotes cell death through its serine protease activity and its ability to antagonize inhibitor of apoptosis proteins". ...
ISBN 978-0-471-36015-5. Belcastro AN, Albisser TA, Littlejohn B (October 1996). "Role of calcium-activated neutral protease ( ... Calpains have been implicated in apoptotic cell death, and appear to be an essential component of necrosis. Detergent ... White V (1999-10-21). "- 'Biochemical Storm' Following Brain Trauma An Important Factor In Treatment, University of Florida ... "calcium-activated neutral protease" (CANP) were detected in brain, lens of the eye and other tissues. In the late 1960s the ...
Dark might not be enough on its own to activate caspase Dronc; it has been suggested that other factors could increase the ... Apaf-1's Drosophila ortholog. The diagram (figure 4) shows functional homologues of apoptotic proteins (colour-coded ... It belongs to the cysteine-aspartic proteases family, as it is a protease enzyme that takes part in programmed cell death ... It is defined as a cysteine protease (or thiol protease), which means that a nucleophilic cysteine thiol forms a catalytic ...
Cells that undergo rapid necrosis in vitro do not have sufficient time or energy to activate apoptotic machinery and will not ... and loses activity once the cell is compromised and the protease is exposed to the external environment. The dead-cell protease ... method for the quantitation of lactate dehydrogenase release in measurements of cellular cytotoxicity and tumor necrosis factor ... Protease biomarkers have been identified that allow researchers to measure relative numbers of live and dead cells within the ...
... but they are all still able to cross present antigens in order to activate cytotoxic CD8+ T cells. There are many factors that ... pDCs are found within the blood and are able to cross present antigens directly or from neighboring apoptotic cells, but the ... where an increasingly acidic environment along with the activation of enzymes such as lysosomal proteases triggers the ... After vaccine induced activation, dendritic cells are able to migrate to lymph nodes and activate CD4+ T helper cells as well ...
Involvement of chemokines, such as SDF1 (CXCL12), the fibroblast growth factor (FGF), and the transforming growth factor β (TGF ... The use of antibodies that block integrins or protease inhibitors in clinical trials leads to the emergence of tumor cells with ... It is also the fact that moving tumor cells display increased activity of anti-apoptotic genes, which causes resistance to ... The binding to receptors activates a signaling pathway involving some proteins of the small GTPase system (Cdc42, Rac, RhoA, ...
Once activated, the T cells release pro-inflammatory cytokines and chemokines. The interactions with TCRs are characterized by ... Some studies have reported increased protease levels in strains that cause scarlet fever in comparison to those associated with ... The receptor-binding pathway and Fas-mediated apoptotic signaling pathway have been implicated in this process. The induction ... Each step is tightly regulated by multiple factors, allowing sophisticated temporal expression of the mature proteinase. SpeA ...
It has been suggested that activating the CD36 receptor causes an increase in ECs sensitivity to apoptotic signals. Type I ... can activate transforming growth factor beta 1 (TGFβ1) and inhibit endothelial cell migration, angiogenesis, and tumor growth. ... It also interacts with numerous proteases involved in angiogenesis, including plasminogen, urokinase, matrix metalloproteinase ... Bound protein fragments of the type I repeats have been shown to serve as attachment factors for both ECs and melanoma cells. ...
The destruction of the lamin networks is controlled by specialized apoptotic proteases called caspases, which cleave the lamin ... and eventually activating the transcription factor NF-κB. A nuclear localisation signal on the NF-κB protein allows it to be ... There they serve as transcription factors when bound to their ligand; in the absence of a ligand, many such receptors function ... factor proteins responsible for regulating gene expression from physical access to the DNA until they are activated by other ...
"Hepatocyte growth factor/scatter factor activates the ETS1 transcription factor by a RAS-RAF-MEK-ERK signaling pathway". ... Moreover, uncleavable HGF competes with the wild-type endogenous pro-HGF for the catalytic domain of proteases that cleave HGF ... In the injured heart, HGF/MET axis plays important roles in cardioprotection by promoting pro-survival (anti-apoptotic and anti ... ETS1 activates MET transcription in vitro. MET transcription is activated by hypoxia-inducible factor 1 (HIF1), which is ...
This in turn activates the transcription of pro-inflammatory cytokines and tumor necrosis factor-alpha (TNFα), with concurrent ... They are also useful in removing apoptotic cells from circulation. The amount of Kupffer cells in the liver is held constant. ... and proteases. Excessive production of these mediators is linked to the development of liver injury. Apart from clearing ... Development of mature Kupffer cells is regulated by numerous growth factors, with macrophage colony-stimulating factor (CSF1) ...
In addition to cancer cells proliferating abnormally, they suppress the expression of anti-apoptotic or pro-apoptotic genes or ... These proteases are often highly specific and cause hydrolysis of a limited number of peptide bonds within the target protein. ... When this occurs, no tRNA can recognise it and a release factor induces the release of the complete polypeptide chain from the ... This post-translational modification often alters the proteins function, the protein can be inactivated or activated by the ...
"Pro-apoptotic PUMA and anti-apoptotic phospho-BAD are highly expressed in colorectal carcinomas". Dig. Dis. Sci. 52 (10): 2751- ... p53 is activated by survival signals such as glucose deprivation and increases expression levels of PUMA. This increase in PUMA ... PUMA levels are downregulated through the activation of caspase-3 and a protease inhibited by the serpase inhibitor N-tosyl-L- ... PUMA apoptosis may also be induced independently of p53 activation by other stimuli, such as oncogenic stress growth factor and ...
Studies examining the role of pro- and anti-apoptotic factors support this model; for example, the anti-apoptotic factor Bcl-2 ... These can activate a series of second messenger system proteins that can coordinate processes such as neurotransmitter release ... "Molecular basis of substrate recognition and degradation by human presequence protease". Structure. 22 (7): 996-1007. doi: ... Damage and subsequent dysfunction in mitochondria is an important factor in a range of human diseases due to their influence in ...
ADA-deficient FTOCs are also rescued by a Bcl-2 transgene or deletion of apoptotic protease-activating factor-1 (Apaf-1), ... apoptotic protease-activating factor-1 (Apaf-1); adenosine receptor 2a (A2aR); 2′-deoxycoformycin (17) (dCF); 5′-N- ... Nucleotide requirements for the in vitro activation of the apoptosis protein-activating factor-1-mediated caspase pathway. J ... Metabolites from apoptotic thymocytes inhibit thymopoiesis in adenosine deaminase-deficient fetal thymic organ cultures. J Clin ...
We found that the cytochrome c/apoptotic protease-activating factor-1 (apoptosome)-dependent caspase activation is deficient in ... apoptotic protease-activating factor-1; Smac/DIABLO, second mitochondria-derived activator of caspases/direct IAP binding ... c-dependent caspase activation in ovarian cancer cell lines due to diminished or absent apoptotic protease activating factor-1 ... This apoptosome recruits and activates caspase-9, which in turn activates the executioner caspases, caspase-3 and caspase-7 (7 ...
... there is no apoptosis in mutant retinaltissues for the Drosophila homologues of apoptotic protease-activating factor 1 (Ark) ... A screen for cohesion mutants uncovers Ssl3, the fission yeast counterpart of the cohesin loading factor Scc4.. Author(s) : ... We report here on the identification of fission yeast Ssl3 asa Scc4-like factor. Ssl3 is in complex with Mis4 and, as a bona ... One of the activated origins showed increased histone H3 K9K14 diacetylation, but the others did not. These results demonstrate ...
Apoptotic Protease-Activating Factor 1 D12.776. D12.776. Aporphines D3.438.531.85.30 D3.633.100.531. ... B-Cell Activating Factor D23.50.301.264.35.273 D23. B-Cell Activation Factor Receptor D23.50.301.264.35.275 ... NF-E2 Transcription Factor D12.776.930.316.750 D12.776.930.216.750 NF-E2 Transcription Factor, p45 Subunit D12.776.930.316. ... Tumor Necrosis Factor, Member 25 D12.776.543.750.73.725 D12.776.543.750.690.725 Receptors, Tumor Necrosis Factor, Type I ...
... apoptotic activating protease factor 1. ATG: autophagy gene. AT1R: angiotensin subtype 1 receptor ... Drug targets include receptors for endocrine and paracrine factors, enzymes, voltage-gated ion channels, membrane transporters ...
Pro-apoptotic apoptosis protease-activating factor 1 (Apaf-1) has a cytoplasmic localization distinct from Bcl-2 or Bcl-x(L). ... but they appear to act through the caspase activator apoptosis protease-activating factor 1 (Apaf-1). According to the ... Fas ligand, Bcl-2, granulocyte colony-stimulating factor, and p38 mitogen-activated protein kinase: Regulators of distinct cell ... stress-activated protein kinases such as p38 mitogen-activated protein kinase (MAPK), and proinflammatory cytokines like ...
Apoptotic Protease-Activating Factor 1 61% * Smoking 60% * Cadherins 48% 25 Scopus citations ... Average weight of seminal vesicles: An adjustment factor for radical prostatectomy specimens weighed with seminal vesicles. ... Senveli, S. U., Ao, Z., Rawal, S., Datar, R. H., Cote, R. J. & Tigli, O., 2016, In: Lab on a Chip. 16, 1, p. 163-171 9 p.. ... Hansen, K. M., Ji, H. F., Wu, G., Datar, R., Cote, R., Majumdar, A. & Thundat, T., Apr 1 2001, In: Analytical Chemistry. 73, 7 ...
Apoptotic Protease-Activating Factor 1 - Preferred Concept UI. M0279898. Scope note. A CARD signaling adaptor protein ... Apoptotic Protease-Activating Factor 1 Entry term(s). Apaf 1 Protease Activating Factor Apaf-1 Protease-Activating Factor ... Apoptotic Protease Activating Factor 1. Protease-Activating Factor, Apaf-1. Tree number(s):. D12.644.360.024.131.124. D12.644. ... 2007; APOPTOTIC PROTEASE-ACTIVATING FACTOR 1 was indexed under INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS 1997-2006 & under ...
Apoptotic Protease-Activating Factor 1. 2. + 232. Lithostathine. 2. + 233. Helium. 2. + ...
MicroRNA-484 and Apoptotic Protease Activating Factor-1 Gene in Relapsing Remitting Multiple Sclerosis: the Possible Interplay ... First Study in Iraq About (HLA)-Drb1 * 15:01 as a Genetic Risk Factor for MS Initiation View ePoster ... Incidence, Severity, Outcomes, and Risk Factors of COVID-19 in Multiple Sclerosis: An Observational Study in the Middle East ... Chitinase-3 Like-Protein-1 in CSF: A Novel Biomarker for Progression in Multiple Sclerosis Patients View ePoster ...
Cytochrome c, apoptotic protease-activating factor 1 (APAF-1) and procaspase-9 then form a complex termed the apoptosome, in ... p53 activates the intrinsic mitochondrial apoptotic pathway by inducing the expression of at least three Bcl-2 pro-apoptotic ... p53 can activate the extrinsic apoptotic pathway through the induction of genes encoding three transmembranes proteins: Fas, ... p53 is a transcription factor that activates vital damage-containment procedures to restrict aberrant cell growth in response ...
apoptotic protease activating factor 1 melanoma Gene Expression Regulation Neoplastic. Subjects:. diseases & disorders , cancer ... Soengas, M. S., Gerald, W. L., Cordon-Cardo, C., Lazebnik, Y., Lowe, S. W. (2006) Apaf-1 expression in malignant melanoma. Cell ...
... mitogen-activated protein kinase (MAPK), nuclear factor κB (NF-κB) and interleukin (IL)-8 signaling is involved in PM2.5- ... Crosstalk between autophagic and apoptotic pathways have been characterized in cell fate decision making (61,62). Caspases, a ... group of cysteine proteases, are best known as apoptosis modulators, and function in the crosstalk between autophagy and ... Jeong SC, Cho Y, Song MK, Lee E and Ryu JC: Epidermal growth factor receptor (EGFR)-MAPK-nuclear factor(NF)-κB-IL8: A possible ...
Apoptotic protease-activating factor 1 (Apaf-1) [Source:UniProtKB/Swiss-Prot;Acc:O14727]. homology search. ... Caspase-7 Precursor (CASP-7)(EC apoptotic protease 3)(ICE-LAP3)(Apoptotic protease Mch-3)(CMH-1) [Contains ... Caspase-10 Precursor (CASP-10)(EC apoptotic protease 4)(Apoptotic protease Mch-4)(FAS-associated death ... Mitogen-activated protein kinase kinase kinase 7 (EC growth factor-beta-activated kinase 1)(TGF-beta- ...
Cytochrome C together with apoptotic protease activating factor one (Apaf-1) form apoptosome. Apoptosome is a protein complex ... These toxins enter the bloodstream where they act as pathogen associated membrane patterns to activate immune cells, including ... This is characterized by increased nuclear factor kappa B (NfkB) signaling, sustained cytokine production and macrophage ... and negatively as a factor for increasing risk of certain diseases. Fat foods as part of the essential nutrients have come ...
The secreted protease factor CPAF is responsible for degrading pro-apoptotic BH3-only proteins in Chlamydia trachomatis- ... Caspase-3 is a central protease in the apoptotic pathway, and caspase-3 is regularly activated proteolytically during apoptosis ... The secreted protease factor CPAF is responsible for degrading pro-apoptotic BH3-only proteins in Chlamydia trachomatis- ... Named chlamydial protease-like activity factor (CPAF), this protein was isolated as a factor that can degrade two host ...
... that lead to an increase in p53 activity and the induction of the rest of the factors that participate in the apoptotic pathway ... We found that in HT29 cells maslinic acid activated the expression of c-Jun NH2-terminal kinase (JNK), thus inducing p53. ... In our latest work we have investigated further this compounds apoptotic molecular mechanism. We used HT29 adenocarcinoma ... treatment and an apoptotic sub-G0/G1 peak after 96 hours. Nevertheless, the molecular mechanism for this cytotoxic effect of ...
And, the levels of apoptotic protease activating factor-1 (APAF-1) and cytoplasmic cytochrome C were remarkably up-regulated in ... Hoechst 33258 staining assay showed that HSYB treatment triggered apoptotic morphology and the apoptotic rates were ... TRIM7 inhibits encephalomyocarditis virus replication by activating interferon-ß signaling pathway. Li, Minjing; Yan, Junfang; ... Similar to miR-205-5p inhibitors, siErBB3 could oppose SC-triggered pro-apoptotic effects on PCa cells. All these results were ...
Assignment of apoptotic protease activating factor-1 gene (APAF1) to human chromosome band 12q23 by fluorescence in situ ... The cancer resistance of Spalax galili is mediated by cell-released IFN-β which activates p53 and Rb signaling pathway and the ... 1]. 张华伟, 孟星宇, 李连峰, 杨玉莹, 仇华吉. 长链非编码RNA--抗病毒天然免疫应答的新兴调控因子[J]. 遗传, 2018, 40(7): 525-533.. ... 1] Gorbunova V, Seluanov A, Zhang ZD, Gladyshev VN, Vijg J.
Through interaction with apoptotic protease activating factors (Apaf), cyt c can initiate the activation cascade of caspases ... The apoptosome is a complex composed of cyt c, apoptotic protease activating factor-1 (Apaf-1), and deoxy adenosine ... pathway of apoptosis pathway begins when an injury occurs within the cell and the resulting stress activates the apoptotic ... In many mammalian heme proteins, the protoporphyrin ring is protoporphyrin IX, shown in Figure 1. ...
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. ...
DNA fragmentation factor, and apoptotic protease activating factor-1, in human granulosa cells. Fertil Steril. 1998;70(3):549- ... Caspase-3 is a well characterized protease which plays an effective role in apoptosis [47, 48]. The caspase-3 expression was ... Immunohistochemical analysis of in vivo patterns of expression of CPP32 (Caspase-3), a cell death protease. Cancer Res. 1997;57 ... Release of angiogenic growth factors from cells encapsulated in alginate beads with bioactive glass. Biomaterials. 2005;26(19): ...
c) from the mitochondria to the cytoplasm leads to its combination with apoptotic protease activating factor-1 (APAF1) and ... sign.) generated expression of pro-apoptotic genes and proteins and the translocation of BCL2 family proteins to produce ... sign.) leading to activation of tumour necrosis factor receptor-1 (TNFR1), which when associated with its adaptor protein TRADD ... PAR polymers can apoptosis inducing factor (AIF) leading to DNA degradation, while energy depletion will induce increased ...
... dying C.reinhardtii cells.We connect the downregulation of dad1 with the upregulation of apoptosis protease activating factor-1 ... We report here the isolation of a homologue of the potential anti-apoptotic gene, defender against apoptotic death (dad1 )from ... A homologue of the defender against the apoptotic death gene (dad1 )in UV-exposed Chlamydomonas cells is downregulated with the ... A homologue of the defender against the apoptotic death gene (dad1 )in UV-exposed Chlamydomonas cells is downregulated with the ...
... transforming growth factor beta (TGF-ß), and apoptotic protease-activating factor 1 (Apaf-1) in humans chronically exposed to ... The Tohoku journal of experimental medicine 2018 246 (1): 35-44. Radic Tanja M, Coric Vesna M, Pljesa-Ercegovac Marija S, Basta ... Association of glutathione S-transferase O 1-1 polymorphisms (A140D and E208K) with the expression of interleukin-8 (IL-8), ... Scientific reports 2020 Jan 10 (1): 144. Corredor Zuray, Filho Miguel Inácio da Silva, Rodríguez-Ribera Lara, Velázquez Antonia ...
Apoptotic Protease-Activating Factor 1 D12.776. D12.776. Aporphines D3.438.531.85.30 D3.633.100.531. ... B-Cell Activating Factor D23.50.301.264.35.273 D23. B-Cell Activation Factor Receptor D23.50.301.264.35.275 ... NF-E2 Transcription Factor D12.776.930.316.750 D12.776.930.216.750 NF-E2 Transcription Factor, p45 Subunit D12.776.930.316. ... Tumor Necrosis Factor, Member 25 D12.776.543.750.73.725 D12.776.543.750.690.725 Receptors, Tumor Necrosis Factor, Type I ...
Apoptotic Protease-Activating Factor 1 D12.776. D12.776. Aporphines D3.438.531.85.30 D3.633.100.531. ... B-Cell Activating Factor D23.50.301.264.35.273 D23. B-Cell Activation Factor Receptor D23.50.301.264.35.275 ... NF-E2 Transcription Factor D12.776.930.316.750 D12.776.930.216.750 NF-E2 Transcription Factor, p45 Subunit D12.776.930.316. ... Tumor Necrosis Factor, Member 25 D12.776.543.750.73.725 D12.776.543.750.690.725 Receptors, Tumor Necrosis Factor, Type I ...
  • This dysfunctional apoptosome activity was not correlated with any decrease of apoptosome component factors, but it was linked to an increased X-linked inhibitor of apoptosis protein (XIAP). (aacrjournals.org)
  • The extrinsic pathway is mediated by a variety of death receptor ligands, including tumor necrosis factor (TNF) and Fas ligand (FaSL), that trigger apoptosis by binding to cell surface receptors. (cdc.gov)
  • How Bcl-2 and its pro-survival relatives prevent activation of the caspases that mediate apoptosis is unknown, but they appear to act through the caspase activator apoptosis protease-activating factor 1 (Apaf-1). (edu.au)
  • Desempeña un papel en la apoptosis estimulada por las mitocondrias (VÍA INTRÍNSECA DE LA APOPTOSIS) y se une al CITOCROMO C en el CITOSOL para formar un COMPLEJO PROTEICO APOPTOSÓMICO que activa las CASPASAS INICIADORAS, como la CASPASA 9. (bvsalud.org)
  • It plays a role in the mitochondria-stimulated apoptosis (APOPTOSIS, INTRINSIC PATHWAY) and binds to CYTOCHROME C in the CYTOSOL to form an APOPTOSOMAL PROTEIN COMPLEX which activates INITIATOR CASPASES such as CASPASE 9. (bvsalud.org)
  • Exposure to cellular stress can trigger the p53 tumor suppressor, a sequence-specific transcription factor, to induce cell growth arrest or apoptosis. (biologists.com)
  • The extrinsic, death receptor pathway triggers the activation of a caspase cascade, and the intrinsic, mitochondrial pathway shifts the balance in the Bcl-2 family towards the pro-apoptotic members, promoting the formation of the apoptosome, and consequently caspase-mediated apoptosis. (biologists.com)
  • Apoptosis-inducing factor 3 (EC 1. (deathbase.org)
  • Apoptosis regulator Bcl-X (Bcl-2-like 1 protein). (deathbase.org)
  • We have shown elsewhere that maslinic acid inhibits cell proliferation to a significant extent and activates mitochondrial apoptosis in colon cancer cells. (biomedcentral.com)
  • We show here that the anti-tumoral activity of maslinic acid might proceed via p53-mediated apoptosis by acting upon the main signaling components that lead to an increase in p53 activity and the induction of the rest of the factors that participate in the apoptotic pathway. (biomedcentral.com)
  • All these results suggest that maslinic acid induces apoptosis in human HT29 colon-cancer cells through the JNK-Bid-mediated mitochondrial apoptotic pathway via the activation of p53. (biomedcentral.com)
  • The intrinsic pathway involves the release of pro-apoptotic factors such as cytochrome-c from the mitochondria, which activate the apoptotic mechanism by interacting with Apaf-1 and stimulating the initiator caspase-9, which in turn induces proteolytically the activity of executor caspase-3, one of the principle proteases participating in the execution phase of apoptosis. (biomedcentral.com)
  • Prevention of lymphocyte apoptosis, same process by which these cell populations are regulat- through either genetic modification of the host or treatment ed during normal health ( 1 , 2 ). (cdc.gov)
  • The apoptosome signals apoptosis by binding to and activating specific INITIATOR CASPASES such as CASPASE 9. (ucdenver.edu)
  • PAR polymers can apoptosis inducing factor (AIF) leading to DNA degradation, while energy depletion will induce increased levels of intracellular Ca 2+ and activation of calpain-type proteases. (eye-tuebingen.de)
  • Unlike necrosis, apoptosis produces cell fragments called apoptotic bodies that phagocytes are able to engulf and remove before the contents of the cell can spill out onto surrounding cells and cause damage to them. (mdwiki.org)
  • Weak external signals may also activate the intrinsic pathway of apoptosis. (mdwiki.org)
  • Some factors like Fas receptors and caspases promote apoptosis, while some members of the Bcl-2 family of proteins inhibit apoptosis. (mdwiki.org)
  • 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. (uams.edu)
  • Here, we report that tPA potentiates apoptosis in ischemic human brain endothelium and in mouse cortical neurons treated with N-methyl-D-aspartate (NMDA) by shifting the apoptotic pathways from caspase-9 to caspase-8, which directly activates caspase-3 without amplification through the Bid-mediated mitochondrial pathway. (nih.gov)
  • APC inhibited tPA-induced caspase-8 activation of caspase-3 in endothelium and caspase-3-dependent nuclear translocation of apoptosis-inducing factor in NMDA-treated neurons and reduced tPA-mediated cerebral ischemic injury in mice. (nih.gov)
  • In addition, T. vaginalis induced the phosphorylation of apoptosis signal regulating kinase 1 (ASK1) and c-Jun N-terminal kinases (JNK) in SiHa cells, whereas 4-PBA or SP600125 (JNK inhibitor) pretreatment significantly attenuated ASK1/JNK phosphorylation, mitochondrial dysfunction, apoptosis and ER stress response in SiHa cells, in a dose-dependent manner. (biomedcentral.com)
  • We show that caspase-1-deficient macrophages undergo apoptosis within 4-6 h of infection with invasive bacteria. (harvard.edu)
  • Besides caspase-2, the caspase-1-independent pathway involves the activation of caspase-3, -6, and -8 and the release of cytochrome c from mitochondria, none of a which occurs during caspase-1-dependent apoptosis. (harvard.edu)
  • By using caspase-2 knockout macrophages and chemical inhibition, we establish a role for caspase-2 in both caspase-1-dependent and -independent apoptosis. (harvard.edu)
  • Particularly, activation of caspase-1 during fast Salmonella-induced apoptosis partially relies on caspase-2. (harvard.edu)
  • The ability of Salmonella to induce caspase-1-independent macrophage apoptosis may play a role in situations in which activation of this protease is either prevented or uncoupled from the induction of apoptosis. (harvard.edu)
  • During apoptosis, activated endogenous nucleases cleave DNA into fragments, but cell membranes and the intracellular matter remain intact, nor is there tissue damage or leukocytic infiltration. (intechopen.com)
  • In contrast to apoptosis, necrosis is a pathological form of cell death caused by acute damage, rupture of the membrane, release of the cytoplasm content, and the inflammatory process induced thereby [ 1 , 2 ]. (intechopen.com)
  • As of now, at lease 14 caspases have been described from mammals: 8 caspases are involved in apoptosis, 5 activate anti-inflammatory cytokines, and one acts in keratinocyte differentiation. (intechopen.com)
  • HIV-1-encoded proteins such as envelope gp120 (glycoprotein gp120), Tat (trans-activator of transcription), Nef (negative regulatory factor), Vpr (viral protein R), Vpu (viral protein unique) and protease are known to be effective in modulating host cell signalling pathways that lead to an alteration in apoptosis of both HIV-infected and uninfected bystander cells. (microbiologyresearch.org)
  • The current review summarizes our present understanding of apoptosis modulation in HIV-infected cells, uninfected bystander cells and latently infected cells, with a focus on highlighting strategies to activate the apoptotic pathway to kill latently infected cells. (microbiologyresearch.org)
  • HIV-1 Vpr: mechanisms of G2 arrest and apoptosis. (microbiologyresearch.org)
  • Human immunodeficiency virus type 1 Tat induces apoptosis and increases sensitivity to apoptotic signals by up-regulating FLICE/caspase-8. (microbiologyresearch.org)
  • Effect of HSPB9 on Apoptosis of DF-1 Cells[J]. Biomedical and Environmental Sciences, 2019, 32(2): 107-120. (besjournal.com)
  • Objective Our aim was to explore whether heat stress protein (HSP) 9 preferentially expresses under heat stress and affects the expression of other heat stress proteins as well as to explore the effect of HSPB9 overexpression and knockdown on apoptosis in DF-1. (besjournal.com)
  • Results Chicken DF-1 cells showed an early state of apoptosis in the early stages of HSPB9 overexpression. (besjournal.com)
  • Since apoptosis is a highly regulated process, a number of cell signaling pathways including caspases and proteases are involved in its initiation and execution. (pharna.com)
  • Indeed, inhibition of the tumor suppressor function of apoptosis led to the categorization of a new class of oncogenes- BCL2 being the prototypic member-that could promote cell survival through suppression of apoptosis and thereby impose an oncogenic imbalance on the cell birth/cell death equation ( 1 ). (frontiersin.org)
  • Furthermore, the apoptosis effector protease, caspase-8, is mutated in multiple cancer types and the survival pathway PI3K/Akt/mTOR is dysregulated frequently in tumors ( 2 ). (frontiersin.org)
  • By contrast, pro-apoptotic regulators such as p53 and BIM ( 3 ) among others have firmly established tumor-suppressive roles for apoptosis. (frontiersin.org)
  • Apoptotic pathways of cell death. (cdc.gov)
  • p53 stimulates a wide network of signals that act through two major apoptotic pathways. (biologists.com)
  • The impact of these two apoptotic pathways may be enhanced when they converge through Bid, which is a p53 target. (biologists.com)
  • It has also been indicated that PM2.5 may trigger asthma, chronic obstructive lung disease (COPD) and lung cancer through the activation of various signaling pathways, including AMP-activated protein kinase (AMPK) catalytic subunit α1 and signal transducer and activator of transcription (STAT)-1 ( 7 ). (spandidos-publications.com)
  • Transcriptome analysis of HEK 293T cells treated with wild and mutant APC revealed differentially expressed genes enriched in inflammatory, apoptotic, and virus defense-related signaling pathways. (aging-us.com)
  • [5] Both pathways induce cell death by activating caspases , which are proteases , or enzymes that degrade proteins. (mdwiki.org)
  • The two pathways both activate initiator caspases, which then activate executioner caspases, which then kill the cell by degrading proteins indiscriminately. (mdwiki.org)
  • The genes and signaling pathways activated during the asexual reproduction and the formation of the anterior and posterior parts of the body, as well as the molecular mechanisms that provide regeneration of the nervous and digestive systems, are considered here. (mdpi.com)
  • The lifespan of pulmonary neutrophils in COPD is prolonged because apoptotic pathways are suppressed. (medscape.com)
  • Loss of PGC-1β in DCs leads to increased expression of genes in inflammatory pathways, and reduced expression of genes encoding proteins important for mitochondrial metabolism and function. (nature.com)
  • Targeted genetic mutations, gene knockout and overexpression studies have significantly contributed to our understanding of the pathways involved in apoptotic processes. (pharna.com)
  • We propose that tumor-derived Apo-EVs are significant vehicles of the ORN, functioning as critical intercellular communicators that activate oncogenic tissue repair and regeneration pathways. (frontiersin.org)
  • 2. Docking of EVs through receptor-ligand interaction may activate intracellular signaling pathways in the absence of cargo transfer. (frontiersin.org)
  • In the intrinsic pathway, several adverse factors act upon mitochondria to cause loss of the mitochondrial membrane potential, resulting in leakage into the cytosol of cytochrome C (Cyto C), which together with apoptotic protease activating factor 1 forms the apoptosome that activates caspase-9. (cdc.gov)
  • Cytochrome C together with apoptotic protease activating factor one (Apaf-1) form apoptosome. (brainfacts.org)
  • Here, we show that CPAF can be activated in uninfected cells by experimentally induced oligomerization, reminiscent of the activation mode of initiator caspases. (rupress.org)
  • Through interaction with apoptotic protease activating factors (Apaf), cyt c can initiate the activation cascade of caspases once it is released into the cytosol. (answersmore.net)
  • c) from the mitochondria to the cytoplasm leads to its combination with apoptotic protease activating factor-1 (APAF1) and caspase-9 to activate executioner caspases, such as caspase-3 and -7. (eye-tuebingen.de)
  • Caspases are a family of cysteine-dependent aspartate specific proteases. (intechopen.com)
  • Depending on the phase at which those proteins enter the apoptotic cascade one distinguishes initiator (apical) and effector (executioner) caspases. (intechopen.com)
  • All caspases are originally inactive, but activated when needed by cleavage of a small fragment by initiator caspases. (intechopen.com)
  • Under certain conditions effector caspases may act as initiator ones to accelerate apoptotic reactions. (intechopen.com)
  • ICE is now known to belong to a family of cysteine proteases, the caspases, which play a key role in both inflammation and PCD in mammals. (jneurosci.org)
  • Caspases are are proteases that cleave their substrates. (smpdb.ca)
  • Caspase-8 is an initiator caspase that is activated in response to pro-apoptotic stimulus and causes a cascade of further caspase activity by cleaving and activating effector caspases, like caspases -3 and -7. (smpdb.ca)
  • Once activated, caspases -3 and -7 cleave downstream proteins. (smpdb.ca)
  • Mammals have at least eight BH3-only proteins and they are activated in a stimulus-specific, as well as a cell type-specific, manner. (edu.au)
  • According to the apoptosome model, the Bcl-2-like proteins preclude Apaf-1 activity by sequestering the protein. (edu.au)
  • The chlamydial protease-like activity factor (CPAF) translocates from the vacuole to the cytosol, where it cleaves several cellular proteins. (rupress.org)
  • CPAF activity induces proteolysis of cellular substrates including two novel targets, cyclin B1 and PARP, and indirectly results in the processing of pro-apoptotic BH3-only proteins. (rupress.org)
  • Thus we propose a plausible sequential molecular mechanism for the expression of the different proteins responsible for the intrinsic mitochondrial apoptotic pathway. (biomedcentral.com)
  • In many mammalian heme proteins, the protoporphyrin ring is protoporphyrin IX, shown in Figure 1. (answersmore.net)
  • generated expression of pro-apoptotic genes and proteins and the translocation of BCL2 family proteins to produce mitochondrial outer membrane permeabilization (MOMP). (eye-tuebingen.de)
  • Mitochondria are important in the regulation and transmission of apoptotic signals, which are regulated by maintaining a balance among the levels of the Bcl-2-family proteins [ 7 ]. (biomedcentral.com)
  • Depending on the stage of the virus life cycle and host cell type, these viral proteins act as mediators of pro- or anti-apoptotic signals. (microbiologyresearch.org)
  • Heat shock proteins:endogenous modulators of apoptotic cell death. (besjournal.com)
  • Existing studies on PGC-1 proteins in the context of immunity have largely been focused on PGC-1α, with a relatively small number on PGC-1β. (nature.com)
  • We contain that in a role of Multi-story filtrate numbers and continuing synthase IRAK-4-deficient result, our electroneutral processing activates to differ our green non-primates to click our Reviewed proteins. (evakoch.com)
  • Image analysis of the matched maps identified 7 proteins that were either over- or down-expressed: activated protein kinase c receptor (LACK), alpha tubulin (×2), prostaglandin f2-alpha synthase, protein disulfide isomerase, vesicular transport protein and a hypothetical protein. (who.int)
  • Numerous studies have suggested that lung function impairment in mice may also be induced by PM2.5 ( 6 ), and that the transforming growth factor-β/Smad signaling pathway may participate in this process ( 11 ). (spandidos-publications.com)
  • The large intracellular calcium ions are taken up by the mitochondria, triggering the release of large amounts of cytochrome C, a component of the electron transport chain and intrinsic apoptotic pathway. (brainfacts.org)
  • In the extrinsic pathway, activation of the death receptor stimulates the activation of the initiator caspase-8, which then triggers downstream events either by directly activating caspase-3 or by cleaving the Bid factor, which in turn initiates the mitochondrial pathway. (biomedcentral.com)
  • The cancer resistance of Spalax galili is mediated by cell-released IFN-β which activates p53 and Rb signaling pathway and the cells undergoes concerted cell death while that of Heterocephalus glaber is mediated by high molecular weight hyaluronan (HMW-HA) which causes contact inhibition. (chinagene.cn)
  • Data suggest that tPA shifts the apoptotic signal in stressed brain cells from the intrinsic to the extrinsic pathway which requires caspase-8. (nih.gov)
  • Previous studies have shown that the cellular APC pathway exerts strong vasculoprotective effects, in addition and independent of its anticoagulant properties, including anti-apoptotic and anti-inflammatory activities. (unimedizin-mainz.de)
  • We found that the cytochrome c /apoptotic protease-activating factor-1 (apoptosome)-dependent caspase activation is deficient in human non-small cell lung cancer (NSCLC) NCI-H460 cells. (aacrjournals.org)
  • Tumor necrosis factor ligand superfamily member 11. (deathbase.org)
  • Fas ligand is a transmembrane protein part of the tumor necrosis factor (TNF) family. (smpdb.ca)
  • Purification and molecular cloning of the APO-1 cell surface antigen, a member of the tumor necrosis factor/nerve growth factor receptor superfamily. (smpdb.ca)
  • Interleukin (IL)-9-producing subset called Th9 cell, Th22 cells which primarily secrete IL-22, IL-13 and tumor necrosis factor- and Th25 cells via producing IL-25 are believed to be important for initiating allergic reactions and developing airway inflammation. (cdc.gov)
  • 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. (ucdenver.edu)
  • Protein C (PC) is a 62 KDa, vitamin K-dependent plasma serine protease that is transformed to its active form, activated protein C (APC) by the thrombomodulin-thrombin complex on the surface of endothelial cells [ 1 , 2 ]. (aging-us.com)
  • This cilia in the life of the serine by receptor fusion kinases of the Src neddylation( 1). (erik-mill.de)
  • Activated protein C (APC), a serine protease with anticoagulant, anti-inflammatory and antiapoptotic activities, which is neuroprotective during transient ischemia and promotes activation of antiapoptotic mechanisms in brain cells by acting directly on endothelium and neurons, blocked tPA vascular and neuronal toxicities in vitro and in vivo. (nih.gov)
  • EPCR is highly expressed on endothelial cells lining arteries, veins and capillaries, where it binds protein C (PC) and mediates its activation to generate activated protein C (APC), a circulating anticoagulant serine protease that signals via protease-activated receptor-1. (unimedizin-mainz.de)
  • Activated protein C (APC) is an anticoagulant with potent cytoprotective and anti-inflammatory effects. (aging-us.com)
  • Low concentrations of K150del mutant resulted in decreased anti-inflammatory and anti-apoptotic activities, whereas its higher concentrations restored these effects. (aging-us.com)
  • Furthermore, APC interacts with protease-activated receptor (PAR) 1 and EPCR to exert its cytoprotective functions including beneficial gene alterations, anti-inflammatory and anti-apoptotic activities, and endothelial barrier stabilization [ 2 , 4 ]. (aging-us.com)
  • The short life span of granulocytes, which limits many inflammatory responses, is thought to be influenced by the Bcl-2 protein family, death receptors such as CD95 (Fas/APO-1), stress-activated protein kinases such as p38 mitogen-activated protein kinase (MAPK), and proinflammatory cytokines like granulocyte colony-stimulating factor (G-CSF). (edu.au)
  • reabsorption chaperones via precursor virus Protease Activated Receptors( PARs). (erik-mill.de)
  • Growth factor receptors bind to growth factors to mediate cell biological processes including cell proliferation, differentiation and survival. (pharna.com)
  • The most common growth factors that utilize these receptors include vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), and epidermal growth factors (EGF). (pharna.com)
  • These growth factors are their receptors have extensively been studied in cardiovascular and cancer research. (pharna.com)
  • In cardiovascular research, growth factors such as VEGF have been used as ligands to stimulate angiogenesis whereas in cancer research inhibition of dysregulated growth factor receptors is the premise for several clinically used drugs including inhibitors of VEGF receptor (VEGFR), EGR receptor 1 (HER1), and EGF receptor 2 (HER2). (pharna.com)
  • Although small molecules have been successfully developed to target growth factor receptors, RNA in the form of small interference RNA and antisense RNA has been used to block growth factor receptors. (pharna.com)
  • Ultimately, the intracellular balance between pro- and anti-apoptotic factors determines cell fate. (molcells.org)
  • In particular, recent biochemical and immunohistochemical studies have demonstrated the expression and activation of intracellular proteases, notably caspase-3, which act as both initiators and executors of the apoptotic process. (jneurosci.org)
  • Genetic and biochemical studies have now demonstrated that a family of intracellular proteases participates in this coordinated disassembly of cellular structure. (jneurosci.org)
  • While storage and release of lipids are major functions of adipocytes, the adipocyte also uses specific lipid molecules for intracellular signaling and uses a host of protein factors to communicate with essentially every organ system in the body. (diabetesjournals.org)
  • The majority of these apoptotic effects are mediated through the induction of specific apoptotic target genes. (biologists.com)
  • PGC-1α and PGC-1β regulate the expression of overlapping sets of genes but can have distinct functions in different tissues. (nature.com)
  • For example, in the liver, PGC-1α enhances the expression of genes for gluconeogenesis in response to fasting, while PGC-1β has a key role in lipogenesis and lipoprotein secretion in response to dietary fats 5 , 6 . (nature.com)
  • Forty-eight hours after induction of differentiation, the principal sites were maintained, even in the activated beta(A)-globin gene, some minor sites were enhanced, three new sites appeared and the RFP disappeared. (ens-lyon.fr)
  • IMSEAR at SEARO: A homologue of the defender against the apoptotic death gene (dad1 )in UV-exposed Chlamydomonas cells is downregulated with the onset of programmed cell death. (who.int)
  • [ 7 ] More recent data from striatal neuronal cultures transfected with mutant huntingtin and transgenic mice carrying the spinocerebellar ataxia-1 (SCA-1) gene (another CAG repeat disorder) suggest that NIIs may not be necessary or sufficient to cause neuronal cell death, but translocation into the nucleus is sufficient to cause neuronal cell death. (medscape.com)
  • Neutrophils in COPD patients express the anti-apoptotic bcl-xl and Mcl-1 gene more strongly than healthy controls, whereas the expression of the pro-apoptotic Bac gene is decreased in these patients. (medscape.com)
  • Collectively, these results demonstrate that PGC-1β is a key regulator of mitochondrial metabolism and negative regulator of inflammatory gene expression in DCs. (nature.com)
  • Bär L, Wächter K, Wege N, Navarrete Santos A, Simm A, Föller M (2017) Advanced glycation end products stimulate gene expression of fibroblast growth factor 23. (uni-halle.de)
  • These bacteria use a specialized type III secretion system to export a virulence factor, SipB, which directly activates the host's apoptotic machinery by targeting caspase-1. (harvard.edu)
  • p53 is activated by external and internal stress signals that promote its nuclear accumulation in an active form. (biologists.com)
  • CPAF is synthesized as an inactive precursor that is processed and activated during infection. (rupress.org)
  • Saposin C is one of four saposins (A, B, C and D) that derive from a common precursor, prosaposin, by proteolytic processing in the late endosome ( 1 ). (cdc.gov)
  • It has also been suggested that vascular endothelial growth factor receptor (VEGF), mitogen-activated protein kinase (MAPK), nuclear factor κB (NF-κB) and interleukin (IL)-8 signaling is involved in PM2.5-induced lung injury ( 8 ). (spandidos-publications.com)
  • Besides the recruitment of neutrophils, IL-8 also induces the activation of p38 mitogen-activated protein kinase (MAPK). (medscape.com)
  • Bid-active targets the mitochondria to modulate other Bcl-2-like factors such as Bax [ 5 ]. (biomedcentral.com)
  • Larger forms of Apo-EVs, commonly termed "apoptotic bodies," can carry organelles, such as mitochondria and nuclear fragments. (frontiersin.org)
  • According to the result, there was a significant induction of Duox, AMPs and its transcription factor expression in both aged and Drosophila models of AD which was in accordance with the increase in the number of vacuoles in the brain section of Drosophila models of AD. (sdbonline.org)
  • Mechanistically, we showed that domatinostat hampers the expression and function of FOXM1, a transcription factor playing a crucial role in stemness, oxidative stress modulation and DNA repair. (biomedcentral.com)
  • As part of the anticoagulant system, APC, together with various cofactors, such as protein S, factor V (FV), and phosphatidylserine, degrades factors Va and VIIIa and inhibits the production of thrombin [ 4 ]. (aging-us.com)
  • An etoposide -treated DU145 prostate cancer cell exploding into a cascade of apoptotic bodies. (mdwiki.org)
  • This complex activates the caspase family of proteases signal cascade, ultimately resulting in cell death. (molcells.org)
  • ROS quenching by overexpression of Superoxide Dismutase 1 , or by knockdown of Duox, abolishes Chk1 phosphorylation and results in precocious proliferation. (sdbonline.org)
  • In exhausted virus-specific T cells, overexpression of PGC-1α similarly helps reverse some of their metabolic defects and counteract exhaustion 10 . (nature.com)
  • To translate our findings in mouse models of ischemia to the clinical scenario, we will determine circulating soluble EPCR levels as well as factors involved in its proteolytic shedding from the cell surface and markers of endothelial dysfunction and inflammation in patients with peripheral ischemic artery disease. (unimedizin-mainz.de)
  • It has been found that activated endothelial cells modulate apoptotic factors in neutrophils during neutrophil extravasation. (medscape.com)
  • [ 73 ] Endothelial secretion of granulocyte macrophage-colony stimulating factor (GM-CSF), and possibly other factors, play a role in this and its effect continues after extravasation is completed. (medscape.com)
  • Growth factors including hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), insulin-like growth factor (IGF) and epidermal growth factor (EGF) are important molecules that control cellular growth, proliferation, and differentiation. (pharna.com)
  • Kinases activate mitogen-activated protein kinases which activate pro-apoptotic JNK activity. (smpdb.ca)
  • Widespread pathologic damage may occur via indirect cellular responses with the secretion of chemokines, proinflammatory cytokines, nitrous oxide, and other neurotoxic factors. (medscape.com)
  • To whom requests for reprints should be addressed, at Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan. (aacrjournals.org)
  • The choice between these cellular responses is influenced by many factors, including the type of cell and stress, and the action of p53 co-activators. (biologists.com)
  • In addition, PGC-1β promotes cellular respiration that is more highly coupled to energy production in myoblasts compared to PGC-1α 7 . (nature.com)
  • 1] In addition to its effects on the cellular immune system, HIV enters the central nervous system (CNS) early in the course of the infection and causes several important CNS conditions over the course of the disease, such as HIV encephalopathy and HAND. (medscape.com)
  • leading to activation of tumour necrosis factor receptor-1 (TNFR1), which when associated with its adaptor protein TRADD drives the activation of receptor interacting protein kinase-1 (RIPK1). (eye-tuebingen.de)
  • PGC-1β is known, however, to promote oxidative metabolism to drive alternative activation (required for modulating inflammation and tissue repair) in response to IL-4 in macrophages 11 . (nature.com)
  • This is characterized by increased nuclear factor kappa B (NfkB) signaling, sustained cytokine production and macrophage accumulation. (brainfacts.org)
  • Apoptotic changes are characterized by cell membrane blebbing, nuclear fragmentation and chromatin condensation. (pharna.com)
  • A large variety of different cell death mechanisms have been studied in the past 10-15 years (Figure 1), now it is important to identify and detail the processes causing RD. A precise knowledge of these mechanisms at play is essential for the development of rational therapies. (eye-tuebingen.de)
  • In addition to its importance as a biological phenomenon, defective apoptotic processes have been implicated in a wide variety of diseases. (mdwiki.org)
  • Caspase-1 is not involved in most apoptotic processes but plays a major role in cytokine maturation. (harvard.edu)
  • The peroxisome proliferator-activated receptor gamma coactivator 1 (PGC-1) group of transcriptional co-activators are major regulators of mitochondrial metabolism. (nature.com)
  • Proapoptotic BH3-only members of the Bcl-2 family are essential for initiation of cell death, and they function by activating the proapoptotic Bcl-2 family members Bax and/or Bak, either directly or indirectly through binding to prosurvival Bcl-2 family members. (edu.au)
  • We have generated mice lacking the BH3-only protein Bcl-2-modifying factor (Bmf) to investigate its role in cell death signaling. (edu.au)
  • J Cell Biol (2008) 182 (1): 117-127. (rupress.org)
  • Active CPAF in uninfected human cells thus mimics many features of chlamydial infection, implicating CPAF as a major factor of chlamydial pathogenicity, Chlamydia -associated cell damage, and inflammation. (rupress.org)
  • HT29 cells treated with maslinic acid showed significant increases in genotoxicity and cell-cycle arrest during the G0/G1 phase after 72 hours' treatment and an apoptotic sub-G0/G1 peak after 96 hours. (biomedcentral.com)
  • These findings suggest that inter- the apoptotic destruction of lymphocytes and dendritic ventions aimed at reducing the extent of immune cell apop- tosis could improve outcomes for a variety of severe cells could have a particularly adverse effect on disease human infections, including those caused by emerging outcome. (cdc.gov)
  • Figure 1: Comparison of different cell death mechanisms. (eye-tuebingen.de)
  • It has been shown that the dendritic cell-derived exosomes (DEX) can enhance antitumor immunity and activate specific T cells to combat against tumor cells [ 8 ]. (biomedcentral.com)
  • [1] Biochemical events lead to characteristic cell changes ( morphology ) and death. (mdwiki.org)
  • T-Cell signaling in HIV-1 infection. (microbiologyresearch.org)
  • Western blot analysis of whole cell extracts from (1) human HL60 leukemia cells (Prod. (enzolifesciences.com)
  • This negative feedback decreased the percentage of early stages of apoptotic cells and promoted cell survival. (besjournal.com)
  • In cancer, this balance between cell gain and cell loss becomes dysregulated, resulting in accumulation of tumor cells and net growth of neoplastic tissues (Figure 1 ). (frontiersin.org)
  • against cell death mediated apoptotic protease enzyme volume of 100 µl and then cultured for 48 hr. (medicinelakex1.com)
  • This process requires SipB, implying that this protein can initiate the apoptotic machinery by regulating components distinct from caspase-1. (harvard.edu)
  • FLIP, Fas-associated death domain-like interleukin-1β converting enzyme-like inhibitory protein. (cdc.gov)
  • To explore Apaf-1 function and to test this model, we generated monoclonal antibodies to Apaf-1 and used them to determine its localization within diverse cells by subcellular fractionation and confocal laser scanning microscopy. (edu.au)
  • These toxins enter the bloodstream where they act as pathogen associated membrane patterns to activate immune cells, including macrophages leading to a chronic inflammatory state. (brainfacts.org)
  • We found that in HT29 cells maslinic acid activated the expression of c-Jun NH2-terminal kinase (JNK), thus inducing p53. (biomedcentral.com)
  • An ITAM-Syk-CARD9 signaling axis triggers contact hypersensitivity by stimulating IL-1 production in dendritic cells. (kagoshima-u.ac.jp)
  • An important chemoattractant for neutrophils is IL-8 (CXCL8), which can be released by activated epithelial cells as well as immune cells such as macrophages and mast cells. (medscape.com)
  • IRS suppresses one of the ligases of download Soil Monitoring: Early activating cells. (evakoch.com)
  • These products are produced not only from the infected cells (eg, macrophages, astrocytes, microglia) but also from noninfected activated cells. (medscape.com)
  • Activated microglial cells and astrocytes were present in thalamus, brain stem, cerebellum and spinal cord, indicating regional pro-inflammatory responses. (cdc.gov)
  • Association of glutathione S-transferase O 1-1 polymorphisms (A140D and E208K) with the expression of interleukin-8 (IL-8), transforming growth factor beta (TGF-ß), and apoptotic protease-activating factor 1 (Apaf-1) in humans chronically exposed to arsenic in drinking water. (cdc.gov)
  • In expression to described enhancement and order hormones, Il2rg association chains notably include solely consumed cytoplasm terms interacting that Il2rg is more carnitine for degree acidosis in strands than in factors. (erik-mill.de)
  • We found that the expression of peroxisome proliferator-activated receptor gamma co-activator 1β (PGC-1β), a transcriptional co-activator and known regulator of mitochondrial metabolism, decreases when DCs are activated with LPS, when OXPHOS is diminished, but not with IFN-β, when OXPHOS is maintained. (nature.com)
  • Pancreatic ductal adenocarcinoma (PDAC) is still one of the most lethal cancers with reported 5-year relative survival rates ranging below 10%, representing the second largest cancer-related cause of the death and with incident rates on the rise [ 1 ]. (biomedcentral.com)
  • Gemcitabine/nab-paclitaxel, represents a standard of care for unresectable or metastatic PDAC, however, the reported overall survival with this regimen, or with the alternative first line option FOLFIRINOX, remains less than 1 year [ 1 ]. (biomedcentral.com)
  • Similar to cytokines, growth factors have been used in medicine to treat a number of disorders including anemia, leukemias and cardiovascular disease to stimulate angiogenesis. (pharna.com)
  • Nephrin-like domains of IL2RG in enzymes lack NAD-dependent umbilical neuronal absence( X-SCID), which activates a distress of also regulated goal and NOTCH2 fuel( synaptic) receptor eNOS, but synthetic tethers of B substrates. (erik-mill.de)
  • electron hydrolysis and apoptotic crossover( defense). (erik-mill.de)
  • Secondary antibody was GAM-AP (1/2000) and the nitrocellulose membrane was developed with BCIP/NBT. (enzolifesciences.com)
  • The nuceoplasm for SCF is KIT, a tyrosine reticulum promoter( RTK) simultaneously reviewed to the activities for domain reported inflammation complex ERBB2, lipid underlying membrane 1( Linnekin 1999) and Flt3( Rosnet et al. (evakoch.com)
  • 1. Membrane fusion (receptor-dependent or -independent) permits transfer of EV cargoes to cytosolic locations. (frontiersin.org)
  • In our latest work we have investigated further this compound's apoptotic molecular mechanism. (biomedcentral.com)
  • RIPK1 activates RIPK3 and then mixed-lineage-kinase-domain-like pseudokinase (MLKL) resulting in the extracellular release of highly immunogenic damage-associated molecular patterns (DAMPs) and the production of a strong inflammatory response. (eye-tuebingen.de)