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Human Caspase 8 Protein expressed in Escherichia coli (E. coli) - ABIN2487286
Appukuttan, Kasseckert, Micoogullari, Flacke, Kumar, Woste, Abdallah, Pott, Reusch, Ladilov: Type 10 adenylyl cyclase mediates mitochondrial Bax translocation and apoptosis of adult rat cardiomyocytes under simulated ischaemia/reperfusion. in Cardiovascular research 2012
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Human Caspase 8 Protein expressed in Escherichia coli (E. coli) - ABIN2688834
Nicholson, Ali, Thornberry, Vaillancourt, Ding, Gallant, Gareau, Griffin, Labelle, Lazebnik: Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis. in Nature 1995
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Furthermore, while activities to process procaspase-8 and procaspase-9 appeared in SAMDC-overexpressed apoptotic embryos, the activity to process procaspase-8 did not appear in p53-overexpressed apoptotic embryos.
tail regression at metamorphosis implicates an apoptotic pathway inducible by T(3) hormone in an organ autonomous manner and involving the cell death executioners BH3 interacting domain death agonist and Caspases-2 and -8
Results uncover a form of caspase-8-mediated pyroptosis and suggest a hypothesis for the increased sensitivity of humans to Yersinia infection compared with the rodent reservoir.
these results demonstrate that Caspase-8 is essential to prevent Salmonella Typhimurium induced enteritis and to ensure host survival
These data demonstrate that caspase-8 functions in synovial antigen-presenting cells to regulate the response to inflammatory stimuli by controlling RIPK3 action, and this delicate balance maintains homeostasis within the joint.
Results illustrate the temporal and spatial activation of caspase-8 and -3 in microglia/macrophages occurring upon ischemic stroke and suggest that the expression of these caspases could be used in neuropathological diagnostic work.
Caspases and their substrates are key mediators of apoptosis.
inhibition of TAK1 triggered two caspase 8 activation pathways through the induction of RIP1-FADD-caspase 8 complex as well as FLIP cleavage/degradation.
this study identifies a crucial role for caspase-8 in the development of allergic airway inflammation
Prolonged treatment of human PMNs or mice bone marrow derived neutrophils (BMDN) with nitric oxide led to enhanced reactive oxygen species generation, caspase-8/caspase-3 cleavage, reduced mitochondrial membrane potential and finally cellular apoptosis.
caspase-8-dependent apoptosis was linked to hepatocellular carcinoma development.
Statistically significant increases in the expression of Fas and caspase-8 were observed, along with other molecules involved in the extrinsic apoptotic pathway such as Dapk1, Traf3, Tnsf12, Tnfrsf1A and Ripk1.
Results suggest that caspase-8 could regulate receptor-interacting protein 3 (RIP3)-mediated necroptosis.
we show that caspase-8 activity promotes cell-intrinsic cytokine expression, independent of its role in cell death in response to Yersinia infection
Data indicate that NLRC4 activation in Intestinal epithelial cells (IECs) leads to cell expulsion and IL-18 release, and implicate Caspase-8 in NLRC4 inflammasome responses in vivo by generation of doubly deficient in Caspase-1 and Caspase-8.
ING4 might suppress proliferation and enhance apoptosis in human malignant melanoma cells by activating Fas-induced apoptosis in a caspase-8-dependent pathway.
studies have uncovered the combined actions of the NLRP3 inflammasome and caspase 8 leading to IL-1beta maturation and the directionality of IL-1beta in driving disease inPstpip2(cmo)mice.
Chronic TLR Stimulation Controls NLRP3 Inflammasome Activation through IL-10 Mediated Regulation of NLRP3 Expression and Caspase-8 Activation
A20 targets caspase-8 and FADD to protect HTLV-I-infected cells.
Data indicate that receptor-interacting serine-threonine kinase 3 (RIPK3) deletion prevents inflammatory phenotypes in CreLysM (lysozyme M) Casp8fl/fl (caspase 8) mice.
CASP8 deletion did not affect the overall number of microglia expressing the pan specific microglia marker, Iba1
We observed that NDMP generation was dependent on the extrinsic caspase apoptotic pathway (caspase 3 and caspase 8), cAMP activation of PKA but not of Epac, and on activation of MLCK.
CASP8 deficiency is a novel cause of very early onset-inflammatory bowel disease associated with lymphocyte dysfunction, impaired inflammasome activation, and defec- tive epithelial cell death responses.
Data show that ionizing radiation (IR) induces apoptosis in THP-1 cells through cas-8-mediated pathways, whereas THP-1-derived macrophages (THP-1-M) are resistant to IR due to impaired casp-8-mediated apoptosis during differentiation and not to a capacity for DSB repair suggesting that the regulation of casp-8-mediated apoptosis during differentiation plays a role in the p53-independent radio-resistance of THP-1-M.
The apoptosis was partially dependent upon caspase-8 concomitant with attenuated NF-kappa B survival signal due to stimulus of TNF-alpha. It suggests that PAK4 as target is a switch between caspase-8 apoptosis and NF-kappa B survival signals induced by TNF-alpha in hepatocarcinoma cells.
The caspase 8 mediated RIPK1 cleavage product has a pro-apoptotic function, and further cleavage of this pro-apoptotic cleavage product by human rhinovirus 3C protease may provide a mechanism by which human rhinovirus limits apoptosis.
results suggest that miR-21 regulates the apoptosis of keloid fibroblasts via targeting FasL, and caspase-8 and the mitochondria-mediated apoptotic signaling pathway is involved in this process.
Caspase-3 and -8 and annexin V may serve as diagnostic markers in Ovarian cancer , also explained that the decrement in control of the S phase in the cell cycle may considered one of the significant factors in the development of ovarian tumors
neither rs13416436 nor rs2037815 associated with pre-eclampsia
High CASP8 expression is associated with Colorectal Cancer.
Sleep duration is associated with plasma caspase-8. Caspase-8 independently predicts diabetes mellitus years before disease onset and modifies the effect of sleep duration on incident diabetes mellitus.
Caspase-8 and Caspase-3 expressions in tumor tissues are novel candidate prognostic markers for colorectal cancer patients
Reactive oxygen species-induced cleavage of NHLRC2 by caspase-8 leads to apoptotic cell death in the HCT116 human colon cancer cells.
this study is the first report on reduced expression of CASP8 in breast cancer versus adjacent normal tissues.
The polymorphisms of CASP8, rs7608692, and haplotype AGAACAG correlated with neutropenia toxicity. The haplotype GGGGAAA was associated with thrombocytopenia toxicity. We conclude that the polymorphisms of CASP8 contribute to the prognosis of advanced lung adenocarcinoma and influence the quality of life and survival.
These results indicated that cMyc and Fas regulated the sensitivity of A549 cells to irradiation by regulating caspase8-mediated Bid activation and the subsequent association with the mitochondrial pathway of apoptosis.
The caspase-8/Bid/cytochrome c axis links signals from death receptors to mitochondrial reactive oxygen species production.
miR-21 was elevated in osteosarcoma, and overexpression of miR-21 suppressed apoptosis via targeting caspase 8.
Our findings indicate the relationship of SNP CASP8 D302H and breast cancer would not be universal but only be sensitive in some particular European countries.
no mutations were detected in the CASP8 gene, but we observed a frequent [32/48 (66.6%)] SNP [rs1045487] in the oral cancer samples.
case-control study, including 600 hepatocellular carcinoma (HCC) and 600 HBsAg positive controls without HCC, was conducted to assess the relationship between 11 tagging SNPs in CASP8, CASP10 and CFLAR and HBV-related HCC risk .These results suggest that the CASP8 -652 6N ins/del polymorphism may play a protective role in the development, progression, and survival of HBV-related HCC among the Chinese Han population.
High caspase-8 is not significantly associated with adverse breast cancer-specific survival. No associations were observed between caspase-8 and clinicopathological criteria.
S. aureus-induced apoptosis in bovine mammary epithelial cells apoptosis was mitigated by caspase-3 and caspase-8 inhibitors, suggesting that apoptosis is initiated via caspase-8 activation.
Endothelial cell apoptosis by H. somnus-activated platelets required activation of both caspase-8 and caspase-9.
mmediately after hypoxia C8 and C1 follow a similar pattern of increase while long term this appears to dissociate
induces apoptosis in porcine ovarian follicles
Nitric oxide-dependent increase in caspase-8 mRNA levels is associated with phosphorylation of STAT-1 at Ser-727 and STAT1 binding to the caspase-8 promoter in cultured lung endothelial cells.
Data show that cysteine significantly reduced the expression of pro-inflammatory cytokines, including TNF-alpha, IL-6, IL-12p40, IL-1beta, and resulted in increased expression of the apoptosis initiator caspase-8 and bcl2L1.
Induction of apoptosis through targeted activation of caspase by tamoxifen (ATTAC(TM)) further expands the repertoire of genetic tools for conditional interrogation of cellular functions.
Targeted gene knockdown of TNFRSF1B in zebrafish embryos results in the induction of a caspase-8, caspase-2 and P53-dependent apoptotic program in endothelial cells that bypasses caspase-3.
These results show that zebrafish casp8 has a structure and function similar to mammalian CASP8 orthologs and the role of caspase-8 in the apoptotic signal pathway has been conserved over at least 450 million years of vertebrate evolution.
This gene encodes a member of the cysteine-aspartic acid protease (caspase) family. Sequential activation of caspases plays a central role in the execution-phase of cell apoptosis. Caspases exist as inactive proenzymes composed of a prodomain, a large protease subunit, and a small protease subunit. Activation of caspases requires proteolytic processing at conserved internal aspartic residues to generate a heterodimeric enzyme consisting of the large and small subunits. This protein is involved in the programmed cell death induced by Fas and various apoptotic stimuli. The N-terminal FADD-like death effector domain of this protein suggests that it may interact with Fas-interacting protein FADD. This protein was detected in the insoluble fraction of the affected brain region from Huntington disease patients but not in those from normal controls, which implicated the role in neurodegenerative diseases. Many alternatively spliced transcript variants encoding different isoforms have been described, although not all variants have had their full-length sequences determined.
, xcaspase 8
, death related ced-3/Nedd2-like protein
, caspase 8, apoptosis-related cysteine peptidase
, caspase 8
, DEATH effector domain caspase
, Fas-linked ICE-like protease
, FADD-homologous ICE/CED-3-like protease
, FADD-like ICE
, ICE-like apoptotic protease 5
, MACH-alpha-1/2/3 protein
, MACH-beta-1/2/3/4 protein
, MORT1-associated ced-3 homolog
, apoptotic cysteine protease
, apoptotic protease Mch-5
, caspase 8, apoptosis-related cysteine protease
, cysteine protease