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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
Show all 6 Pubmed References
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
Show all 3 Pubmed References
Human Caspase 8 Protein expressed in Escherichia coli (E. coli) - ABIN2688831
Patel, Gores, Kaufmann: The role of proteases during apoptosis. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 1996
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Furthermore, while activities to process procaspase-8 and procaspase-9 appeared in SAMDC (show AMD1 Proteins)-overexpressed apoptotic embryos, the activity to process procaspase-8 did not appear in p53 (show TP53 Proteins)-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 (show BID Proteins) and Caspases-2 and -8
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.
inhibition of TAK1 (show NR2C2 Proteins) triggered two caspase 8 activation pathways through the induction of RIP1 (show RALBP1 Proteins)-FADD (show FADD Proteins)-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 (show CASP3 Proteins) 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 (show FAS Proteins) and caspase-8 were observed, along with other molecules involved in the extrinsic apoptotic pathway such as Dapk1 (show DAPK1 Proteins), Traf3 (show TRAF3 Proteins), Tnsf12, Tnfrsf1A (show TNFRSF1A Proteins) and Ripk1 (show RIPK1 Proteins).
Results suggest that caspase-8 could regulate receptor-interacting protein 3 (RIP3 (show RIPK3 Proteins))-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 (show NLRC4 Proteins) activation in Intestinal epithelial cells (IECs) leads to cell expulsion and IL-18 (show IL18 Proteins) release, and implicate Caspase-8 in NLRC4 (show NLRC4 Proteins) inflammasome responses in vivo by generation of doubly deficient in Caspase-1 (show CASP1 Proteins) and Caspase-8.
ING4 (show ING4 Proteins) might suppress proliferation and enhance apoptosis in human malignant melanoma cells by activating Fas (show FAS Proteins)-induced apoptosis in a caspase-8-dependent pathway.
High caspase-8 is not significantly associated with adverse breast cancer-specific survival. No associations were observed between caspase-8 and clinicopathological criteria.
we found that plumbagin could enhance TRAIL-induced apoptosis in Kasumi-1 cells, and the mechanisms include ROS (show ROS1 Proteins)-mediated upregulation of DR5 (show TNFRSF10B Proteins) expression, caspase-8 activation and inhibition of cFLIP (show CFLAR Proteins) expression
this study shows that mitochondrial DNA oxidation induces imbalanced activity of NLRP3 (show NLRP3 Proteins)/NLRP6 inflammasomes by activation of caspase-8 and BRCC36 (show BRCC3 Proteins) in dry eye
Importantly, the bioinformatics analysis of microarray gene expression data derived from a set of high-grade human gliomas, shows that high Caspase-8 expression levels correlate with a worse prognosis.
this review describes the role of caspase-8 in the initiation of extrinsic apoptosis execution and the mechanism by which caspase-8 inhibits necroptosis
Data indicate that elevated levels of Polo-like kinase 3 (Plk3 (show PLK3 Proteins))and pT273 caspase-8 are correlated with favorable clinical outcome in patients with anal squamous cell carcinoma (anal SCC (show CYP11A1 Proteins)) treated with concomitant chemoradiotherapy (CRT (show SLC6A8 Proteins)).
Caspase-8 binding via FADD to the receptor is an indispensable initiating step in death-inducing signaling complex formation and NF-kB activation.
The procaspase-8 Q482H mutation in AML (show RUNX1 Proteins) patients abolishes caspase-8-mediated apoptosis by impairing procaspase-8 dimerization.
These findings suggest that intracellular cholesterol level affects TMZ treatment of GBM mediated via a DR5 (show TNFRSF10B Proteins)-caspase-8 mechanism.
study shows genetic association of rare variants in CASP8 with Alzheimer's disease and proposes a mechanism of action mediated by decreased enzyme activity; for two CASP8 variants, p.K148R and p.I298V, the association remained significant in a large combined sample
S. aureus-induced apoptosis in bovine mammary epithelial cells apoptosis was mitigated by caspase-3 (show CASP3 Proteins) 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 (show CASP9 Proteins).
Nitric oxide-dependent increase in caspase-8 mRNA levels is associated with phosphorylation of STAT-1 (show STAT1 Proteins) at Ser (show SIGLEC1 Proteins)-727 and STAT1 (show STAT1 Proteins) 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 (show TNF Proteins), IL-6 (show IL6 Proteins), IL-12p40, IL-1beta (show IL1B Proteins), and resulted in increased expression of the apoptosis initiator caspase-8 and bcl2L1 (show BCL2L1 Proteins).
Induction of apoptosis through targeted activation of caspase (show CASP3 Proteins) by tamoxifen (ATTAC(TM)) further expands the repertoire of genetic tools for conditional interrogation of cellular functions.
Targeted gene knockdown of TNFRSF1B (show TNFRSF1B Proteins) in zebrafish embryos results in the induction of a caspase-8, caspase-2 (show CASP2 Proteins) and P53 (show TP53 Proteins)-dependent apoptotic program in endothelial cells that bypasses caspase-3 (show CASP3 Proteins).
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