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Patil, Kim, Jayaprakasha: Berberine induces apoptosis in breast cancer cells (MCF-7) through mitochondrial-dependent pathway. in European journal of pharmacology 2010
Show all 35 Pubmed References
Anginot, Espeli, Chasson, Mancini, Schiff: Galectin 1 modulates plasma cell homeostasis and regulates the humoral immune response. in Journal of immunology (Baltimore, Md. : 1950) 2013
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Patel, Wilson, ODea, Takata: TNF-induced death signaling triggers alveolar epithelial dysfunction in acute lung injury. in Journal of immunology (Baltimore, Md. : 1950) 2013
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Abdel-Latif, Murray, Renberg, ONeill, Porter, Jensen, Johnson: Cell death in bovine parvovirus-infected embryonic bovine tracheal cells is mediated by necrosis rather than apoptosis. in The Journal of general virology 2006
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Teachey, Obzut, Axsom, Choi, Goldsmith, Hall, Hulitt, Manno, Maris, Rhodin, Sullivan, Brown, Grupp: Rapamycin improves lymphoproliferative disease in murine autoimmune lymphoproliferative syndrome (ALPS). in Blood 2006
Rat (Rattus) Caspase 8 ELISA Kit für Sandwich ELISA - ABIN416145
Abdelkader, Safar, Salem: Ursodeoxycholic Acid Ameliorates Apoptotic Cascade in the Rotenone Model of Parkinson's Disease: Modulation of Mitochondrial Perturbations. in Molecular neurobiology 2015
Furthermore, while activities to process procaspase-8 and procaspase-9 appeared in SAMDC (zeige AMD1 ELISA Kits)-overexpressed apoptotic embryos, the activity to process procaspase-8 did not appear in p53 (zeige TP53 ELISA Kits)-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 (zeige BID ELISA Kits) 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 (zeige NR2C2 ELISA Kits) triggered two caspase 8 activation pathways through the induction of RIP1 (zeige RALBP1 ELISA Kits)-FADD (zeige FADD ELISA Kits)-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 (zeige CASP3 ELISA Kits) 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 (zeige FAS ELISA Kits) and caspase-8 were observed, along with other molecules involved in the extrinsic apoptotic pathway such as Dapk1 (zeige DAPK1 ELISA Kits), Traf3 (zeige TRAF3 ELISA Kits), Tnsf12, Tnfrsf1A (zeige TNFRSF1A ELISA Kits) and Ripk1 (zeige RIPK1 ELISA Kits).
Results suggest that caspase-8 could regulate receptor-interacting protein 3 (RIP3 (zeige RIPK3 ELISA Kits))-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 (zeige NLRC4 ELISA Kits) activation in Intestinal epithelial cells (IECs) leads to cell expulsion and IL-18 (zeige IL18 ELISA Kits) release, and implicate Caspase-8 in NLRC4 (zeige NLRC4 ELISA Kits) inflammasome responses in vivo by generation of doubly deficient in Caspase-1 (zeige CASP1 ELISA Kits) and Caspase-8.
ING4 (zeige ING4 ELISA Kits) might suppress proliferation and enhance apoptosis in human malignant melanoma cells by activating Fas (zeige FAS ELISA Kits)-induced apoptosis in a caspase-8-dependent pathway.
The procaspase-8 Q482H mutation in AML (zeige RUNX1 ELISA Kits) 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 (zeige TNFRSF10B ELISA Kits)-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
Knockout (KO) or knockdown of caspase-8, CD95 (zeige FAS ELISA Kits) or FADD (zeige FADD ELISA Kits) prevents activation of Plk3 (zeige PLK3 ELISA Kits) upon CD95 (zeige FAS ELISA Kits) stimulation, suggesting a requirement of a functional death-inducing signaling complex for Plk3 (zeige PLK3 ELISA Kits) activation.
CASP8: rs1045494 (C > T), PIK3R1: rs3756668 (A > G) and CASP7 (zeige CASP7 ELISA Kits): rs4353229 (T > C), were associated with longer overall survival in limited disease-small cell lung cancer patients after chemoradiotherapy
SP-D (zeige SFTPD ELISA Kits) increases the formation of nuclear and membrane blebs. Inhibition of caspase-8 confirms the effect of SP-D (zeige SFTPD ELISA Kits) is unique to the caspase-8 pathway.
This is the first report, showing negative and independent prognostic impact of the CASP8 -652 6N Del and the 302His variant for breast cancer.
The C-terminal helical conformation of Bax (zeige BAX ELISA Kits), not its primary sequence, appears to be critical for CASP8 recruitment and activation culminating in cell death.
Data suggest that pro-death signals through TIR-domain-containing adapter-inducing interferon-beta (zeige IFNB1 ELISA Kits) (TRIF (zeige TRIM69 ELISA Kits)) are regulated by autophagy and propose that pro-apoptotic signalling through TRIF (zeige TRIM69 ELISA Kits)/RIPK1 (zeige RIPK1 ELISA Kits)/caspase-8 occurs in fibrillary platforms.
S. aureus-induced apoptosis in bovine mammary epithelial cells apoptosis was mitigated by caspase-3 (zeige CASP3 ELISA Kits) 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 (zeige CASP9 ELISA Kits).
Nitric oxide-dependent increase in caspase-8 mRNA levels is associated with phosphorylation of STAT-1 (zeige STAT1 ELISA Kits) at Ser (zeige SIGLEC1 ELISA Kits)-727 and STAT1 (zeige STAT1 ELISA Kits) 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 (zeige TNF ELISA Kits), IL-6 (zeige IL6 ELISA Kits), IL-12p40, IL-1beta (zeige IL1B ELISA Kits), and resulted in increased expression of the apoptosis initiator caspase-8 and bcl2L1 (zeige BCL2L1 ELISA Kits).
Induction of apoptosis through targeted activation of caspase (zeige CASP3 ELISA Kits) by tamoxifen (ATTAC(TM)) further expands the repertoire of genetic tools for conditional interrogation of cellular functions.
Targeted gene knockdown of TNFRSF1B (zeige TNFRSF1B ELISA Kits) in zebrafish embryos results in the induction of a caspase-8, caspase-2 (zeige CASP2 ELISA Kits) and P53 (zeige TP53 ELISA Kits)-dependent apoptotic program in endothelial cells that bypasses caspase-3 (zeige CASP3 ELISA Kits).
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