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Patil, Kim, Jayaprakasha: Berberine induces apoptosis in breast cancer cells (MCF-7) through mitochondrial-dependent pathway. dans 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. dans Journal of immunology (Baltimore, Md. : 1950) 2013
Show all 16 Pubmed References
Patel, Wilson, ODea, Takata: TNF-induced death signaling triggers alveolar epithelial dysfunction in acute lung injury. dans 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. dans 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). dans Blood 2006
Rat (Rattus) Caspase 8 Kit ELISA pour Sandwich ELISA - ABIN416145
Abdelkader, Safar, Salem: Ursodeoxycholic Acid Ameliorates Apoptotic Cascade in the Rotenone Model of Parkinson's Disease: Modulation of Mitochondrial Perturbations. dans Molecular neurobiology 2015
Furthermore, while activities to process procaspase-8 and procaspase-9 appeared in SAMDC (Montrer AMD1 Kits ELISA)-overexpressed apoptotic embryos, the activity to process procaspase-8 did not appear in p53 (Montrer TP53 Kits ELISA)-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 (Montrer BID Kits ELISA) 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 (Montrer NR2C2 Kits ELISA) triggered two caspase 8 activation pathways through the induction of RIP1 (Montrer RALBP1 Kits ELISA)-FADD (Montrer FADD Kits ELISA)-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 (Montrer CASP3 Kits ELISA) 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 (Montrer FAS Kits ELISA) and caspase-8 were observed, along with other molecules involved in the extrinsic apoptotic pathway such as Dapk1 (Montrer DAPK1 Kits ELISA), Traf3 (Montrer TRAF3 Kits ELISA), Tnsf12, Tnfrsf1A (Montrer TNFRSF1A Kits ELISA) and Ripk1 (Montrer RIPK1 Kits ELISA).
Results suggest that caspase-8 could regulate receptor-interacting protein 3 (RIP3 (Montrer RIPK3 Kits ELISA))-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 (Montrer NLRC4 Kits ELISA) activation in Intestinal epithelial cells (IECs) leads to cell expulsion and IL-18 (Montrer IL18 Kits ELISA) release, and implicate Caspase-8 in NLRC4 (Montrer NLRC4 Kits ELISA) inflammasome responses in vivo by generation of doubly deficient in Caspase-1 (Montrer CASP1 Kits ELISA) and Caspase-8.
ING4 (Montrer ING4 Kits ELISA) might suppress proliferation and enhance apoptosis in human malignant melanoma cells by activating Fas (Montrer FAS Kits ELISA)-induced apoptosis in a caspase-8-dependent pathway.
The procaspase-8 Q482H mutation in AML (Montrer RUNX1 Kits ELISA) 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 (Montrer TNFRSF10B Kits ELISA)-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 (Montrer FAS Kits ELISA) or FADD (Montrer FADD Kits ELISA) prevents activation of Plk3 (Montrer PLK3 Kits ELISA) upon CD95 (Montrer FAS Kits ELISA) stimulation, suggesting a requirement of a functional death-inducing signaling complex for Plk3 (Montrer PLK3 Kits ELISA) activation.
CASP8: rs1045494 (C > T), PIK3R1: rs3756668 (A > G) and CASP7 (Montrer CASP7 Kits ELISA): rs4353229 (T > C), were associated with longer overall survival in limited disease-small cell lung cancer patients after chemoradiotherapy
SP-D (Montrer SFTPD Kits ELISA) increases the formation of nuclear and membrane blebs. Inhibition of caspase-8 confirms the effect of SP-D (Montrer SFTPD Kits ELISA) 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 (Montrer BAX Kits ELISA), 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 (Montrer IFNB1 Kits ELISA) (TRIF (Montrer TRIM69 Kits ELISA)) are regulated by autophagy and propose that pro-apoptotic signalling through TRIF (Montrer TRIM69 Kits ELISA)/RIPK1 (Montrer RIPK1 Kits ELISA)/caspase-8 occurs in fibrillary platforms.
S. aureus-induced apoptosis in bovine mammary epithelial cells apoptosis was mitigated by caspase-3 (Montrer CASP3 Kits ELISA) 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 (Montrer CASP9 Kits ELISA).
Nitric oxide-dependent increase in caspase-8 mRNA levels is associated with phosphorylation of STAT-1 (Montrer STAT1 Kits ELISA) at Ser (Montrer SIGLEC1 Kits ELISA)-727 and STAT1 (Montrer STAT1 Kits ELISA) 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 (Montrer TNF Kits ELISA), IL-6 (Montrer IL6 Kits ELISA), IL-12p40, IL-1beta (Montrer IL1B Kits ELISA), and resulted in increased expression of the apoptosis initiator caspase-8 and bcl2L1 (Montrer BCL2L1 Kits ELISA).
Induction of apoptosis through targeted activation of caspase (Montrer CASP3 Kits ELISA) by tamoxifen (ATTAC(TM)) further expands the repertoire of genetic tools for conditional interrogation of cellular functions.
Targeted gene knockdown of TNFRSF1B (Montrer TNFRSF1B Kits ELISA) in zebrafish embryos results in the induction of a caspase-8, caspase-2 (Montrer CASP2 Kits ELISA) and P53 (Montrer TP53 Kits ELISA)-dependent apoptotic program in endothelial cells that bypasses caspase-3 (Montrer CASP3 Kits ELISA).
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