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Human BID Kit ELISA pour Sandwich ELISA - ABIN365900
Lim, Loh, Ting, Bradshaw, Zeenathul: Antiproliferation and induction of caspase-8-dependent mitochondria-mediated apoptosis by ?-tocotrienol in human lung and brain cancer cell lines. dans Biomedicine & pharmacotherapy 2014
Stage-specific expression of TNFalpha (Montrer TNF Kits ELISA) regulates bad/bid-mediated apoptosis and RIP1 (Montrer RALBP1 Kits ELISA)/ROS (Montrer ROS1 Kits ELISA)-mediated secondary necrosis in Birnavirus-infected fish cells.
Hyperosmotic Shock Engages Two Positive Feedback Loops through Caspase-3 (Montrer CASP3 Kits ELISA)-dependent Proteolysis of JNK1 (Montrer MAPK8 Kits ELISA)-2 and Bid.
tail regression at metamorphosis implicates an apoptotic pathway inducible by T(3) hormone in an organ autonomous manner and involving the cell death executioners BID and Caspases-2 and -8
Here, we identified and characterized the Xenopus homologs of caspase-10 (Montrer CASP10 Kits ELISA) (xCaspase-10beta), a novel initiator caspase (Montrer CASP3 Kits ELISA), and Bid (xBid), a BH3-only (Montrer BBC3 Kits ELISA) molecule of the Bcl-2 (Montrer BCL2 Kits ELISA) family involved in both the extrinsic and intrinsic pathways.
diubiquitylation is a specific feature of xBid.
the results establish that cleavage by caspase 8 (Montrer CASP8 Kits ELISA) and the subsequent association with the outer mitochondrial membrane are two critical events that activate Bid during death receptor-mediated apoptosis.
The results indicate that BID-independent pathways are responsible for FAS (Montrer FAS Kits ELISA)-dependent human islet cell death in Type 1 diabetes.
The BID-MTCH2 (Montrer MTCH2 Kits ELISA) axis regulates the differentiation/apoptosis of stem cells and mitochondrial metabolism. (Review)
Data suggest, in models of spatial propagation of mitochondrial permeabilization during apoptosis, there appears to be requirement for cooperative signaling involving truncated-BID and ROS (Montrer ROS1 Kits ELISA) (reactive oxygen species) for efficient/ robust propagation.
this study emphasizes that the coordinated action of hGzmB-activated p53 (Montrer TP53 Kits ELISA) and GzmB (Montrer Gzmb Kits ELISA)-cleaved Bid is important for GzmB (Montrer Gzmb Kits ELISA)-induced cell death and for cytotoxic lymphocyte/Natural Killer Cell-mediated killing of target cells.
Motifs of VDAC2 (Montrer VDAC2 Kits ELISA) required for mitochondrial Bak (Montrer BAK1 Kits ELISA) import and tBid-induced apoptosis.
Tax (Montrer CNTN2 Kits ELISA) confers apoptosis resistance to HTLV-1-infected T cells by suppressing the expression of Bim (Montrer BCL2L11 Kits ELISA) and Bid.
EG also activated the death receptor-dependent pathway of apoptosis by enhancing the expression of caspases-8, -9, and -3 and the Bcl-2 (Montrer BCL2 Kits ELISA) interacting domain (Bid).
Inhibition of NANOGP8 or NANOG enhances the cytotoxicity of BH3 mimetics.
JNK1 (Montrer MAPK8 Kits ELISA)/2 regulate Bid by direct phosphorylation at Thr59.
In the present study, we identified the proapoptotic Bcl-2 (Montrer BCL2 Kits ELISA) family protein Bid as a positive regulator of mutant SOD1 (Montrer SOD1 Kits ELISA)-induced TLR-nuclear factor-kappaB (NF-kappaB (Montrer NFKB1 Kits ELISA)) signaling in microglia.
ATM (Montrer ATM Kits ELISA)-BID-MTCH2 (Montrer MTCH2 Kits ELISA) pathway that we have identified plays a critical role in the DDR (Montrer DDR1 Kits ELISA) via regulation of mitochondrial metabolism.
DRP1 (Montrer CRMP1 Kits ELISA)-dependent apoptotic mitochondrial fission occurs independently of BAX (Montrer BAX Kits ELISA), BAK (Montrer BAK1 Kits ELISA) and APAF1 (Montrer APAF1 Kits ELISA) to amplify cell death by BID and oxidative stress.
A phosphorylation-deficient mutant of BID, MTCH2 (Montrer MTCH2 Kits ELISA)'s ligand, induces an increase in OXPHOS, but with higher ROS (Montrer ROS1 Kits ELISA) and reduced ATP levels than Mtch2 (Montrer MTCH2 Kits ELISA) loss, and is associated with hypersensitivity to irradiation.
BID protein suppresses p38 (Montrer CRK Kits ELISA) activity and induce malignant cell transformation of hepatocytes.
compare membrane permeabilization by Bax (Montrer BAX Kits ELISA) activated by either cBid [cleaved Bid (p7 and p15 (Montrer CDKN2B Kits ELISA))] or Bim (Montrer BCL2L11 Kits ELISA) and examine the role of membrane lipids in the recruitment and activation of these three Bcl-2 (Montrer BCL2 Kits ELISA) pro-apoptotic proteins
Hepatocyte Bid suppression is critical for the resistance to the lethal effects of Fas (Montrer FAS Kits ELISA) activation. Fas (Montrer FAS Kits ELISA) signaling induces differential activation of non-canonical interleukin-1beta maturation, amplified in the absence of apoptotic Bid in hepatocytes.
Data demonstrate a new role for Bid as a mediator of astrocyte activation during neuroinflammation, and suggest that Bid activation may contribute to non-cell autonomous motoneuron degeneration in amyotrophic lateral sclerosis
BID is required for tumor suppression by NSAIDs in APCMin/+ mice. It mediates these chemopreventive effects via selective killing of APC (Montrer APC Kits ELISA)-deficient intestinal stem cells.
Bid and Bax (Montrer BAX Kits ELISA) are signal transduction factors in granulosa cells and play proapoptotic roles.
This gene encodes a death agonist that heterodimerizes with either agonist BAX or antagonist BCL2. The encoded protein is a member of the BCL-2 family of cell death regulators. It is a mediator of mitochondrial damage induced by caspase-8 (CASP8)\; CASP8 cleaves this encoded protein, and the COOH-terminal part translocates to mitochondria where it triggers cytochrome c release. Multiple alternatively spliced transcript variants have been found, but the full-length nature of some variants has not been defined.
BH3 interacting domain death agonist
, BH3-interacting domain death agonist
, BID isoform ES(1b)
, BID isoform L(2)
, BID isoform Si6
, Human BID coding sequence
, apoptic death agonist
, desmocollin type 4
, p22 BID
, apoptotic death agonist BID