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caspase-10 (show CASP10 Proteins) was dispensable for enhancement of cisplatin/LA-12 and TRAIL combination-induced cell death and stimulation of Bid cleavage
an oligomeric arrangement of Bid, Bax (show BAX Proteins), and possibly other members of the Bcl-2 (show BCL2 Proteins) family of proteins that form a self-propagating network that permeabilizes the outer-mitochondrial membrane.
Combined therapy with Seliciclib((R)) and Belinostat((R)) results in eradication of non-small cell lung cancer via apoptosis induction and BID activation.
Results from genome-wide DNA methylation, functional network analysis and pyrosequencing, show selective CpG sites (NOS1AP, BID, and GABRB1) differentially methylated in smokers and chronic obstructive pulmonary disease patients compared to nonsmokers.
The adenovirus-mediated truncated Bid overexpression induced by the Cre/LoxP system can effectively eliminate CD133+ ovarian cancer stem cells, representing a novel therapeutic strategy for the treatment of ovarian cancer.
MiR (show MLXIP Proteins)-20a-directed regulation of BID in colorectal cancer.
the results establish that cleavage by caspase 8 (show CASP8 Proteins) 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 (show FAS Proteins)-dependent human islet cell death in Type 1 diabetes.
The BID-MTCH2 (show MTCH2 Proteins) 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 (show ROS1 Proteins) (reactive oxygen species) for efficient/ robust propagation.
Cleaved Bid did not permeabilize the membrane, but lowered the membrane breakthrough force.
toxic reactive oxygen species levels in Mll5(-/-) mice are critically dependent on type 1 interferon (show IFNA Proteins) (IFN-1) signaling, which triggers mitochondrial accumulation of full-length Bid.
In the present study, we identified the proapoptotic Bcl-2 (show BCL2 Proteins) family protein Bid as a positive regulator of mutant SOD1 (show SOD1 Proteins)-induced TLR-nuclear factor-kappaB (NF-kappaB (show NFKB1 Proteins)) signaling in microglia.
ATM (show ATM Proteins)-BID-MTCH2 (show MTCH2 Proteins) pathway that we have identified plays a critical role in the DDR (show DDR1 Proteins) via regulation of mitochondrial metabolism.
DRP1 (show CRMP1 Proteins)-dependent apoptotic mitochondrial fission occurs independently of BAX (show BAX Proteins), BAK (show BAK1 Proteins) and APAF1 (show APAF1 Proteins) to amplify cell death by BID and oxidative stress.
A phosphorylation-deficient mutant of BID, MTCH2 (show MTCH2 Proteins)'s ligand, induces an increase in OXPHOS, but with higher ROS (show ROS1 Proteins) and reduced ATP levels than Mtch2 (show MTCH2 Proteins) loss, and is associated with hypersensitivity to irradiation.
Motifs of VDAC2 (show VDAC2 Proteins) required for mitochondrial Bak (show BAK1 Proteins) import and tBid-induced apoptosis.
BID protein suppresses p38 (show CRK Proteins) activity and induce malignant cell transformation of hepatocytes.
compare membrane permeabilization by Bax (show BAX Proteins) activated by either cBid [cleaved Bid (p7 and p15 (show CDKN2B Proteins))] or Bim (show BCL2L11 Proteins) and examine the role of membrane lipids in the recruitment and activation of these three Bcl-2 (show BCL2 Proteins) pro-apoptotic proteins
Hepatocyte Bid suppression is critical for the resistance to the lethal effects of Fas (show FAS Proteins) activation. Fas (show FAS Proteins) signaling induces differential activation of non-canonical interleukin-1beta maturation, amplified in the absence of apoptotic Bid in hepatocytes.
Stage-specific expression of TNFalpha (show TNF Proteins) regulates bad/bid-mediated apoptosis and RIP1 (show RALBP1 Proteins)/ROS (show ROS1 Proteins)-mediated secondary necrosis in Birnavirus-infected fish cells.
Bid and Bax (show BAX Proteins) are signal transduction factors in granulosa cells and play proapoptotic roles.
Hyperosmotic Shock Engages Two Positive Feedback Loops through Caspase-3 (show CASP3 Proteins)-dependent Proteolysis of JNK1 (show MAPK8 Proteins)-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 (show CASP10 Proteins) (xCaspase-10beta), a novel initiator caspase (show CASP3 Proteins), and Bid (xBid), a BH3-only (show BBC3 Proteins) molecule of the Bcl-2 (show BCL2 Proteins) family involved in both the extrinsic and intrinsic pathways.
diubiquitylation is a specific feature of xBid.
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
, 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
, BH3 interacting domain death agonist