Gene interactions and pathways from curated databases and text-mining

◀ Back to CASP7

BID — CASP7

Text-mined interactions from Literome

Slee et al., Cell Death Differ 2000 : Activation of caspase-8 in the latter pathways results in cleavage of BID , translocation of activated BID to mitochondria, followed by redistribution of cytochrome c to the cytosol
Kulik et al., Cancer Res 2001 (Prostatic Neoplasms) : Treatment with TNF-alpha resulted in activation of caspase 8 and cleavage of BID , which in turn induced cytochrome c release and caspase 9-dependent activation of effector caspases
Srivastava et al., Neoplasia (New York, N.Y.) 2001 (Neoplasms) : The apoptotic processes, therefore, follow two signaling pathways, namely the mitochondrial independent activation of caspase-3, and mitochondrial dependent apoptosis due to cleavage of BID by caspase-8, the formation of apoptosomes, and activation of caspase-9 and the downstream caspases
Ravi et al., Cancer Res 2002 (Adenocarcinoma...) : Apo2L/TRAIL induced apoptosis involves caspase-8 mediated cleavage of BID ... The active truncated form of BID ( tBID ) triggers the mitochondrial activation of caspase-9 by inducing the activation of BAK or BAX ... We find that CK2 inhibits Apo2L/TRAIL induced caspase-8 mediated cleavage of BID , thereby reducing the formation of tBID
Kasahara et al., Antioxid Redox Signal 2002 : IR at 10-40 Gy induced significant DNA fragmentation, activation of caspase-3 and -8 , the processing of a proapoptotic BID , and mitochondrial release of cytochrome c in the parental or HL-60/Vect cells, whereas no significant DNA fragmentation or no other concurring events were observed in the HL-60/FAK cells
Akay et al., Cell cycle (Georgetown, Tex.) 2004 : ATO rapidly induced Apo2/TRAIL, activation of caspase 8, cleavage of BID , depolarization of mitochondrial membrane ( MM ) and release of AIF from mitochondria in a Bcl-2 independent fashion
Soriano et al., J Biol Chem 2004 (Inflammation) : CsA exerted a marked PTP inhibition ex vivo, with an effect that peaked between 2 and 9 h of drug treatment and decayed with an apparent half-time of about 13 h. Administration of LPS plus D-GalN to naive rats caused the expected increased serum levels of tumor necrosis factor (TNF)-alpha, liver inflammation with BID cleavage, activation of caspase 3, appearance of terminal deoxynucleotidyltransferase mediated dUTP nick-end labeling positive nuclei, and release of alanine aminotransferase and aspartate aminotransferase into the bloodstream
Tamagiku et al., Biochem Biophys Res Commun 2004 : TRAIL at 500 ng/ml induced significant DNA fragmentation, activation of caspase-8 and 3, the processing of a proapoptotic BID , and mitochondrial release of cytochrome c in HL-60/Vect cells, whereas no such events were observed in the HL-60/FAK cells
Kaufmann et al., Cell Death Differ 2012 (Neoplasms) : This can be achieved through caspase-8 mediated proteolytic activation of the pro-apoptotic Bcl-2 homology domain (BH)3-only protein BH3 interacting domain death agonist ( Bid ), which then causes mitochondrial outer membrane permeabilisation
Hanzel et al., Arch Toxicol 2012 : Supporting that, BID cleavage and the activation of caspase 3 by Tl ( III ) were fully prevented when cells were preincubated with cathepsin D inhibitor ( pepstatin A ) and only partially prevented when cathepsin B inhibitor ( E64d ) was used
Gupta et al., PloS one 2012 (Prostatic Neoplasms) : However, GTP induced FAS upregulation through activation of c-jun-N-terminal kinase resulted in FADD phosphorylation, caspase-8 activation and truncation of BID , leading to apoptosis in both LNCaPshV and LNCaPshp53 cells