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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