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BAD — CASP4
Text-mined interactions from Literome
Kim et al., Mol Cell Biol 2002
(Carcinoma, Hepatocellular...) :
However, TGF-beta 1 induced
caspase dependent cleavage of
BAD at its N terminus to generate a 15-kDa truncated protein
Stoica et al., Mol Cell Neurosci 2003
:
We show that ceramide treatment initiates a cascade of biochemical alterations associated with cell death : earliest signal transduction changes involve Akt dephosphorylation and inactivation followed by dephosphorylation of proapoptotic regulators such as
BAD ( proapoptotic Bcl-2 family member ), Forkhead family transcription factors, glycogen synthase kinase 3-beta, mitochondrial depolarization and permeabilization, release of cytochrome c into the cytosol, and
caspase-3 activation
Benetti et al., J Virol 2003
:
The herpes simplex virus 1 US3 protein kinase blocks
caspase dependent double cleavage and activation of the proapoptotic protein
BAD
Spencer et al., J Biol Chem 2003
(MAP Kinase Signaling System) :
Quercetin induced potent inhibition of both Akt/PKB and ERK phosphorylation, resulting in reduced phosphorylation of
BAD and a strong
activation of
caspase-3
Xi et al., Biochem Biophys Res Commun 2005
:
Inactivation of Akt was associated with dephosphorylation of
BAD , increased cytochrome c release, and
activation of
caspase-3 and caspase-9
Lin et al., Apoptosis 2008
(Glioblastoma) :
In addition, ardipusilloside III exposure resulted in time dependent
BAD dephosphorylation and cleavage as well as
activation of
caspase-8 and caspase-3
Jiang et al., Cancer cell international 2013
:
BAD overexpression also
induced apoptosis in all cell types, in which process expression of mitochondrial cytochrom c ( cyto-c ) and
caspase 3 were increased, whereas Bcl-xl, Bcl-2, Bax and caspase 8 expressions did not changed