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BAD — CASP7

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