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CASP7 — PLCG1
Text-mined interactions from Literome
Woo et al., Biochem Biophys Res Commun 2004
:
Overexpression of a constitutively active Akt ( myr-Akt ) in U937 cells inhibited the induction of apoptosis,
activation of
caspase 3, and
PLC-gamma1 cleavage by chrysin
Hachimura et al., Ann N Y Acad Sci 2004
:
Thus, as a
consequence of
caspase activation, orally tolerant CD4 T cells could not form normal TCR signaling complexes associated with GADS and showed downregulated
PLC-gamma1 activation, which resulted in impairment of TCR induced calcium signaling
Park et al., Biol Pharm Bull 2007
:
The increase in apoptosis induced by beta-sitosterol was associated with down-regulation of Bcl-2, degradation of poly- ( ADP-ribose ) polymerase ( PARP ) and phospholipase C
(PLC)-gamma1 protein, and
activation of
caspase-3
Park et al., Biochem Biophys Res Commun 2008
:
The
caspase-8 inhibitor ( z-IETD-fmk ), which failed to influence pFPhe induced caspase-9 activation, completely
blocked caspase-8 activation and
PLCgamma-1 degradation with a marked reduction in caspase-3 activation and PARP degradation, indicating pFPhe induced caspase-8 activation as a downstream event of mitochondria dependent activation of caspase-9
Oh et al., Apoptosis 2008
(Leukemia) :
Furthermore, we have shown that overexpression of Bcl-2 and active Akt ( myr-Akt ) in U937 cells inhibited the induction of apoptosis,
activation of
caspase-3 , and
PLC-gamma1 cleavage by withaferin A. Taken together, our results indicated that the JNK and Akt pathways and inhibition of NF-kappaB activity were key regulators of apoptosis in response to withaferin A in human leukemia U937 cells