◀ Back to PPP2R1A
CASP10 — PPP2R1A
Text-mined interactions from Literome
Liu et al., Biochem Pharmacol 2002
(Leukemia) :
Moreover, although salvicine induced HL-60 cell apoptosis in a caspase-3 dependent manner, a specific
caspase-3 inhibitor, Z-DEVD-FMK, did not
prevent a decrease in telomerase activity or an increase in
PP2A activity in apoptotic HL-60 cells, ruling out a role for caspase-3 in PP2A activation by salvicine
Alvarado-Kristensson et al., J Biol Chem 2005
:
Consequently, the early and temporary activation of
PP2A in neutrophils
impaired not only the p38 MAPK mediated inhibition of
caspase 3 but also restored the activity to caspase 3 that had already been phosphorylated and thereby inactivated
Ray et al., J Biol Chem 2005
:
These results indicate that polyamines regulate
PP2A activity, and inhibition of PP2A in response to polyamine depletion increases steady state levels of Bad and Bcl-2 proteins and their phosphorylation and thereby
prevents cytochrome c release,
caspase-9 , and caspase-3 activation
Chen et al., Mol Pharmacol 2006
:
Overexpression of
PP2A resulted in
caspase-2 activation, mitochondrial damage, and cell apoptosis that were inhibited by okadaic acid ( OA ) and lithium
Calvo et al., Biochim Biophys Acta 2010
:
Furthermore, our results suggest that
PP2A plays a role in hormone dependent Caco-2 cells viability and in the cleavage of
caspase-3 and its substrate PARP
Santoro et al., J Biol Chem 1998
:
The effects on
PP2A could be
prevented by the
caspase family inhibitors acetyl-Asp-Glu-Val-Asp ( DEVD ) aldehyde or Ac-DEVD fluoromethyl ketone