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CASP5 — PPP2R1A

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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