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CASP10 — SNAP25

Text-mined interactions from Literome

Stefanelli et al., Biochim Biophys Acta 1999 : N-Acetylcysteine (NAC) at a concentration of 10 mM blocks depletion of cellular glutathione and cell death in SNAP treated CEHC, but it poorly affects the ability of SNAP to inhibit caspase activity ... Consequently, in the presence of NAC, SNAP attenuates not only caspase activity but also cell death of staurosporine treated CEHC
Chae et al., Biol Pharm Bull 2001 : Our data show that DBcAMP or forskolin blocked SNAP induced caspase-3-like cysteine protease activation and that H-89, a PKA inhibitor, reversed the cAMP induced regulatory effect of caspase-3 like protease
Chen et al., Cell Immunol 2001 : The gamma-irradiation induced increase in caspase 3 and 6 activities was inhibited in the presence of SNAP
Török et al., Cancer Res 2002 (Cholangiocarcinoma) : In contrast, SNAP did prevent activation of caspase 9 in etoposide treated cells ... Furthermore, SNAP also blocked caspase 9 activation in a cell-free system and reversibly inhibited catalytic activity of human recombinant caspase 9
Maejima et al., J Mol Cell Cardiol 2005 : After 24 h DOX-treatment, SNAP reduced the increased caspase-3 activity by 63 %, and this effect was reversed by treatment with HgCl2. Immunoblot analysis showed that accumulation of the cleaved caspase-3 protein, an active form that induces apoptosis was inhibited significantly by SNAP
Figueroa et al., J Neurosci Res 2006 : SNAP , an NO donor, induces apoptosis in these cells because it 1 ) increases the p53 and 2 ) induces cytochrome c release and activation of caspase-9 and caspase-3