◀ Back to CASP5

CASP5 — MAGT1

Text-mined interactions from Literome

Troy et al., J Neurosci 2001 : The mechanism underlying the shift is the result of a threefold compensatory elevation of caspase-9 expression and a doubling of levels of direct IAP binding protein with low pI/ ( DIABLO ) /second mitochondria derived activator of caspase ( Smac ), an IAP inhibitor , both at the mRNA and protein levels [ corrected ]
Liao et al., Biochem Biophys Res Commun 2002 : Caspase inhibition assays indicated that recombinant Tn-IAP1v could specifically inhibit human caspase-9 in vitro instead of caspase-3, -7, and -8, which was further confirmed by the observation that recombinant Tn-IAP1v can directly bind caspase-9 in the protein pull-down assay
Bae et al., Biochem Biophys Res Commun 2003 : Curcumin induces apoptosis in U937 cells via a mechanism that appears to involve down-regulation of the anti-apoptotic Bcl-xL, and IAP proteins, release of cytochrome c, and activation of caspase 3
Martins et al., J Biol Chem 2003 : Thus although IAP overexpression can suppress caspase activation, it could have the opposite effect on HtrA2/Omi dependent cell death
Yang et al., Cancer Res 2003 (Neoplasms) : These results suggest that up-regulated IAP expression counteracts the high basal caspase-3 activity observed in these tumor cells and that apoptosis in tumor cells but not normal cells can be induced by blocking IAP activity
Li et al., Science 2004 (Glioblastoma) : We describe the synthesis and properties of a small molecule mimic of Smac, a pro-apoptotic protein that functions by relieving inhibitor-of-apoptosis protein (IAP) mediated suppression of caspase activity
Yang et al., Cell Biol Toxicol 2010 (Carcinoma, Hepatocellular...) : Taken together, the results of the present study indicate that intracellularly transported adenosine activates caspase-3 by neutralizing caspase-3 inhibition due to IAP as a result of decreased IAP2 expression and reduced IAP activity in response to increased DIABLO expression and perhaps DIABLO release from damaged mitochondria, in addition to caspase-8 activation