◀ Back to CASP7
CASP7 — 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