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CASP3 — HTRA2
Text-mined interactions from Literome
Verhagen et al., J Biol Chem 2002
:
HtrA2 can, like DIABLO/Smac,
prevent XIAP inhibition of
active caspase 3 in vitro and is able to counteract XIAP protection of mammalian NT2 cells against UV-induced cell death
Yamaguchi et al., Cancer Res 2003
(Colonic Neoplasms) :
Treating HCT116 cells with THG results in caspase-8 activation ; Bid cleavage ; Bax conformational change and mitochondrial translocation ; the release of cytochrome c, Smac/Diablo, and
Omi/HtrA2 into the cytosol
; caspase-3 activation ; and apoptosis
Srinivasula et al., J Biol Chem 2003
:
In contrast, ectopic expression of mature wildtype
Omi/HtrA2 , but not an active site mutant,
induces potent
caspase activation and apoptosis
Tillman et al., Cancer Res 2003
(Colonic Neoplasms) :
In RKO, rottlerin
induced the release of cytochrome c,
HtrA2/Omi , Smac/DIABLO, and AIF from the mitochondria, potentiated in combination with TRAIL, with concomitant
caspase activation and down-regulation of XIAP ... In RKO, rottlerin
induced the release of cytochrome c,
HtrA2/Omi , Smac/DIABLO, and AIF from the mitochondria, potentiated in combination with TRAIL, with concomitant
caspase activation and down-regulation of XIAP
Suzuki et al., Cell Death Differ 2004
:
Mitochondrial protease
Omi/HtrA2 enhances
caspase activation through multiple pathways ...
Omi/HtrA2 is a mitochondrial serine protease that is released into the cytosol during apoptosis and
promotes cytochrome c ( Cyt c ) dependent
caspase activation by neutralizing inhibitor of apoptosis proteins ( IAPs ) via its IAP binding motif ... Extramitochondrial expression of
Omi/HtrA2 indirectly
induced permeabilization of the outer mitochondrial membrane and subsequent Cyt c-dependent
caspase activation in HeLa cells
Wu et al., Clin Exp Pharmacol Physiol 2004
:
3. The apoptotic effect induced by cinnamaldehyde could be further supported by the release of cytochrome c, Smac/Diablo and
Omi/HtrA2 from mitochondria to the cytosol and
activation of
caspase 3
Liu et al., Circulation 2005
(Myocardial Infarction...) :
Taken together, these results demonstrate for the first time that ischemia/reperfusion results in
Omi/HtrA2 translocation from the mitochondria to the cytosol, where it promotes cardiomyocyte apoptosis via a protease activity dependent,
caspase mediated pathway
Zhang et al., Sci China C Life Sci 2008
:
The release of Cyt c,
HtrA2 and Smac from mitochondria did not occur via the same mechanism, the release of Cyt c and HtrA2 was caspase independent and the release of Smac was
caspase dependent ... The release of Cyt c, HtrA2 and Smac from mitochondria did not occur via the same mechanism, the release of Cyt c and
HtrA2 was caspase independent and the release of Smac was
caspase dependent
Winkler et al., Thromb Haemost 2013
:
Inhibition of
Omi/HtrA2 led to decreased levels of activated
caspase-3/7 and caspase-9, but did not abolish loss of ??m or prevent release of Omi/HtrA2 from mitochondria