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BIRC2 — CASP2
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Steinman et al., Mol Med 2000
:
c-IAP1 loss
involved proteasomal, rather than
caspase , degradation pathways
Partheniou et al., Biochem Biophys Res Commun 2001
(Leukemia) :
In contrast, there was a
caspase dependent cleavage of XIAP, but not
c-IAP1 , during treatment with TNFalpha for 7 days
Choi et al., Int J Oncol 2002
:
Co-treatment with NAC markedly prevented dephosphorylation of Akt,
activation of
caspase 3, and down-regulation of
cIAP1
Vaziri et al., Anticancer Res 2003
:
VP-16 and KN-62 co-treatment was associated with
caspase activation via the mitochondrial pathway and significant reductions ( p = 0.002 ) in
c-IAP1 protein expression but not with c-IAP2 or XIAP
Zhao et al., J Toxicol Environ Health 2004
(Inflammation...) :
The release of cytochrome c from mitochrondria, the
activation of
caspase-3 , -8, and -9, the cleavage of nuclear poly ( ADP-ribose ) polymerase ( PARP ), and the expression of TNF receptors ( TNF-R1/p55 and TNF-R2/p75 ), TNF-R associated factor 2 (TRAF2), and cellular inhibitor of apoptosis 1 (
c-IAP1 ) were determined by immunoblotting
Peng et al., J Neurosci Res 2005
(Nerve Degeneration) :
Further, inhibition of cellular inhibitors of apoptosis protein 1 ( c-IAP1 ) expression by small interfering RNA ( siRNA ) increased TRAIL mediated caspase-3 activation and apoptosis ; thus,
c-IAP1 protects NPCs against TRAIL induced apoptosis and
suppresses caspase-3 activation
Liu et al., Mol Cancer Ther 2006
(Breast Neoplasms) :
Interestingly, the nonspecific
caspase inhibitor, z-VAD-FMK,
inhibited the down-regulation of Akt, XIAP, and
cIAP-1 in cerulenin- and LY294002 treated cells
Das et al., Cancer 2007
(Glioblastoma) :
Other events in apoptosis included overexpression of Bax, down-regulation of Bcl-2 and some
BIRC proteins, mitochondrial release of cytochrome c and Smac into the cytosol, and
activation of calpain,
caspase-9 , and caspase-3
Ribeiro et al., J Cell Biol 2007
:
Here, we show that Drosophila melanogaster
inhibitor of apoptosis protein 2 ( DIAP2 )
controls the level of
caspase activity in living cells
Das et al., Brain Res 2008
(Brain Neoplasms...) :
Besides, apoptosis was associated with alterations in expression of pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins resulting in an increase in Bax : Bcl-2 ratio, mitochondrial release of cytochrome c and Smac, downregulation of selective baculoviral inhibitor-of-apoptosis repeat containing (
BIRC ) molecules, an increase in intracellular free [Ca2+ ], and
activation of calpain and
caspase-3
Karmakar et al., Neuroscience 2009
(Body Weight...) :
Combination of 4-HPR and GST increased Bax : Bcl-2 ratio, mitochondrial release of Smac, downregulation of baculovirus inhibitor-of-apoptosis repeat containing (
BIRC ) proteins including BIRC-2 and BIRC-3, and activation of
caspase-3 and apoptosis
inducing factor ( AIF )
Yang et al., Cell Biol Toxicol 2010
(Carcinoma, Hepatocellular...) :
Adenosine downregulated the expression of mRNAs and proteins for Bcl-X ( L ) and
inhibitor of apoptosis protein 2 (IAP2) to directly
inhibit caspase-3 , -7, and -9, but it otherwise upregulated the expression of mRNA and protein for DIABLO, an inhibitor of IAPs
Farhana et al., Cell Death Differ 2011
:
3-Cl-AHPC activation of the noncanonical pathway was preceded by
caspase mediated decrease in the E3-ligase
c-IAP1 with subsequent stabilization of NF-?B inducing kinase ( NIK ) expression, increased binding of NIK by TRAF3, activation of IKKa, and the resultant increased levels of RelB and p52