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CASP12 — HSPA5
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Rao et al., FEBS Lett 2002
:
GRP78 inhibits cytochrome c-mediated
caspase activation in a cell-free system, and expression of GRP78 blocks both caspase activation and caspase mediated cell death ...
GRP78 forms a complex with caspase-7 and -12 and
prevents release of
caspase-12 from the ER
Xie et al., Hepatology 2002
(Liver Diseases) :
TUDCA abolished TG-induced markers of ER stress ; reduced calcium efflux, induction of
Bip/GRP78 , and
caspase-12 activation ; and subsequently inhibited activation of effector caspases and apoptosis
Tessitore et al., Mol Cell 2004
(Disease Models, Animal...) :
Here we demonstrate that activation of an unfolded protein response ( UPR ) associated with the upregulation of
BiP and CHOP and the
activation of JNK2 and
caspase-12 leads to neuronal apoptosis in the mouse model of GM1-gangliosidosis
Hao et al., J Biol Chem 2006
(Reperfusion Injury) :
Induction of the endoplasmic reticulum stress response by anoxia/recovery or tunicamycin ( monitored by induction of
Bip or Grp94 expression, phosphorylation of eukaryotic translation initiation factor 2alpha subunit, expression of CHOP, and
activation of
caspase-12 ) was attenuated in cells that overexpress SLK
Hwang et al., J Cell Physiol 2008
(Colonic Neoplasms) :
The induction of drug resistance can be partly explained by the fact that
GRP78 can
block activation of
caspase-7 induced by treatment with etoposide
Kusunoki et al., Neurosci Lett 2008
:
Here we report that p-nonylphenol, one of the EDCs, induced apoptosis with up-regulation of
glucose regulated protein 78 (GRP78) expression and
activation of
caspase-12 , which are involved in endoplasmic reticulum ( ER ) stress specific phenomena, in NGF treated neuronally differentiated PC12 cells
Xu et al., Yao Xue Xue Bao 2008
:
The cleavage and
activation of
caspase-3 , -6, -7, -9, -12 and upregulation of
GRP78 expression were determined by Western blotting
Ji et al., J Agric Food Chem 2009
(Carcinoma, Non-Small-Cell Lung...) :
Western blotting and flow cytometric analysis also demonstrated that GA increased protein levels of GADD153 and
GRP78 ,
activation of
caspase-8 , -9, and -3, loss of DeltaPsi ( m ) and cytochrome c, and AIF release from mitochondria
Park et al., Biochem Pharmacol 2011
:
MG132 induced apoptotic changes, including upregulation of
Grp78/BiP and CHOP/GADD153 levels,
activation of
caspase-12 , p38MAPK and Bak, and mitochondria dependent activation of caspase cascade were more significant in p56 ( lck ) -stable transfectant JCaM1.6/lck than in p56 ( lck ) -deficient JCaM1.6/vector
Wang et al., Nutr Cancer 2012
(Calcium Signaling...) :
Exposure to DATS additionally induced endogenous endoplasmic reticulum stress markers and intracellular Ca2? mobilization, upregulation of
Bip/GRP78 and CHOP/GADD153, and
activation of
caspase-4
Barateiro et al., Neuromolecular Med 2012
:
Our results show that OPC display increased apoptosis and necrosis-like cell death upon UCB exposure, mediated by early signals of endoplasmic reticulum ( ER ) stress [ e.g. upregulation of glucose regulated protein
(GRP)78 , inositol requiring enzyme ( IRE ) -1a and activation transcription factor (ATF)-6, as well as
activation of
caspase-2 and c-Jun N-terminal kinase (JNK) ], followed by mitochondrial dysfunction ( e.g. loss of mitochondria membrane potential and caspase-9 activation )
Kong et al., J Nephrol 2013
(Acute Kidney Injury) :
The over-expression of CP-induced endoplasmic reticulum ( ER ) stress markers ( CHOP and
GRP78 ) and
activation of
caspase-12 were suppressed by rHuEPO, which also attenuated the CP-induced suppression of phosphatidylinositol-3kinase/Akt ( PI3K/Akt ) signaling in rat kidneys
Ou et al., Toxicol Lett 2012
:
The results demonstrated that phycocyanin suppressed SRA01/04 cells ' morphologic changes and apoptosis induced by d-galactose,
inhibited the expression and activation of
caspase 3, alternated the Bax/Bcl-2 ratio, and down-regulated the level of p53,
GRP78 , and CHOP in d-galactose treated SRA01/04 cells
Wu et al., Apoptosis 2013
(Reperfusion Injury) :
SB202190 ( an inhibitor of p38 MAPK ) abolished HPC induced cytoprotection, downregulation of
GRP78 and CHOP, and
activation of
caspase-12 , as well as PERK phosphorylation