Gene interactions and pathways from curated databases and text-mining

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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