Gene interactions and pathways from curated databases and text-mining

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CASP7 — HSPA5

Pathways - manually collected, often from reviews:

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
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
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
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 )
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