Gene interactions and pathways from curated databases and text-mining

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CASP7 — STAT1

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Zhou et al., J Biol Chem 2003 : Moreover, the phosphorylation of STAT1 by IFNgamma was blocked by an inhibitor of caspase 8, indicating that STAT1 had a suppressive effect on MMP-9
Kim et al., Mol Cell Biol 2005 : STAT1 level and activity were reciprocally regulated by caspase activation and were associated with cell death
Li et al., Mol Cell Biochem 2007 : Nitric oxide upregulation of caspase-8 mRNA expression in lung endothelial cells : role of JAK2/STAT-1 signaling
Müerköster et al., Int J Cancer 2008 (Carcinoma, Pancreatic Ductal...) : This involved a reduced expression of caspases and the caspase inducing transcription factor STAT1 , both caused by diminished gene transcription
Benco et al., Reproduction 2009 : Overexpression of STAT1 reversed the effect of ghrelin on STAT1, PCNA, PGF, OXT ( from stimulatory to inhibitory ), BCL2, P ( 4 ) ( from inhibitory to stimulatory ), prevented ghrelin effect on caspase-3 and BAX, but did not affect ghrelin 's effect on MAPK/ERK1,2 expression
Doeppner et al., Acta Neuropathol 2011 (Brain Ischemia...) : Whereas inhibition of caspase-3 had no effect on brain injury in ephrin-B3 ( +/+ ) animals, infarct size in ephrin-B3 ( -/- ) mice was strongly reduced, suggesting that aggravated brain injury in these animals might involve a caspase-3 dependent activation of STAT1
Fielhaber et al., J Biol Chem 2012 : KPNA1, or its interaction with STAT1, was required for the nuclear import of latent STAT1, transcriptional induction of the STAT1 gene, and caspase-3 activation under conditions of reduced mTOR activity ( i.e. rapamycin, glucose starvation, serum withdrawal )