◀ Back to CASP2
CASP2 — STAT1
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 )