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IRF8 — STAT1
Text-mined interactions from Literome
Contursi et al., Proc Natl Acad Sci U S A 2000
:
These results suggest that
ICSBP , when
induced by IFNgamma through
STAT1 , in turn generates a second wave of transcription from GAS containing promoters, thereby contributing to the elicitation of IFNgamma 's unique activities in immune cells
Guo et al., J Immunol 2005
:
IRF-2 constitutively binds to the two ISRE/IRF-E sites at the DRR, while IRF-1 and
STAT1 are
induced to bind to the two
ISRE/IRF-E sites and the ISRE/IRF-E1, respectively, only after IFN-beta treatment
Dimberg et al., Scand J Immunol 2006
:
Taken together, our data suggest that ATRA induced regulation of Stat2,
ICSBP and C/EBPepsilon is
dependent on active
Stat1 , and that a failure to correctly regulate these transcription factors is associated with the inhibition of monocytic differentiation
Unlu et al., Mol Immunol 2007
:
We report here that non-tyrosine phosphorylated ( NTP )
-Stat1 is
involved in a cooperative interaction with Spi-1/PU.1 and
IRF8 to form a pre associated, poised complex for IL1B gene induction
Huang et al., J Clin Invest 2007
(Inflammation...) :
Enforced expression of STAT1,
IRF-1 , or GATA-1
enhanced phosphorylation of
STAT1 , STAT3, and STAT5 in cultured Gata1-deficient murine megakaryocytes, with concomitant megakaryocyte maturation
Zimmerman et al., Cancer Res 2012
(Neoplasms, Experimental...) :
Mechanistic investigations revealed that
IRF8 suppressed
STAT1 transcription by binding the STAT1 promoter
Amadi-Obi et al., PloS one 2012
(Macular Degeneration...) :
In this study, we have shown that the anti-inflammatory cytokine, IL-27, induced CFH expression in mouse retinal cells and human retinal pigmented epithelial cells (RPE) through
STAT1 mediated up-regulation of Interferon Regulatory Factor-1 (IRF-1) and
IRF-8
Nguyen et al., Oncogene 1997
:
Most strikingly, induction of IRF-1 and
IRF/RelA expression
resulted in a significant increase in
STAT1 ( p91 ) protein and increased ISGF3 DNA binding activity, suggesting that IRF-1 tumor suppressor activity may involve a novel mechanism which activates the JAK-STAT pathway through STAT1