Gene interactions and pathways from curated databases and text-mining

◀ Back to STAT1

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