◀ Back to STAT1
IRF9 — STAT1
Pathways - manually collected, often from reviews:
-
KEGG Osteoclast differentiation:
STAT1/STAT2
→
IRF9
(protein-protein, binding/association)
-
KEGG Jak-STAT signaling pathway:
IRF9
→
STAT1/STAT2/STAT3/STAT4/STAT5A/STAT5B/STAT6
(protein-protein, binding/association)
-
KEGG Hepatitis C:
STAT1/STAT2
→
IRF9
(protein-protein, binding/association)
-
KEGG Measles:
STAT1/STAT2
→
IRF9
(protein-protein, binding/association)
-
KEGG Measles:
STAT1
→
IRF9
(protein-protein, binding/association)
-
KEGG Influenza A:
STAT1/STAT2
→
IRF9
(protein-protein, binding/association)
-
Reactome Reaction:
IRF9
→
STAT1
(indirect_complex)
Wesoly et al., Acta biochimica Polonica 2007, Qureshi et al., Proc Natl Acad Sci U S A 1995*, Li et al., J Biol Chem 1996, Martinez-Moczygemba et al., J Biol Chem 1997*
-
Reactome Reaction:
IRF9
→
STAT1
(reaction)
Qureshi et al., Proc Natl Acad Sci U S A 1995*, Li et al., J Biol Chem 1996, Martinez-Moczygemba et al., J Biol Chem 1997*
-
WikiPathways Type II interferon signaling (IFNG):
Complex of STAT2-STAT1-IRF9-IRF9
→
EIF2AK2
(activation)
-
WikiPathways Type II interferon signaling (IFNG):
Complex of STAT2-STAT1-IRF9-IRF9
→
CXCL10
(activation)
-
WikiPathways Type II interferon signaling (IFNG):
Complex of STAT2-STAT1-IRF9-IRF9
→
IFIT2
(activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
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
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
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