| Function |
Transcription factor that plays an essential role in anti-viral immunity. It mediates signaling by type I IFNs (IFN-alpha and IFN-beta). Following type I IFN binding to cell surface receptors, Jak kinases (TYK2 and JAK1) are activated, leading to tyrosine phosphorylation of STAT1 and STAT2. IRF9/ISGF3G associates with the phosphorylated STAT1:STAT2 dimer to form a complex termed ISGF3 transcription factor, that enters the nucleus. ISGF3 binds to the IFN stimulated response element (ISRE) to activate the transcription of interferon stimulated genes, which drive the cell in an antiviral state.
|
| Gene References into Functions |
- Priming cells with IFNbeta synergistically enhances IL6 induction in response to treatments that activate NF-kappaB, in a process that depends upon the recruitment of STAT2, IRF9. PMID: 29581268
- Surface features in the interacting domains of IRF9 and STAT2 have diverged to enable specific interaction between these family members and to enable the antiviral response. PMID: 29317535
- Recent studies have revealed a unique role for IRF9 as a conductor of the cellular responses to IFN-Is. Intriguingly, novel roles for IRF9 outside of the antiviral response are also being identified. PMID: 26987614
- these findings identify miR-302d as a key regulator of type I IFN driven gene expression via its ability to target IRF9 and regulate ISG expression, underscoring the importance of non-coding RNA in regulating the IFN pathway in SLE. PMID: 28318807
- Decreased IRF9 expression was accompanied by increased replication of hepatitis C virus and hepatitis E virus. PMID: 28442624
- PKV VP3 associated with STAT2 and IRF9, and interfered with the formation of the STAT2-IRF9 and STAT2-STAT2 complex. PMID: 28441586
- Interferonstimulated gene factor 3 complex, which consists of STAT1, STAT2 and IRF9, is required for the induction of SAMHD1 expression by IFN-alpha in SMMC-7721 cells. PMID: 26397446
- U-ISGF3 induced by IFN-lambdas and -beta drives prolonged expression of a set of IFN-stimulated genes during HCV infection PMID: 26216956
- IRF9 is a vascular injury-response molecule that promotes VSMC proliferation. IRF9 expression is upregulated during neointima formation. PMID: 25319116
- DC-SIGN-induced ISGF3 by fucose-based PAMPs has an essential role in driving IL-27 and subsequent TFH polarization, which might be harnessed for vaccination design PMID: 25278262
- IRF9 mediated myocardial reperfusion injury PMID: 25150882
- STAT2 and IRF9 overexpression is sufficient to drive interferon-related DNA damage signature expression upon cell crowding. PMID: 25156627
- IL6 is an inducer of IRF9 expression in prostate cancer and a sensitizer for the antiproliferative effects of IFNalpha2. PMID: 23913484
- The hepatitis C virus (HCV) non-structural 5A (NS5A) protein, which is known to modulate the IFN response, competes with IRF9 for CypA binding and can prevent the formation of IRF9-CypA complexes. PMID: 22902549
- HDAC1 and HDAC2 differentially modulate STAT activity in response to IFNalpha2: while they are required for the induction of ISGF3-responsive genes, they impair the transcription of STAT3-dependent genes. PMID: 21957129
- Western blot and electrophoretic mobility-shift assays identified the interferon-stimulated gene factor-3 (ISGF-3) components STAT1 and IRF-9 as the proximal targets of human herpesvirus 8 vIRF-2 activity. PMID: 21697347
- STAT2 may interact with IRF-9 in a STAT1-independent manner. The complex STAT2/IRF-9 is the key factor mediating the expression of RIG-G gene regulated by IFN-alpha. PMID: 20403236
- Signals ensued by IFN-alpha and IL-4 induce cytoplasmic sequestration of IL-4-activated STAT6 and IFN-alpha-activated STAT2:p48 in B cells through the formation of pY-STAT6:pY-STAT2:p48 complex. PMID: 21268015
- analysis of IFN-stimulated response elements (ISREs) that bind to both the IFN-stimulated gene factor 3 (ISGF3) as well as to IFN response factor 7 (IRF7) PMID: 20943654
- Results suggest that the amount of cellular IRF9 is a crucial determinant for amplification of early dynamics of IFNalpha-mediated signal transduction. PMID: 20964804
- a key factor for eliciting the antiproliferative activity of IFN-alpha in tumors PMID: 19752753
- NOD1 can activate the ISGF3 signaling pathway that is usually associated with protection against viral infection to provide robust type I IFN-mediated protection from H. pylori and possibly other mucosal infections PMID: 20389019
- the IFN-activated ISGF3 transcription factor regulates transcription through contact with DRIP150 PMID: 12509459
- IRF9 functions to recruit RNA polymerase II to the promoter of interferon-stimulated genes and requires histone deacetylases PMID: 15194680
- the conserved DNA-binding domain of STAT2 has a role specific to the activity of ISGF3-independent STAT2-containing complexes PMID: 15668228
- defects in ISGF3 can cause resistance to IFN-alpha(2a) treatment PMID: 15714000
- GBF1 is recruited to the endogenous IRF-9 promoter, and interacts with C/EBP-beta, IL-1, and IL-6 PMID: 16318580
- Pretreatment of Huh-7 cells with 0.5-1 mM H2O2 resulted in the suppression of the IFN-alpha-induced antiviral protein MxA and of IRF-9 mRNA expression. PMID: 16595158
- Data reveal the existence of a collection of GAS-regulated target genes whose expression is interferon-inducible and independent of ISGF3 but highly dependent on the STAT2 DNA binding domain. PMID: 16689942
- Results identify Viperin as a tightly regulated ISGF3 target gene, which is counter-regulated by PRDI-BF1. PMID: 16849320
- Suggest that the JAK-STAT pathway may play a major role in mediating the effects of IFN-alpha against hepatitis b virus, and that ISGF3 might be a key factor. PMID: 17559358
- These data define the role of the ISGF3 members in IFN-beta inhibitory signaling. PMID: 18370868
- The data suggest that liberation of the IFNaR2-ICD by regulated proteolysis could trigger a novel mechanism for moving the transcription factor Stat2 to the nucleus. PMID: 18456457
Show More
Hide All
|
