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Single nucleotide polymorphism c.459A > G in the IRF9 gene significantly decreased the IFN-gamma concentration and increased the ratio of IFN-gamma/IL-10 in serum of piglets after challenged with classical swine fever vaccine.
this review outlines the structural basis of IRF9 that guides its regulation and interaction in antiviral immunity and other diseases
findings show that human IRF9- and ISGF3-dependent type I and III IFN responsive pathways are essential for controlling IAV.
the type I IFN receptor signal elicits an increase in PD-L1 expression in lung cancer cells through IRF9-dependent and independent pathways.
Thus after VHL inactivation, HIF induces ISGF3, which is reversed by the loss of secondary tumor suppressors, suggesting that this is a key negative feedback loop in clear cell renal cell carcinoma.
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.
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.
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.
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.
Decreased IRF9 expression was accompanied by increased replication of hepatitis C virus and hepatitis E virus.
PKV VP3 associated with STAT2 and IRF9, and interfered with the formation of the STAT2-IRF9 and STAT2-STAT2 complex.
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.
U-ISGF3 induced by IFN-lambdas and -beta drives prolonged expression of a set of IFN-stimulated genes during HCV infection
IRF9 is a vascular injury-response molecule that promotes VSMC proliferation. IRF9 expression is upregulated during neointima formation.
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
IRF9 mediated myocardial reperfusion injury
STAT2 and IRF9 overexpression is sufficient to drive interferon-related DNA damage signature expression upon cell crowding.
IL6 is an inducer of IRF9 expression in prostate cancer and a sensitizer for the antiproliferative effects of IFNalpha2.
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.
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.
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.
Much more significant induction of zebrafish IRF9 by zebrafish IFNgamma2.
Both type I IFN and IFN-gamma cause promoter binding of a complete ISGF3 complex containing STAT1, STAT2 and IRF9.
findings illustrate an essential role for IRF9, as a mediator downstream of IFNAR, in preventing overwhelming antigen exposure causing CD8(+) T cell exhaustion and leading to chronic viral infection.
We found that STAT-1(-/-) MRL lpr m, but not IRF-9(-/-) or IFNAR-2(-/-) mice, developed interstitial nephritis characterized by infiltration with RORgammat-positive lymphocytes, macrophages, and eosinophils.
IFN-I can mediate ISG expression inmixed glial cell cultures (MGCs) via ISGF3-independent signaling pathways but with reduced efficiency, with delayed and prolonged kinetics, and is more dependent on STAT1 and STAT2 than IRF9; and 2) signaling pathways not involving STAT1, STAT2, or IRF9 play a minor role only in mediating IFN-alpha-stimulated genes expression in MGCs.
IFN-alpha/beta is able to drive the formation of a Stat2 and IRF-9 complex that drives the expression of a subset of IFN-stimulated genes, but with substantially delayed kinetics.
In a murine model of dextran sodium sulfate -induced colitis, IRF9 deficiency protects animals, whereas the combined loss of interferon I and interferon III receptors worsens their condition.
STAT2/IRF9 regulates antiviral activity through a prolonged ISGF3-like transcriptional response.
IRF9 directly activates neuronal death signaling pathways through the downregulation of Sirt1 deacetylase in response to acute I/R stress.
IFN-beta-induced necroptosis of macrophages proceeds through tonic IFN-stimulated gene factor 3 (ISGF3) signaling, which leads to persistent expression of STAT1, STAT2, and IRF9 and sustained Rip3 activation.
IRF9 inhibits the development of cardiac hypertrophy by suppressing the transcriptional activity of myocardin in the heart.
Interferon regulatory factor 9 protects against hepatic insulin resistance and steatosis in male mice.
STAT1, not STAT2 or IRF9, prevent the emergence of a lethal antiviral CD4(+) T-cell response after lymphocytic choriomeningitis virus infection.
role for IRF9 in immune regulation within the gut mucosa
Through association of IFN-responsive factor 9 (IRF9) with the IFN stimulation response element, IFN-alpha enhances both the induction and maintenance of programmed death (PD)-1 expression on T cell receptor-engaged primary mouse T cells.
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)
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
Transcriptional amplification requires recruitment of the interferon-stimulated gene factor 3 (ISGF3) complex upon activation of myeloid dendritic cells.
Transcription regulatory factor that 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. The phosphorylated STATs dimerize, associate with IRF9/ISGF3G 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.
interferon regulatory factor 9
, interferon-stimulated transcription factor 3, gamma 48kDa
, IFN-alpha-responsive transcription factor subunit
, ISGF-3 gamma
, ISGF3 p48 subunit
, interferon-stimulated gene factor 3 gamma
, interferon-stimulated transcription factor 3, gamma (48kD)
, transcriptional regulator ISGF3 subunit gamma
, interferon dependent positive acting transcription factor 3 gamma