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Single nucleotide polymorphism c.459A > G in the IRF9 gene significantly decreased the IFN-gamma (show IFNG ELISA Kits) concentration and increased the ratio of IFN-gamma (show IFNG ELISA Kits)/IL-10 (show IL10 ELISA Kits) in serum of piglets after challenged with classical swine fever vaccine.
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 (show MLXIP ELISA Kits)-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 (show STAT2 ELISA Kits) and IRF9, and interfered with the formation of the STAT2 (show STAT2 ELISA Kits)-IRF9 and STAT2-STAT2 (show STAT2 ELISA Kits) complex.
Interferonstimulated gene factor 3 complex, which consists of STAT1 (show STAT1 ELISA Kits), STAT2 (show STAT2 ELISA Kits) and IRF9, is required for the induction of SAMHD1 (show SAMHD1 ELISA Kits) expression by IFN-alpha (show IFNA ELISA Kits) in SMMC-7721 cells.
U-ISGF3 (show STAT1 ELISA Kits) 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 (show CD209 ELISA Kits)-induced ISGF3 (show STAT1 ELISA Kits) by fucose-based PAMPs has an essential role in driving IL-27 (show IL27 ELISA Kits) and subsequent TFH polarization, which might be harnessed for vaccination design
IRF9 mediated myocardial reperfusion injury
STAT2 (show STAT2 ELISA Kits) and IRF9 overexpression is sufficient to drive interferon (show IFNA ELISA Kits)-related DNA damage signature expression upon cell crowding.
Much more significant induction of zebrafish IRF9 by zebrafish IFNgamma2.
findings illustrate an essential role for IRF9, as a mediator downstream of IFNAR (show IFNAR1 ELISA Kits), in preventing overwhelming antigen exposure causing CD8 (show CD8A ELISA Kits)(+) T cell exhaustion and leading to chronic viral infection.
We found that STAT-1 (show STAT1 ELISA Kits)(-/-) MRL lpr (show FAS ELISA Kits) m, but not IRF-9(-/-) or IFNAR-2 (show IFNAR2 ELISA Kits)(-/-) 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 (show STAT1 ELISA Kits) and STAT2 (show STAT2 ELISA Kits) than IRF9; and 2) signaling pathways not involving STAT1 (show STAT1 ELISA Kits), STAT2 (show STAT2 ELISA Kits), or IRF9 play a minor role only in mediating IFN-alpha (show IFNA ELISA Kits)-stimulated genes expression in MGCs.
IFN-alpha (show IFNA ELISA Kits)/beta is able to drive the formation of a Stat2 (show STAT2 ELISA Kits) 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 (show IFNA ELISA Kits) I and interferon (show IFNA ELISA Kits) III receptors worsens their condition.
STAT2 (show STAT2 ELISA Kits)/IRF9 regulates antiviral activity through a prolonged ISGF3-like transcriptional response.
IRF9 directly activates neuronal death signaling pathways through the downregulation of Sirt1 (show SIRT1 ELISA Kits) deacetylase in response to acute I/R stress.
IFN-beta (show IFNB1 ELISA Kits)-induced necroptosis of macrophages proceeds through tonic IFN-stimulated gene factor 3 (ISGF3) signaling, which leads to persistent expression of STAT1 (show STAT1 ELISA Kits), STAT2 (show STAT2 ELISA Kits), and IRF9 and sustained Rip3 (show MPRIP ELISA Kits) activation.
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