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Single nucleotide polymorphism c.459A > G in the IRF9 gene significantly decreased the IFN-gamma (show IFNG Proteins) concentration and increased the ratio of IFN-gamma (show IFNG Proteins)/IL-10 (show IL10 Proteins) 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 Proteins)-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 Proteins) and IRF9, and interfered with the formation of the STAT2 (show STAT2 Proteins)-IRF9 and STAT2-STAT2 (show STAT2 Proteins) complex.
Interferonstimulated gene factor 3 complex, which consists of STAT1 (show STAT1 Proteins), STAT2 (show STAT2 Proteins) and IRF9, is required for the induction of SAMHD1 (show SAMHD1 Proteins) expression by IFN-alpha (show IFNA Proteins) in SMMC-7721 cells.
U-ISGF3 (show STAT1 Proteins) 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 Proteins)-induced ISGF3 (show STAT1 Proteins) by fucose-based PAMPs has an essential role in driving IL-27 (show IL27 Proteins) and subsequent TFH polarization, which might be harnessed for vaccination design
IRF9 mediated myocardial reperfusion injury
STAT2 (show STAT2 Proteins) and IRF9 overexpression is sufficient to drive interferon (show IFNA Proteins)-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 Proteins), in preventing overwhelming antigen exposure causing CD8 (show CD8A Proteins)(+) T cell exhaustion and leading to chronic viral infection.
We found that STAT-1 (show STAT1 Proteins)(-/-) MRL lpr (show FAS Proteins) m, but not IRF-9(-/-) or IFNAR-2 (show IFNAR2 Proteins)(-/-) 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 Proteins) and STAT2 (show STAT2 Proteins) than IRF9; and 2) signaling pathways not involving STAT1 (show STAT1 Proteins), STAT2 (show STAT2 Proteins), or IRF9 play a minor role only in mediating IFN-alpha (show IFNA Proteins)-stimulated genes expression in MGCs.
IFN-alpha (show IFNA Proteins)/beta is able to drive the formation of a Stat2 (show STAT2 Proteins) 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 Proteins) I and interferon (show IFNA Proteins) III receptors worsens their condition.
STAT2 (show STAT2 Proteins)/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 Proteins) deacetylase in response to acute I/R stress.
IFN-beta (show IFNB1 Proteins)-induced necroptosis of macrophages proceeds through tonic IFN-stimulated gene factor 3 (ISGF3) signaling, which leads to persistent expression of STAT1 (show STAT1 Proteins), STAT2 (show STAT2 Proteins), and IRF9 and sustained Rip3 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