IRF7

IRF7 encodes interferon regulatory factor 7, a member of the interferon regulatory transcription factor (IRF) family. IRF7 has been shown to play a role in the transcriptional activation of virus-inducible cellular genes, including interferon beta chain genes. Inducible expression of IRF7 is largely restricted to lymphoid tissue. Multiple IRF7 transcript variants have been identified, although the functional consequences of these have not yet been established. [provided by RefSeq, Jul 2008]

Interferon Regulatory Factor 7

Key transcriptional regulator of type I interferon (IFN)-dependent immune responses and plays a critical role in the innate immune response against DNA and RNA viruses. Regulates the transcription of type I IFN genes (IFN-alpha and IFN-beta) and IFN-stimulated genes (ISG) by binding to an interferon-stimulated response element (ISRE) in their promoters (PubMed:17574024, PubMed:32972995).
Can efficiently activate both the IFN-beta (IFNB) and the IFN-alpha (IFNA) genes and mediate their induction via both the virus-activated, MyD88-independent pathway and the TLR-activated, MyD88-dependent pathway. Induces transcription of ubiquitin hydrolase USP25 mRNA in response to lipopolysaccharide (LPS) or viral infection in a type I IFN-dependent manner (By similarity).
Required during both the early and late phases of the IFN gene induction but is more critical for the late than for the early phase. Exists in an inactive form in the cytoplasm of uninfected cells and following viral infection, double-stranded RNA (dsRNA), or toll-like receptor (TLR) signaling, becomes phosphorylated by IKBKE and TBK1 kinases. This induces a conformational change, leading to its dimerization and nuclear localization where along with other coactivators it can activate transcription of the type I IFN and ISG genes. Can also play a role in regulating adaptive immune responses by inducing PSMB9/LMP2 expression, either directly or through induction of IRF1. Binds to the Q promoter (Qp) of EBV nuclear antigen 1 a (EBNA1) and may play a role in the regulation of EBV latency. Can activate distinct gene expression programs in macrophages and regulate the anti-tumor properties of primary macrophages (By similarity) (PubMed:11073981, PubMed:12374802, PubMed:15361868, PubMed:17404045).

Cellular response to DNA damage stimulusManual Assertion Based On ExperimentTAS:UniProtKB
Defense response to virusManual Assertion Based On ExperimentIDA:UniProtKB
Establishment of viral latencyManual Assertion Based On ExperimentTAS:UniProtKB
Immune system processManual Assertion Based On ExperimentIBA:GO_Central
Immunoglobulin mediated immune responseIEA:Ensembl
Innate immune responseManual Assertion Based On ExperimentTAS:UniProtKB
MDA-5 signaling pathwayManual Assertion Based On ExperimentTAS:UniProtKB
Negative regulation of macrophage apoptotic processManual Assertion Based On ExperimentTAS:UniProtKB
Negative regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentTAS:ProtInc
Positive regulation of interferon-alpha productionManual Assertion Based On ExperimentIDA:BHF-UCL
Positive regulation of interferon-beta productionManual Assertion Based On ExperimentIMP:CACAO
Positive regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of transcription, DNA-templatedManual Assertion Based On ExperimentIMP:UniProtKB
Positive regulation of type I interferon-mediated signaling pathwayIEA:Ensembl
Regulation of adaptive immune responseManual Assertion Based On ExperimentIDA:UniProtKB
Regulation of immune responseManual Assertion Based On ExperimentTAS:UniProtKB
Regulation of monocyte differentiationManual Assertion Based On ExperimentTAS:UniProtKB
Regulation of MyD88-dependent toll-like receptor signaling pathwayISS:UniProtKB
Regulation of MyD88-independent toll-like receptor signaling pathwayISS:UniProtKB
Regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentIBA:GO_Central
Regulation of type I interferon productionManual Assertion Based On ExperimentTAS:UniProtKB
Response to virusManual Assertion Based On ExperimentTAS:UniProtKB
Type I interferon signaling pathwayIEA:Ensembl

Cytoplasm; Nucleus. The phosphorylated and active form accumulates selectively in the nucleus.

Immunodeficiency 39 (IMD39):
A primary immunodeficiency causing severe, life-threatening acute respiratory distress upon infection with H1N1 influenza A.

Acetylation inhibits its DNA-binding ability and activity.
In response to a viral infection, phosphorylated on Ser-477 and Ser-479 by TBK1 and IKBKE1. Phosphorylation, and subsequent activation is inhibited by vaccinia virus protein E3. In TLR7- and TLR9-mediated signaling pathway, phosphorylated by IRAK1.
TRAF6-mediated ubiquitination is required for IRF7 activation (By similarity).
TRIM35 mediates IRF7 'Lys-48'-linked polyubiquitination and subsequent proteasomal degradation (PubMed:25907537).
Ubiquitinated by UBE3C, leading to its degradation (PubMed:21167755).
Sumoylated by TRIM28, which inhibits its transactivation activity.
(Microbial infection) Cleaved and inactivated by the protease 3C of enterovirus 71 allowing the virus to disrupt the host type I interferon production.
(Microbial infection) Cleaved and inactivated by the protease 3C of human enterovirus 68D (EV68) allowing the virus to disrupt the host type I interferon production.
'Lys-48'-linked polyubiquitination and subsequent proteasomal degradation is NMI-dependent in response to Sendai virus infection.