Protein / target
Interferon regulatory factor 7
Protein at a glance
Biological role
Sequence-specific double-stranded DNA binding
Strongest disease association
Hypothyroidism
Research activity
Emerging research
Derived from structured UniProt, Open Targets and literature data on this page.
Protein profile
Canonical identity and biological annotation from UniProt.
Function overview
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.
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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 (PubMed:28342865, PubMed:28768858). 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)
Subcellular location
Domains and Gene Ontology detail (34)Hide
Gene Ontology
- Cchromatin
- Ccytoplasm
- Ccytosol
- Cendosome membrane
- Cnucleoplasm
- Cnucleus
- FDNA binding
- FDNA-binding transcription factor activity, RNA polymerase II-specific
- FRNA polymerase II cis-regulatory region sequence-specific DNA binding
- Fsequence-specific double-stranded DNA binding
- Pcytoplasmic pattern recognition receptor signaling pathway
- Pdefense response to virus
Biological roles
What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.
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Immune signalling
- ·Key transcriptional regulator of type I interferon (IFN)-dependent immune responses and…
- ·innate immune response
- ·regulation of adaptive immune response
- ·regulation of immune response
Transcriptional regulation
- ·Key transcriptional regulator of type I interferon (IFN)-dependent immune responses and…
- ·DNA-binding transcription factor activity, RNA polymerase II-specific
- ·RNA polymerase II cis-regulatory region sequence-specific DNA binding
- ·DNA-templated transcription
Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.
Translational evidence
Why this target matters therapeutically, strongest evidence first. Disease associations are gene-level (via the gene that encodes this protein) and open into the full confidence synthesis; the development universe, tractability and safety annotations are target-level, from Open Targets.
Strongest disease associations · via encoding gene IRF7
Gene-level evidence surfaced through the gene IRF7that encodes this protein — not a direct protein–disease relationship. Ranked by Forefront's causal-directness weighting, so genetically- and clinically-evidenced diseases lead over ones that merely share the literature.
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The evidence agreement range shows how closely the independent evidence families agree — it is not a statistical confidence interval, and nothing here is fitted to outcome data. Derived from Open Targets evidence types under Forefront weighting; the per-type scores above show the calculation.
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Tractability
Protein degraders — Emerging
View underlying tractability evidence (2)Hide
Raw Open Targets tractability assessment buckets, by modality.
Research activity
Papers linked directly to this protein. This is the protein's own literature — descriptor-derived papers are kept separate below.
Most cited
Recent
Europe PMC papers linked directly to this protein.
Related family literature
Papers about “Interferon Regulatory Factors” — a broader family this protein belongs to. Shown as context; not counted as papers specifically about this protein.
via Interferon Regulatory Factors
via Interferon Regulatory Factors
Europe PMC literature, reached through curated HGNC family membership. Membership is a taxonomic relationship — it does not imply this protein participates in every mechanism these papers discuss.