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Protein / target

Interferon regulatory factor 7

Encoded byIRF7Q92985Homo sapiensSwiss-Prot
Degrader-tractable
Druggability
UniProt Ubiquitination
2
Research papers

Protein at a glance

Biological role

Sequence-specific double-stranded DNA binding

Strongest disease association

Hypothyroidism

Via encoding gene IRF7 · Genetic evidence · score 0.55

Research activity

Emerging research

2 papers · latest 2023

Derived from structured UniProt, Open Targets and literature data on this page.

Protein profile

UniProt 2026_02

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.

View complete UniProt function annotation

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

NucleusCytoplasm
Domains and Gene Ontology detail (34)

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

503 aa · 54 kDa · 4 isoforms

Biological roles

What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.

Immune signallingUniProt · GOTranscriptional regulationUniProt · GO
View supporting evidence

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

Open Targets 26

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.

Hypothyroidism
0.55Moderately supported

Genetic evidence dominant · Open Targets 0.33

Lupus Erythematosus, Systemic
0.55Moderately supported

Genetic evidence dominant · Open Targets 0.31

Myxedema
0.32Limited support

Genetic evidence dominant · Open Targets 0.19

Scleroderma, Systemic
0.32Limited support

Genetic evidence dominant · Open Targets 0.16

COVID-19
0.32Limited support

Genetic evidence dominant · Open Targets 0.18

View evidence synthesis (5)
HypothyroidismModerately supported
0.55
agreement 0.410.69
Genetic99%Literature1%

Open Targets aggregate 0.33 · 2 independent evidence families

Lupus Erythematosus, SystemicModerately supported
0.55
agreement 0.420.67
Genetic77%Literature20%RNA expression3%

Open Targets aggregate 0.31 · 3 independent evidence families

MyxedemaLimited support
0.32
agreement 0.200.44
Genetic100%

Open Targets aggregate 0.19 · 1 independent evidence family

Scleroderma, SystemicLimited support
0.32
agreement 0.180.46
Genetic67%Literature33%

Open Targets aggregate 0.16 · 2 independent evidence families

COVID-19Limited support
0.32
agreement 0.180.45
Genetic81%Literature19%

Open Targets aggregate 0.18 · 2 independent evidence families

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.

Show all associations
Hypothyroidism0.33
Lupus Erythematosus, Systemic0.31
Myxedema0.19
Diabetes Mellitus, Type 20.18
Diabetes Mellitus0.18
COVID-190.18
Scleroderma, Systemic0.16
Arthritis, Rheumatoid0.15
Myositis0.14

Tractability

Protein degradersEmerging

Feasibility evidence (uniprot ubiquitination and database ubiquitination) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (2)
PR · UniProt UbiquitinationPR · Database Ubiquitination

Raw Open Targets tractability assessment buckets, by modality.

Research activity

2 papers · to 2023

Papers linked directly to this protein. This is the protein's own literature — descriptor-derived papers are kept separate below.

Most cited

Zhang Q · Science (New York, N.Y.) · 2020

Ma W · Frontiers in immunology · 2023

Recent

Europe PMC papers linked directly to this protein.

Related family literature

2

Papers about “Interferon Regulatory Factors” — a broader family this protein belongs to. Shown as context; not counted as papers specifically about this protein.

Interferon-Stimulated Genes: What Do They All Do?

Schoggins JW · Annual review of virology · 2019

via Interferon Regulatory Factors

Genetic programming of macrophages to perform anti-tumor functions using targeted mRNA nanocarriers.

Zhang F · Nature communications · 2019

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.