ArticleMolecular and cellular biology1999
Structural and functional analysis of interferon regulatory factor 3: localization of the transactivation and autoinhibitory domains.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers.
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Who cites it
157 citing papers in PubMed, 325 citations in OpenAlex.
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- Foot-and-mouth disease virus VP4 interferes with host interferon response by targeting the nuclear translocation of interferon regulatory factor 3 (IRF3).Veterinary research · 2026Article
- CircCLMP Suppresses Anti-Tumor Immunity by Inhibiting Activation of IRF3 and Interferon Response in Microsatellite Instability-high Endometrial Cancer.International journal of biological sciences · 2026Article
- Lumpy skin disease virus 001/156 protein is a virulence factor that suppresses interferon production through impairing IRF3 dimerization.PLoS pathogens · 2025Article
- Virtual Screening, Molecular Docking and Molecular Dynamics Simulation of Bioactive Compounds from Various Indonesian Medicinal Plants as Potential Inhibitors of Human Papillomavirus Type 16 E6 Protein in Cervical Cancer Development.Tropical life sciences research · 2025Article
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- PBLD enhances antiviral innate immunity by promoting the p53-USP4-MAVS signaling axis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- The multiple roles of interferon regulatory factor family in health and disease.Signal transduction and targeted therapy · 2024Review
- Indomethacin restrains cytoplasmic nucleic acid-stimulated immune responses by inhibiting the nuclear translocation of IRF3.Journal of molecular cell biology · 2024Article
- Activation of the cGAS-STING-IRF3 Axis by Type I and II Interferons Contributes to Host Defense.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- R-loops and impaired autophagy trigger cGAS-dependent inflammation via micronuclei formation in Senataxin-deficient cells.Cellular and molecular life sciences : CMLS · 2024Article
- ORF48 is required for optimal lytic replication of Kaposi's sarcoma-associated herpesvirus.PLoS pathogens · 2024Article
- African swine fever virus pB318L, a trans-geranylgeranyl-diphosphate synthase, negatively regulates cGAS-STING and IFNAR-JAK-STAT signaling pathways.PLoS pathogens · 2024Article
- IRF3 function and immunological gaps in sepsis.Frontiers in immunology · 2024Review
- Downstream STING pathways IRF3 and NF-κB differentially regulate CCL22 in response to cytosolic dsDNA.Cancer gene therapy · 2024Article
- Phase separation in cGAS-STING signaling.Frontiers of medicine · 2023Review
- eIF4A3 Promotes RNA Viruses' Replication by Inhibiting Innate Immune Responses.Journal of virology · 2022Article
- Peste des Petits Ruminants Virus Upregulates STING to Activate ATF6-Mediated Autophagy.Journal of virology · 2022Article
97 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The interferon regulatory factor 3 (IRF-3) gene encodes a 55-kDa protein which is expressed constitutively in all tissues. In unstimulated cells, IRF-3 is present in an inactive cytoplasmic form; following Sendai virus infection, IRF-3 is posttranslationally modified by protein phosphorylation at multiple serine and threonine residues located in the carboxy terminus. Virus-induced phosphorylation of IRF-3 leads to cytoplasmic to nuclear translocation of phosphorylated IRF-3, association with the transcriptional coactivator CBP/p300, and stimulation of DNA binding and transcriptional activities of virus-inducible genes. Using yeast and mammalian one-hybrid analysis, we now demonstrate that an extended, atypical transactivation domain is located in the C terminus of IRF-3 between amino acids (aa) 134 and 394. We also show that the C-terminal domain of IRF-3 located between aa 380 and 427 participates in the autoinhibition of IRF-3 activity via an intramolecular association with the N-terminal region between aa 98 and 240. After Sendai virus infection, an intermolecular association between IRF-3 proteins is detected, demonstrating a virus-dependent formation of IRF-3 homodimers; this interaction is also observed in the absence of virus infection with a constitutively activated form of IRF-3. Substitution of the C-terminal Ser-Thr phosphorylation sites with the phosphomimetic Asp in the region ISNSHPLSLTSDQ between amino acids 395 and 407 [IRF-3(5D)], but not the adjacent S385 and S386 residues, generates a constitutively activated DNA binding form of IRF-3. In contrast, substitution of S385 and S386 with either Ala or Asp inhibits both DNA binding and transactivation activities of the IRF-3(5D) protein. These studies thus define the transactivation domain of IRF-3, two domains that participate in the autoinhibition of IRF-3 activity, and the regulatory phosphorylation sites controlling IRF-3 dimer formation, DNA binding activity, and association with the CBP/p300 coactivator.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.