ArticlePloS one2014
TRIpartite motif 21 (TRIM21) differentially regulates the stability of interferon regulatory factor 5 (IRF5) isoforms.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 71 citations in OpenAlex.
- Unraveling the Multifaceted Role of TRIM21 in Virus-Triggered Innate Immunity and Diseases.Biomolecules · 2026Review
- Loss of Tripartite Motif-Containing Protein 21 and UVB-Induced Systemic Inflammation by Regulating DNA-Sensing Pathways.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- KDM1A-driven RNF81 downregulation promotes gastric cancer progression via KLF4 destabilization.Oncogene · 2025Article
- Disruption of the novel nested geneeLife · 2025Article
- Interferon regulatory factor 5: a potential target for therapeutic intervention in inflammatory diseases.Frontiers in immunology · 2025Review
- TRIM21 regulation of IRF-mediated type I interferon signaling in systemic autoimmune diseases.Frontiers in immunology · 2025Review
- Keratinocytes - Amplifiers of Immune Responses in Systemic Lupus Erythematosus.Current rheumatology reports · 2024Review
- TLR7 signaling: a central nexus in autoimmunity and cGVHD.Blood advances · 2024Article
- Roles of TRIM21/Ro52 in connective tissue disease-associated interstitial lung diseases.Frontiers in immunology · 2024Review
- The interconnected roles of TRIM21/Ro52 in systemic lupus erythematosus, primary Sjögren's syndrome, cancers, and cancer metabolism.Cancer cell international · 2023Review
- Anti-Ro52 positivity is associated with progressive interstitial lung disease in systemic sclerosis-an exploratory study.Arthritis research & therapy · 2023Article
- Renal involvement in Sjőgren's syndrome: predictors and impact on patient outcomes.Rheumatology international · 2023Review
- Mechanism of action of IC 100, a humanized IgG4 monoclonal antibody targeting apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC).Translational research : the journal of laboratory and clinical medicine · 2023Article
- TRIM21 suppresses CHK1 activation by preferentially targeting CLASPIN for K63-linked ubiquitination.Nucleic acids research · 2022Article
- Deubiquitylating enzymes: potential target in autoimmune diseases.Inflammopharmacology · 2021Review
- Epithelial-immune cell interplay in primary Sjögren syndrome salivary gland pathogenesis.Nature reviews. Rheumatology · 2021Review
- Ubiquitination modification: critical regulation of IRF family stability and activity.Science China. Life sciences · 2021Review
- Review
- TRIMming Type I Interferon-Mediated Innate Immune Response in Antiviral and Antitumor Defense.Viruses · 2021Review
- TRIM21/Ro52 - Roles in Innate Immunity and Autoimmune Disease.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IRF5 is a member of the Interferon Regulatory Factor (IRF) family of transcription factors activated downstream of the Toll-Like receptors (TLRs). Polymorphisms in IRF5 have been shown to be associated with the autoimmune disease Systemic Lupus Erythematosus (SLE) and other autoimmune conditions, suggesting a central role for IRF5 in the regulation of the immune response. Four different IRF5 isoforms originate due to alternative splicing and to the presence or absence of a 30 nucleotide insertion in IRF5 exon 6. Since the polymorphic region disturbs a PEST domain, a region associated with protein degradation, we hypothesized that the isoforms bearing the insertion might have increased stability, thus explaining the association of individual IRF5 isoforms with SLE. As the E3 ubiquitin ligase TRIpartite Motif 21 (TRIM21) has been shown to regulate the stability and hence activity of members of the IRF family, we investigated whether IRF5 is subjected to regulation by TRIM21 and whether dysregulation of this mechanism could explain the association of IRF5 with SLE. Our results show that IRF5 is degraded following TLR7 activation and that TRIM21 is involved in this process. Comparison of the individual IRF5 variants demonstrates that isoforms generated by alternative splicing are resistant to TRIM21-mediated degradation following TLR7 stimulation, thus providing a functional link between isoforms expression and stability/activity which contributes to explain the association of IRF5 with SLE.
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