ArticleThe Journal of experimental medicine2019
Phosphorylation-dependent Regnase-1 release from endoplasmic reticulum is critical in IL-17 response.
Article in The Journal of experimental medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
38 citing papers in PubMed, 65 citations in OpenAlex.
- The regnase family in autoimmune diseases: a regnase-1-centered perspective on cellular heterogeneity.Molecular biology reports · 2026Review
- The ribonuclease ZC3H12A stabilizes BRCA1 mRNA in DNA damage response.Redox biology · 2026Article
- Decoding Regnase-1's role in skin inflammation: potential therapeutic implication for dermatological disorders.Journal of advanced research · 2026Review
- Single-nucleus RNA sequencing identifies conserved structural cell programs in allergic lung inflammation.The journal of allergy and clinical immunology. Global · 2026Article
- The Role of Regnase-1 in Autoimmune Diseases - A Future Therapeutic Target for Clinical Use.Clinical reviews in allergy & immunology · 2026Review
- The Double-Edged Sword of Type 17 Immunity in Wound Healing and Skin Barrier Repair: Microenvironment-Driven Functional Plasticity.Biomolecules · 2026Review
- Machine learning meets psoriasis: identifying key lactylation biomarkers as potential targets for diagnosis and therapies.Frontiers in immunology · 2026Article
- Epithelial Regnase-1 inhibits colorectal tumor growth by regulating IL-17 signaling via degradation ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- A Novel Missense Variant ofCirculation reports · 2025Article
- Article
- Role and functional mechanisms of IL‑17/IL‑17R signaling in pancreatic cancer (Review).Oncology reports · 2024Review
- Regulation of inflammatory diseases via the control of mRNA decay.Inflammation and regeneration · 2024Review
- Suppression of TCF4 promotes a ZC3H12A-mediated self-sustaining inflammatory feedback cycle involving IL-17RA/IL-17RE epidermal signaling.JCI insight · 2024Article
- RNA Metabolism Governs Immune Function and Response.Advances in experimental medicine and biology · 2024Review
- The IL-17 family in diseases: from bench to bedside.Signal transduction and targeted therapy · 2023Review
- Regnase-1 downregulation promotes pancreatic cancer through myeloid-derived suppressor cell-mediated evasion of anticancer immunity.Journal of experimental & clinical cancer research : CR · 2023Article
- The intricate relationship between autoimmunity disease and neutrophils death patterns: a love-hate story.Apoptosis : an international journal on programmed cell death · 2023Review
- The Role of IL-17 in the Pathogenesis of Oral Squamous Cell Carcinoma.International journal of molecular sciences · 2023Review
- IL-17A and TNF synergistically drive expression of proinflammatory mediators in synovial fibroblasts via IκBζ-dependent induction of ELF3.Rheumatology (Oxford, England) · 2023Article
- An inflammatory bowel disease-associated SNP increases local thyroglobulin expression to develop inflammation in miniature dachshunds.Frontiers in veterinary science · 2023Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Regnase-1 (also known as Zc3h12a or MCPIP-1) is an endoribonuclease involved in mRNA degradation of inflammation-associated genes. Regnase-1 is inactivated in response to external stimuli through post-translational modifications including phosphorylation, yet the precise role of phosphorylation remains unknown. Here, we demonstrate that interleukin (IL)-17 induces phosphorylation of Regnase-1 in an Act1-TBK1/IKKi-dependent manner, especially in nonhematopoietic cells. Phosphorylated Regnase-1 is released from the endoplasmic reticulum (ER) into the cytosol, thereby losing its mRNA degradation function, which leads to expression of IL-17 target genes. By using CRISPR/Cas-9 technology, we generated Regnase-1 mutant mice, in which IL-17-induced Regnase-1 phosphorylation is completely blocked. Mutant mice (
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Registered trials
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.