ArticleNature communications2015
Phosphorylation status determines the opposing functions of Smad2/Smad3 as STAT3 cofactors in TH17 differentiation.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 121 citations in OpenAlex.
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- Palmitoylation Induced Activation of SMAD3 Exacerbates Colitis by Promoting Tissue-resident Memory T Cells Differentiation.Inflammation · 2026Article
- TRPM7 and magnesium orchestrate human CD4 T-cell activation and differentiation.Life science alliance · 2026Article
- Stem cell-derived extracellular vesicles as immunomodulatory agents: targeting pathological crosstalk in systemic lupus erythematosus and multiple sclerosis.Frontiers in medicine · 2026Review
- Regulatory dynamics of Th17 lymphocytes in oral squamous cell carcinoma: immune modulation and emerging immunotherapies.Immunologic research · 2025Review
- Th17 cell pathogenicity in autoimmune disease.Experimental & molecular medicine · 2025Review
- SMAD2 S-palmitoylation promotes its linker region phosphorylation and TScience signaling · 2025Article
- Integrative Roles of Pro-Inflammatory Cytokines on Airway Smooth Muscle Structure and Function in Asthma.Immunological reviews · 2025Review
- Anti-inflammatory effects of LCB 03-0110 on human corneal epithelial and murine T helper 17 cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Mechanistic Insights into Qin Bi Yin for Psoriasis Treatment Using Network Pharmacology, Experimental Validation, and Molecular Docking.Journal of inflammation research · 2025Article
- Article
- Repression of SMAD3 by STAT3 and c-Ski induces conventional dendritic cell differentiation.Life science alliance · 2024Article
- Developmental self-reactivity determines pathogenic Tc17 differentiation potential of naive CD8Nature communications · 2024Article
- Th17/Treg balance: the bloom and wane in the pathophysiology of sepsis.Frontiers in immunology · 2024Review
- Integrin α3 promotes TScience immunology · 2023Article
- Intricacies of TGF-β signaling in Treg and Th17 cell biology.Cellular & molecular immunology · 2023Review
- Article
- TThe Journal of allergy and clinical immunology · 2022Article
- Interleukin 27 is a novel cytokine with anti-inflammatory effects against spondyloarthritis through the suppression of Th17 responses.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
16 authors at 10 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-β (TGF-β) and interleukin-6 (IL-6) are the pivotal cytokines to induce IL-17-producing CD4(+) T helper cells (TH17); yet their signalling network remains largely unknown. Here we show that the highly homologous TGF-β receptor-regulated Smads (R-Smads): Smad2 and Smad3 oppositely modify STAT3-induced transcription of IL-17A and retinoic acid receptor-related orphan nuclear receptor, RORγt encoded by Rorc, by acting as a co-activator and co-repressor of STAT3, respectively. Smad2 linker phosphorylated by extracellular signal-regulated kinase (ERK) at the serine 255 residue interacts with STAT3 and p300 to transactivate, whereas carboxy-terminal unphosphorylated Smad3 interacts with STAT3 and protein inhibitor of activated STAT3 (PIAS3) to repress the Rorc and Il17a genes. Our work uncovers carboxy-terminal phosphorylation-independent noncanonical R-Smad-STAT3 signalling network in TH17 differentiation.
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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.