ArticleAnnals of the rheumatic diseases2013
Confirmation of TNIP1 but not RHOB and PSORS1C1 as systemic sclerosis risk factors in a large independent replication study.
Article in Annals of the rheumatic diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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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
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- A genome-wide association study follow-up suggests a possible role for PPARG in systemic sclerosis susceptibility.Arthritis research & therapy · 2014Pooled it
- Association ofInternational journal of molecular sciences · 2026Article
- Critical Analysis of Cytoplasmic Progression of Inflammatory Signaling Suggests Potential Pharmacologic Targets for Wound Healing and Fibrotic Disorders.Biomedicines · 2024Review
- Profiling of Toll-like Receptors and Related Signaling Mediators in the Pathogenesis of Morphea.Dermatology practical & conceptual · 2024Article
- Rho GTPase signaling in rheumatic diseases.iScience · 2022Review
- The Immunogenetics of Systemic Sclerosis.Advances in experimental medicine and biology · 2022Article
- [Application of lymphocytes test in peripheral blood of patients with systemic sclerosis during the treatment].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2021Article
- Updates on genetics in systemic sclerosis.Inflammation and regeneration · 2021Review
- Genetics of systemic sclerosis.Journal of scleroderma and related disorders · 2020Review
- Role of Systemic Lupus Erythematosus Risk Variants With Opposing Functional Effects as a Driver of Hypomorphic Expression of TNIP1 and Other Genes Within a Three-Dimensional Chromatin Network.Arthritis & rheumatology (Hoboken, N.J.) · 2020Article
- Enhanced Wound Healing- and Inflammasome-Associated Gene Expression in TNFAIP3-Interacting Protein 1- (TNIP1-) Deficient HaCaT Keratinocytes Parallels Reduced Reepithelialization.Mediators of inflammation · 2020Article
- TNIP1-mediated TNF-α/NF-κB signalling cascade sustains glioma cell proliferation.Journal of cellular and molecular medicine · 2020Article
- Towards a Better Classification and Novel Therapies Based on the Genetics of Systemic Sclerosis.Current rheumatology reports · 2019Review
- TNFAIP3 genetic polymorphisms reduce ankylosing spondylitis risk in Eastern Chinese Han population.Scientific reports · 2019Article
- Article
- TNIP1 Inhibits Proliferation And Promotes Apoptosis In Clear Cell Renal Carcinoma Through Targeting C/Ebpβ.OncoTargets and therapy · 2019Article
- Association of a single nucleotide polymorphism in TNIP1 with type-1 autoimmune hepatitis in the Japanese population.Journal of human genetics · 2018Article
- Gene-level association analysis of systemic sclerosis: A comparison of African-Americans and White populations.PloS one · 2018Article
- Immune Regulatory Genes Are Major Genetic Factors to Behcet Disease: Systematic Review.The open rheumatology journal · 2018Review
- TNIP1 in Autoimmune Diseases: Regulation of Toll-like Receptor Signaling.Journal of immunology research · 2018Review
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Authors and funding
38 authors at 20 institutions in 7 countries.
Funding
Abstract
introductionA recent genome-wide association study in European systemic sclerosis (SSc) patients identified three loci (PSORS1C1, TNIP1 and RHOB) as novel genetic risk factors for the disease. The aim of this study was to replicate the previously mentioned findings in a large multicentre independent SSc cohort of Caucasian ancestry.
methods4389 SSc patients and 7611 healthy controls from different European countries and the USA were included in the study. Six single nucleotide polymorphisms (SNP): rs342070, rs13021401 (RHOB), rs2233287, rs4958881, rs3792783 (TNIP1) and rs3130573 (PSORS1C1) were analysed. Overall significance was calculated by pooled analysis of all the cohorts. Haplotype analyses and conditional logistic regression analyses were carried out to explore further the genetic structure of the tested loci.
resultsPooled analyses of all the analysed SNPs in TNIP1 revealed significant association with the whole disease (rs2233287 p(MH)=1.94×10(-4), OR 1.19; rs4958881 p(MH)=3.26×10(-5), OR 1.19; rs3792783 p(MH)=2.16×10(-4), OR 1.19). These associations were maintained in all the subgroups considered. PSORS1C1 comparison showed association with the complete set of patients and all the subsets except for the anti-centromere-positive patients. However, the association was dependent on different HLA class II alleles. The variants in the RHOB gene were not associated with SSc or any of its subsets.
conclusionsThese data confirmed the influence of TNIP1 on an increased susceptibility to SSc and reinforced this locus as a common autoimmunity risk factor.
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