ArticlePLoS genetics2016
The Rheumatoid Arthritis Risk Variant CCR6DNP Regulates CCR6 via PARP-1.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- PARP1 as a novel therapeutic and diagnostic tool in autoimmune rheumatic diseases: a systematic literature review.Rheumatology international · 2026Pooled it
- Association of DNA damage response pathway genes with rheumatoid arthritis risks: a case-control study.Scientific reports · 2025Article
- Functional Validation of Noncoding Variants Associated With Nonsyndromic Orofacial Cleft.Human mutation · 2025Review
- From genetic variants to therapeutic targets: insights into understanding rheumatoid arthritis.Frontiers in immunology · 2025Review
- Association of CCR6 functional polymorphisms with Primary Biliary Cholangitis.Journal of translational autoimmunity · 2024Article
- Non-coding autoimmune risk variant defines role for ICOS in T peripheral helper cell development.Nature communications · 2024Article
- Computational Assessment of the Expression-modulating Potential for Non-coding Variants.Genomics, proteomics & bioinformatics · 2023Article
- A functional variant of CD40 modulates clearance of hepatitis B virus in hepatocytes via regulation of the ANXA2/CD40/BST2 axis.Human molecular genetics · 2023Article
- Chemokines and chemokine receptors as promising targets in rheumatoid arthritis.Frontiers in immunology · 2023Review
- Coupling high-throughput mapping with proteomics analysis delineates cis-regulatory elements at high resolution.Nucleic acids research · 2022Article
- The potential of PARP inhibitors in targeted cancer therapy and immunotherapy.Frontiers in molecular biosciences · 2022Review
- Review
- Post-GWAS functional studies reveal an RA-associated CD40-induced NF-kB signal transduction and transcriptional regulation network targeted by class II HDAC inhibitors.Human molecular genetics · 2021Article
- An integrative drug repositioning framework discovered a potential therapeutic agent targeting COVID-19.Signal transduction and targeted therapy · 2021Article
- A catalog of GWAS fine-mapping efforts in autoimmune disease.American journal of human genetics · 2021Review
- Editing GWAS: experimental approaches to dissect and exploit disease-associated genetic variation.Genome medicine · 2021Review
- Polymerase independent repression of FoxO1 transcription by sequence-specific PARP1 binding to FoxO1 promoter.Cell death & disease · 2020Article
- Review
- Implications of juvenile idiopathic arthritis genetic risk variants for disease pathogenesis and classification.Current opinion in rheumatology · 2019Review
- High-throughput identification of noncoding functional SNPs via type IIS enzyme restriction.Nature genetics · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Understanding the implications of genome-wide association studies (GWAS) for disease biology requires both identification of causal variants and definition of how these variants alter gene function. The non-coding triallelic dinucleotide polymorphism CCR6DNP is associated with risk for rheumatoid arthritis, and is considered likely causal because allelic variation correlates with expression of the chemokine receptor CCR6. Using transcription activator-like effector nuclease (TALEN) gene editing, we confirmed that CCR6DNP regulates CCR6. To identify the associated transcription factor, we applied a novel assay, Flanking Restriction Enhanced Pulldown (FREP), to identify specific association of poly (ADP-ribose) polymerase 1 (PARP-1) with CCR6DNP consistent with the established allelic risk hierarchy. Correspondingly, manipulation of PARP-1 expression or activity impaired CCR6 expression in several lineages. These findings show that CCR6DNP is a causal variant through which PARP-1 regulates CCR6, and introduce a highly efficient approach to interrogate non-coding genetic polymorphisms associated with human disease.
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What OpenQuestion holds
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.