期刊
NATURE GENETICS
卷 40, 期 10, 页码 1216-1223出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ng.233
关键词
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资金
- T32 NIH training grant [AR007530-23]
- NIH [KAR055688A, AI55314-3, RO1-AR44422, NO1-AR-2-2263, R01 AR49880, CA87969, P60 AR047782, K24 AR0524-01, BIRCWH K12 HD051959]
- Fox Trot Fund
- William Randolph Hearst Fund of Harvard University
- Burroughs Wellcome Fund
- UO1 NIH [UO1 HG004171]
- Millennium Pharmaceuticals and Biogen-Idec
- National Center for Research Resources [U54 RR020278]
- National Institutes of Health
- Swedish Medical Research Council
- Swedish Council for Working Life and Social Research
- King Gustaf V's 80-year Foundation
- Swedish Rheumatic Foundation
- Stockholm County Council
- Arbetsmarknadens Forrsarkringsaktiebolag
- lCounty of Sormland Research and Development Center
- Agency for Science Technology and Research (Singapore)
- Doris Duke Charitable Foundation
- US National Institute of Mental Health
- National Institute of Allergy and Infectious Diseases
- National Institute of Child Health and Human Development
- American College of Rheumatology Arthritis Investigator Award
- Katherine Swan Ginsburg Memorial Award
- Kirkland Scholar Awardee [K24 AR02175, R01 AI065841, 5 M01 RR-00079]
- European Community's FP6 funding
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [K12HD051959] Funding Source: NIH RePORTER
- NATIONAL CANCER INSTITUTE [P01CA087969] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR000079, U54RR020278] Funding Source: NIH RePORTER
- NATIONAL HUMAN GENOME RESEARCH INSTITUTE [U01HG004171] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI065841, K08AI055314] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [P60AR047782, K24AR002175, R01AR049880, K08AR055688, N01AR022263, Z01AR041180, ZIAAR041139, T32AR007530, R01AR044422] Funding Source: NIH RePORTER
To identify rheumatoid arthritis risk loci in European populations, we conducted a meta-analysis of two published genome-wide association (GWA) studies totaling 3,393 cases and 12,462 controls(1,2). We genotyped 31 top-ranked SNPs not previously associated with rheumatoid arthritis in an independent replication of 3,929 autoantibody-positive rheumatoid arthritis cases and 5,807 matched controls from eight separate collections. We identified a common variant at the CD40 gene locus (rs4810485, P = 0.0032 replication, P = 8.2 x 10(-9) overall, OR = 0.87). Along with other associations near TRAF1 (refs. 2,3) and TNFAIP3 (refs. 4,5), this implies a central role for the CD40 signaling pathway in rheumatoid arthritis pathogenesis. We also identified association at the CCL21 gene locus (rs2812378, P = 0.00097 replication, P = 2.8 x 10(-7) overall), a gene involved in lymphocyte trafficking. Finally, we identified evidence of association at four additional gene loci: MMEL1-TNFRSF14 (rs3890745, P = 0.0035 replication, P = 1.1 x 10(-7) overall), CDK6 (rs42041, P = 0.010 replication, P = 4.0 x 10(-6) overall), PRKCQ (rs4750316, P = 0.0078 replication, P = 4.4 x 10(-6) overall), and KIF5A-PIP4K2C (rs1678542, P = 0.0026 replication, P = 8.8 x 10(-8) overall).
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