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A genome-wide association study identifies two new risk loci for Graves' disease

Nature Genetics, ISSN: 1061-4036, Vol: 43, Issue: 9, Page: 897-901
2011
  • 236
    Citations
  • 0
    Usage
  • 152
    Captures
  • 1
    Mentions
  • 26
    Social Media
Metric Options:   Counts1 Year3 Year

Metrics Details

  • Citations
    236
    • Citation Indexes
      234
    • Clinical Citations
      1
      • PubMed Guidelines
        1
    • Patent Family Citations
      1
      • Patent Families
        1
  • Captures
    152
  • Mentions
    1
    • News Mentions
      1
      • News
        1
  • Social Media
    26
    • Shares, Likes & Comments
      26
      • Facebook
        26

Most Recent News

Genetic and Plasma Proteomic Approaches to Identify Therapeutic Targets for Graves’ Disease and Graves’ Ophthalmopathy

Introduction Graves’ disease (GD) is an autoimmune disorder specifically targeting the thyroid gland and is the most common cause of hyperthyroidism. It is driven by

Article Description

Graves' disease is a common autoimmune disorder characterized by thyroid stimulating hormone receptor autoantibodies (TRAb) and hyperthyroidism. To investigate the genetic architecture of Graves' disease, we conducted a genome-wide association study in 1,536 individuals with Graves' disease (cases) and 1,516 controls. We further evaluated a group of associated SNPs in a second set of 3,994 cases and 3,510 controls. We confirmed four previously reported loci (in the major histocompatibility complex, TSHR, CTLA4 and FCRL3) and identified two new susceptibility loci (the RNASET2-FGFR1OP-CCR6 region at 6q27 (P combined = 6.85 ×10 for rs9355610) and an intergenic region at 4p14 (P combined = 1.08 ×10 for rs6832151)). These newly associated SNPs were correlated with the expression levels of RNASET2 at 6q27, of CHRNA9 and of a previously uncharacterized gene at 4p14, respectively. Moreover, we identified strong associations of TSHR and major histocompatibility complex class II variants with persistently TRAb-positive Graves' disease. © 2011 Nature America, Inc. All rights reserved.

Bibliographic Details

Chu, Xun; Pan, Chun-Ming; Zhao, Shuang-Xia; Liang, Jun; Gao, Guan-Qi; Zhang, Xiao-Mei; Yuan, Guo-Yue; Li, Chang-Gui; Xue, Li-Qiong; Shen, Min; Liu, Wei; Xie, Fang; Yang, Shao-Ying; Wang, Hai-Feng; Shi, Jing-Yi; Sun, Wei-Wei; Du, Wen-Hua; Zuo, Chun-Lin; Shi, Jin-Xiu; Liu, Bing-Li; Guo, Cui-Cui; Zhan, Ming; Gu, Zhao-Hui; Zhang, Xiao-Na; Sun, Fei; Wang, Zhi-Quan; Song, Zhi-Yi; Zou, Cai-Yan; Sun, Wei-Hua; Guo, Ting; Cao, Huang-Ming; Ma, Jun-Hua; Han, Bing; Li, Ping; Jiang, He; Huang, Qiu-Hua; Liang, Liming; Liu, Li-Bin; Chen, Gang; Su, Qing; Peng, Yong-De; Zhao, Jia-Jun; Ning, Guang; Chen, Zhu; Chen, Jia-Lun; Chen, Sai-Juan; Huang, Wei; Song, Huai-Dong; China Consortium for Genetics of Autoimmune Thyroid Disease

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Biochemistry, Genetics and Molecular Biology

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