Journal
HUMAN MOLECULAR GENETICS
Volume 22, Issue 16, Pages 3347-3362Publisher
OXFORD UNIV PRESS
DOI: 10.1093/hmg/ddt183
Keywords
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Funding
- National Natural Science Foundation of China [30971595, 30971383, 81100553, 81200568, 81270863, 31171127]
- National Basic Research Program of China (973) [2010CB529204, 2012C B517604]
- Shanghai Science and Technology Committee [10JC1410400]
- Program for Graves' Disease Innovative Research Team of Shanghai Municipal Education Commission
- Natural Science Foundation of Jiangsu Province, China [BK2009208, SBK201221245]
- National Natural Science Foundation of China [30971595, 30971383, 81100553, 81200568, 81270863, 31171127]
- National Basic Research Program of China (973) [2010CB529204, 2012C B517604]
- Shanghai Science and Technology Committee [10JC1410400]
- Program for Graves' Disease Innovative Research Team of Shanghai Municipal Education Commission
- Natural Science Foundation of Jiangsu Province, China [BK2009208, SBK201221245]
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Graves disease (GD), characterized by autoantibodies targeting antigens specifically expressed in thyroid tissues causing hyperthyroidism, is triggered by a combination of genetic and environmental factors. However, only a few loci for GD risk were confirmed in the various ethnic groups, and additional genetic determinants have to be detected. In this study, we carried out a three-stage study in 9529 patients with GD and 9984 controls to identify new risk loci for GD and found genome-wide significant associations in the overall populations for five novel susceptibility loci: the GPR174-ITM2A at Xq21.1, C1QTNF6-RAC2 at 22q12.313.1, SLAMF6 at 1q23.2, ABO at 9q34.2 and an intergenic region harboring two non-coding RNAs at 14q32.2 and one previous indefinite locus, TG at 8q24.22 (P-combined 5 10(8)). The genotypes of corresponding variants at 14q32.2 and 8q24.22 were correlated with the expression levels of C14orf64 and a TG transcript skipping exon 46, respectively. This study increased the number of GD loci with compelling evidence and indicated that non-coding RNAs might be potentially involved in the pathogenesis of GD.
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