tailieunhanh - Báo cáo y học: "Association of the FCRL3 gene with rheumatoid arthritis: a further example of population specificity"
Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Association of the FCRL3 gene with rheumatoid arthritis: a further example of population specificity? | Available online http content 8 4 R117 Research article Association of the FCRL3 gene with rheumatoid arthritis a further example of population specificity Stephen Eyre John Bowes Catherine Potter Jane Worthington and Anne Barton ARC-EU University of Manchester UK Corresponding author Stephen Eyre Received 15 Jun 2006 Revisions requested 28 Jun 2006 Revisions received 4 Jul 2006 Accepted 6 Jul 2006 Published 19 Jul 2006 Arthritis Research Therapy 2006 8 R117 doi ar2006 This article is online at http content 8 4 R117 2006 Eyre et al. licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Open Access Abstract Association of a functional promoter polymorphism mapping to the Fc receptor-like 3 FCRL3 gene has recently been reported and replicated with rheumatoid arthritis RA in Japanese populations. The aim of this study was to investigate association of the FCRL3 gene with RA in UK subjects. DNA was available from 1065 patients with RA and 2073 population controls from the UK. Four single nucleotide polymorphism SNP markers FCRL3-169 C T fclr3_3 rs7528684 f clr3_4 rs11264799 fclr3_5 rs945635 fclr3_6 rs3761959 all previously associated with RA in a Japanese population were genotyped in 761 RA samples and 484 controls. In the remaining samples only the putative disease causal polymorphism FCRL3-169 C T was tested. Genotyping was performed using either the Sequenom MassArray iPlex platform or a 5 Allelic discrimination assay Taqman ABI . Extensive linkage disequilibrium was present across the promoter SNPs genotyped r2 values . Allele frequencies did not differ between RA cases and controls either for the putative disease causal polymorphism odds
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