Genetic and molecular basis of quantitative trait loci of arthritis in rat: genes and polymorphisms.
Genetic and molecular basis of quantitative trait loci of arthritis in rat: genes and polymorphisms.
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DOI：
10.4049/jimmunol.181.2.859
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发表时间：
2008-07-15
期刊：
影响因子：
--
通讯作者：
Gu W
中科院分区：
文献类型：
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作者：
Xiong Q;Jiao Y;Hasty KA;Stuart JM;Postlethwaite A;Kang AH;Gu W
类风湿性关节炎（RA）是一种自身免疫性疾病，其发病机制受到多种遗传和环境因素的影响。为了了解RA的遗传和分子基础，人们使用各种RA大鼠模型鉴定了大量调节实验性自身免疫性关节炎的数量性状基因座（QTL）。然而，确定这些QTL中的特定责任基因仍然是一个重大挑战。利用现有的基因组数据和基因注释信息，我们系统地研究了整个大鼠基因组中RA相关基因和QTL内外的多态性。通过全基因组基因和多态性分析，我们发现在QTL区域的RA相关基因显著多于非QTL区域。进一步的实验研究是必要的，以确定这些已知的RA相关基因或多态性的遗传成分引起的QTL效应。
Rheumatoid arthritis (RA) is an autoimmune disease, the pathogenesis of which is affected by multiple genetic and environmental factors. To understand the genetic and molecular basis of RA, a large number of quantitative trait loci (QTL) that regulate experimental autoimmune arthritis have been identified using various rat models for RA. However, identifying the particular responsible genes within these QTL remains a major challenge. Using currently available genome data and gene annotation information, we systematically examined RA-associated genes and polymorphisms within and outside QTL over the whole rat genome. By the whole genome analysis of genes and polymorphisms, we found that there are significantly more RA-associated genes in QTL regions as contrasted with non-QTL regions. Further experimental studies are necessary to determine whether these known RA-associated genes or polymorphisms are genetic components causing the QTL effect.