期刊
GENETICA
卷 136, 期 2, 页码 333-340出版社
SPRINGER
DOI: 10.1007/s10709-008-9305-3
关键词
Genome screen; Haseman-Elston; IBD; Quantitative traits; Variance components
资金
- NHLBI NIH HHS [R01 HL45522, R01 HL070751-07, P01 HL045522-15, P01 HL045522, R01 HL070751] Funding Source: Medline
- NIAAA NIH HHS [U10 AA008403-15, U10 AA08403] Funding Source: Medline
- NIGMS NIH HHS [R01 GM031575-25, R01 GM031575, R01 GM31575] Funding Source: Medline
- NIMH NIH HHS [R01 MH59490, R01 MH078111-03, R01 MH78111, R37 MH059490, R01 MH059490, R37 MH059490-11, R01 MH078111] Funding Source: Medline
Human quantitative trait locus (QTL) linkage mapping, although based on classical statistical genetic methods that have been around for many years, has been employed for genome-wide screening for only the last 10-15 years. In this time, there have been many success stories, ranging from QTLs that have been replicated in independent studies to those for which one or more genes underlying the linkage peak have been identified to a few with specific functional variants that have been confirmed in in vitro laboratory assays. Despite these successes, there is a general perception that linkage approaches do not work for complex traits, possibly because many human QTL linkage studies have been limited in sample size and have not employed the family configurations that maximize the power to detect linkage. We predict that human QTL linkage studies will continue to be productive for the next several years, particularly in combination with RNA expression level traits that are showing evidence of regulatory QTLs of large effect sizes and in combination with high-density genome-wide SNP panels. These SNP panels are being used to identify QTLs previously localized by linkage and linkage results are being used to place informative priors on genome-wide association studies.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据