ArticleJournal of lipid research2010
A genome-wide linkage scan identifies multiple quantitative trait loci for HDL-cholesterol levels in families with premature CAD and MI.
Article in Journal of lipid research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Chronic stress, epigenetics, and adipose tissue metabolism in the obese state.Nutrition & metabolism · 2020Review
- The Relationship Between Premature Myocardial Infarction with TC/HDL-C Ratio Subgroups in a Multiple Risk Factor Model.Advanced journal of emergency medicine · 2019Article
- Genome-wide linkage scan identifies two novel genetic loci for coronary artery disease: in GeneQuest families.PloS one · 2014Article
- Apolipoprotein A-I: insights from redox proteomics for its role in neurodegeneration.Proteomics. Clinical applications · 2013Review
- The interaction of ApoA-I and ABCA1 triggers signal transduction pathways to mediate efflux of cellular lipids.Molecular medicine (Cambridge, Mass.) · 2012Review
- Genetic susceptibility to atherosclerosis.Stroke research and treatment · 2012Article
- Genetic loci for blood lipid levels identified by linkage and association analyses in Caribbean Hispanics.Journal of lipid research · 2011Article
- Glucuronic acid epimerase is associated with plasma triglyceride and high-density lipoprotein cholesterol levels in Turks.Annals of human genetics · 2011Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Plasma HDL cholesterol levels (HDL-C) are an independent predictor of coronary artery disease (CAD). We have completed a genome-wide linkage scan for HDL-C in a US cohort consisting of 388 multiplex families with premature CAD (GeneQuest). The heritability of HDL-C in GeneQuest was 0.37 with gender and age as covariates (P = 5.1 x 10(-4)). Two major quantitative trait loci (QTL) for log-transformed HDL-C adjusted for age and gender were identified onto chromosomes 7p22 and 15q25 with maximum multipoint logarithm of odds (LOD) scores of 3.76 and 6.69, respectively. Fine mapping decreased the 7p22 LOD score to a nonsignificant level of 3.09 and split the 15q25 QTL into two loci, one minor QTL on 15q22 (LOD = 2.73) that spanned the LIPC gene, and the other at 15q25 (LOD = 5.63). A family-based quantitative transmission disequilibrium test (QTDT) revealed significant association between variant rs1800588 in LIPC and HDL-C in the GeneQuest population (P = 0.0067), which may account for the minor QTL on 15q22. The 15q25 QTL is the most significant locus identified for HDL-C to date, and these results provide a framework for the ultimate identification of the underlying HDL-C variant and gene on chromosomes 15q25, which will provide insights into novel regulatory mechanisms of HDL-C metabolism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.