<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ke T</submitter><funding>National University of Singapore</funding><funding>National Research Foundation Singapore</funding><funding>NCI NIH HHS</funding><funding>National Medical Research Council</funding><funding>National Institutes of Health</funding><pagination>282-93</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4991635</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>80(5)</volume><pubmed_abstract>Peroxisome proliferator activated receptors (PPARs) are transcription factors involved in the regulation of key metabolic pathways. Numerous in vivo and in vitro studies have established their important roles in lipid metabolism. A few SNPs in PPAR genes have been reported to be associated with lipid levels. In this study, we aimed to investigate the interactive effects between single nucleotide polymorphisms (SNPs) in three PPAR isoforms α/δ/γ and other genetic variants across the genome on plasma high-density lipoprotein-cholesterol (HDL-C) levels. Study subjects (N = 2003) were genotyped using Illumina HumanOmniZhongHua-8 Beadchip. Fifty-three tag SNPs ± 100 kb of PPAR α, δ, and γ (r(2) &lt; 0.2) were selected. The effect of interactions between PPAR SNPs and those across the genome on HDL</pubmed_abstract><journal>Annals of human genetics</journal><pubmed_title>Interaction Between Peroxisome Proliferator Activated Receptor δ and Epithelial Membrane Protein 2 Polymorphisms Influences HDL-C Levels in the Chinese Population.</pubmed_title><pmcid>PMC4991635</pmcid><funding_grant_id>R01 CA144034</funding_grant_id><funding_grant_id>0796/2003</funding_grant_id><funding_grant_id>UM1 CA182876</funding_grant_id><funding_grant_id>370062002</funding_grant_id><funding_grant_id>NMRC/1270/2010</funding_grant_id><funding_grant_id>CSA/033/2012</funding_grant_id><funding_grant_id>STaR/2008</funding_grant_id><funding_grant_id>CG 2010</funding_grant_id><funding_grant_id>IRG07nov013</funding_grant_id><funding_grant_id>IRG09nov014</funding_grant_id><funding_grant_id>STaR/2013;</funding_grant_id><funding_grant_id>CG 2013</funding_grant_id><pubmed_authors>Yuan JM</pubmed_authors><pubmed_authors>Goh DY</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Dorajoo R</pubmed_authors><pubmed_authors>Heng CK</pubmed_authors><pubmed_authors>Han Y</pubmed_authors><pubmed_authors>van Dam RM</pubmed_authors><pubmed_authors>Tai ES</pubmed_authors><pubmed_authors>Ke T</pubmed_authors><pubmed_authors>Cheng CY</pubmed_authors><pubmed_authors>Wong TY</pubmed_authors><pubmed_authors>Koh WP</pubmed_authors><pubmed_authors>Khor CC</pubmed_authors><pubmed_authors>Teo YY</pubmed_authors><pubmed_authors>Friedlander Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Interaction Between Peroxisome Proliferator Activated Receptor δ and Epithelial Membrane Protein 2 Polymorphisms Influences HDL-C Levels in the Chinese Population.</name><description>Peroxisome proliferator activated receptors (PPARs) are transcription factors involved in the regulation of key metabolic pathways. Numerous in vivo and in vitro studies have established their important roles in lipid metabolism. A few SNPs in PPAR genes have been reported to be associated with lipid levels. In this study, we aimed to investigate the interactive effects between single nucleotide polymorphisms (SNPs) in three PPAR isoforms α/δ/γ and other genetic variants across the genome on plasma high-density lipoprotein-cholesterol (HDL-C) levels. Study subjects (N = 2003) were genotyped using Illumina HumanOmniZhongHua-8 Beadchip. Fifty-three tag SNPs ± 100 kb of PPAR α, δ, and γ (r(2) &lt; 0.2) were selected. The effect of interactions between PPAR SNPs and those across the genome on HDL</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Sep</publication><modification>2026-04-29T02:02:00.005Z</modification><creation>2019-03-27T02:21:05Z</creation></dates><accession>S-EPMC4991635</accession><cross_references><pubmed>27530449</pubmed><doi>10.1111/ahg.12164</doi></cross_references></HashMap>