The Entire Engineering Powering MAPK

6% of the lipid variance [5]. This insatiable need for increasingly bigger samples to detect common variants with diminishing effect sizes suggests that alternative approaches may facilitate the discovery of novel lipid loci with potentially larger effect sizes. We leveraged the dynamic nature of genetic EPZ5676 cell line effects over a lifetime to enhance the discovery of lipid loci which may contain rare (minor allele frequency (MAF)?MAPK than common variants and explain substantial proportions of lipid variance. One recent study suggested that rare variants may collectively explain up to 7.8% of the variance in high-density lipoprotein levels [21], while another found that rare variants in four genes (LPL, GCKR, APOB, and APOA5) explained 1.1% of total variation in the diagnosis of hypertriglyceridemia [22]. In this investigation, our primary aim was to detect novel quantitative trait loci (QTLs) with age-dependent effects on fasting (��8?h) serum levels of total cholesterol (TC), high-density LY2109761 in vivo lipoprotein cholesterol (HDLC), low-density lipoprotein cholesterol (LDLC), and triglycerides (TG). We fit a highly flexible generalized variance components model [23], which allowed both the heritability and the correlations among relatives to depend on age [23], in each of nine population groups from the Family Blood Pressure Program (FBPP) [24]. These nine groups represented 3600 African Americans (AAs), 1283 Asians, 3218 European Americans (EAs), and 2026 Mexican Americans (MAs) [24]. We subsequently performed overall (across all races) and race-specific meta-analyses of these genome-wide linkage analyses to capitalize on the sharing of lipid loci across populations [3].