rs11954686 - FST - NDUFS4

Magnitude 2.0 · 3 studies on file

Reported associations

  • Genetic Risk for Smoking: Disentangling Interplay Between Genes and Socioeconomic Status - Unknown journal (n.d.) · Unknown authors · PubMed 34855049

    ABSTRACT: This study aims to disentangle the contribution of genetic liability, educational attainment (EA), and their overlap and interaction in lifetime smoking. We conducted genome-wide association studies (GWASs) in UK Biobank (N = 394,718) to (i) capture variants for lifetime smoking, (ii) variants for EA, and (iii) variants that contribute to lifetime smoking independently from EA ('smoking-without-EA'). Based on the GWASs, three polygenic scores (PGSs) were created for individuals from the Netherlands Twin Register (NTR, N = 17,805) and the Netherlands Mental Health Survey and Incidence Study-2 (NEMESIS-2, N = 3090). We tested gene-environment (G × E) interactions between each PGS, neighborhood socioeconomic status (SES) and EA on lifetime smoking. To assess i

  • Polygenic prediction of occupational status GWAS elucidates genetic and environmental interplay in intergenerational transmission, careers and health in UK Biobank - Unknown journal (n.d.) · Unknown authors · PubMed 39715877

    ABSTRACT: Socioeconomic status (SES) impacts health and life-course outcomes. This genome-wide association study (GWAS) of sociologically informed occupational status measures (ISEI, SIOPS, CAMSIS) using the UK Biobank (N = 273,157) identified 106 independent single-nucleotide polymorphisms of which 8 are novel to the study of SES. Genetic correlations with educational attainment (rg = 0.96-0.97) and income (rg = 0.81-0.91) point to a common genetic factor for SES. We observed a 54-57% reduction in within-family predictions compared with population-based predictions, attributed to indirect parental effects (22-27% attenuation) and assortative mating (21-27%) following our calculations. Using polygenic scores from population predictions of 5-10% (incremental R2 =

  • A saturated map of common genetic variants associated with human height - Unknown journal (n.d.) · Unknown authors · PubMed 36224396

    ABSTRACT: Common single-nucleotide polymorphisms (SNPs) are predicted to collectively explain 40-50% of phenotypic variation in human height, but identifying the specific variants and associated regions requires huge sample sizes. Here, using data from a genome-wide association study of 5.4 million individuals of diverse ancestries, we show that 12,111 independent SNPs that are significantly associated with height account for nearly all of the common SNP-based heritability. These SNPs are clustered within 7,209 non-overlapping genomic segments with a mean size of around 90 kb, covering about 21% of the genome. The density of independent associations varies across the genome and the regions of increased density are enriched for biologically relevant genes. In out-of-sample estimation


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