rs10122845 - PTPRD

Magnitude 2.2 · 2 studies on file

Reported associations

• Metabolome-wide association identifies ferredoxin-1 (FDX1) as a determinant of cholesterol metabolism and cardiovascular risk in Asian populations. - Nature cardiovascular research (2025) · Sadhu N, Dalan R, Jain PR, Lee CJM, Pakkiri LS, Tay KY, Mina TH, Low D, Min Y, Ackers-Johnson M, Thi TT, Kota VG, Shi Y, Liu Y, Yu H, Lai V, Yang Y, Tay D, Ng HK, Wang X, Wong KE, Lam M, Guan XL, Bertin N, Wong E, Best J, Sarangarajan R, Elliott P, Riboli E, Lee J, Lee ES, Ngeow J, Tan P, Cheung C, Drum CL, Foo RS, Michelotti GA, Yu H, Sheridan PA, Loh M, Chambers JC · PubMed 40360795

  The burden of cardiovascular disease is rising in the Asia-Pacific region, in contrast to falling cardiovascular disease mortality rates in Europe and North America. Here we perform quantification of 883 metabolites by untargeted mass spectroscopy in 8,124 Asian adults and investigate their relationships with carotid intima media thickness, a marker of atherosclerosis. Plasma concentrations of 3beta-hydroxy-5-cholestenoate (3BH5C), a cholesterol metabolite, were inversely associated with carotid intima media thickness, and Mendelian randomization studies supported a causal relationship between 3BH5C and coronary artery disease. The observed effect size was 5- to 6-fold higher in Asians than Europeans. Colocalization analyses indicated the presence of a shared causal variant between 3BH5C p

• Polygenic prediction of educational attainment within and between families from genome-wide association analyses in 3 million individuals - Unknown journal (n.d.) · Unknown authors · PubMed 35361970

  ABSTRACT: We conduct a genome-wide association study (GWAS) of educational attainment (EA) in a sample of ~3 million individuals and identify 3,952 approximately uncorrelated genome-wide-significant single-nucleotide polymorphisms (SNPs). A genome-wide polygenic predictor, or polygenic index (PGI), explains 12-16% of EA variance and contributes to risk prediction for ten diseases. Direct effects (i.e., controlling for parental PGIs) explain roughly half the PGI's magnitude of association with EA and other phenotypes. The correlation between mate-pair PGIs is far too large to be consistent with phenotypic assortment alone, implying additional assortment on PGI-associated factors. In an additional GWAS of dominance deviations from the additive model, we identify no genome-wide-significan

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