Expressive

rs12022410 - LEPR - RN7SL854P

Magnitude 2.2 · 3 studies on file

Reported associations

  • Discovery, fine-mapping, and conditional analyses of genetic variants associated with C-reactive protein in multiethnic populations using the Metabochip in the Population Architecture using Genomics and Epidemiology (PAGE) study. - Human molecular genetics (2019) · Kocarnik JM, Richard M, Graff M, Haessler J, Bien S, Carlson C, Carty CL, Reiner AP, Avery CL, Ballantyne CM, LaCroix AZ, Assimes TL, Barbalic M, Pankratz N, Tang W, Tao R, Chen D, Talavera GA, Daviglus ML, Chirinos-Medina DA, Pereira R, Nishimura K, Bužková P, Best LG, Ambite JL, Cheng I, Crawford DC, Hindorff LA, Fornage M, Heiss G, North KE, Haiman CA, Peters U, Le Marchand L, Kooperberg C · PubMed 29878111

    C-reactive protein (CRP) is a circulating biomarker indicative of systemic inflammation. We aimed to evaluate genetic associations with CRP levels among non-European-ancestry populations through discovery, fine-mapping and conditional analyses. A total of 30 503 non-European-ancestry participants from 6 studies participating in the Population Architecture using Genomics and Epidemiology study had serum high-sensitivity CRP measurements and ∼200 000 single nucleotide polymorphisms (SNPs) genotyped on the Metabochip. We evaluated the association between each SNP and log-transformed CRP levels using multivariate linear regression, with additive genetic models adjusted for age, sex, the first four principal components of genetic ancestry, and study-specific factors. Differential linkage di

  • Characterising metabolomic signatures of lipid-modifying therapies through drug target mendelian randomisation - Unknown journal (n.d.) · Unknown authors · PubMed 35213538

    ABSTRACT: Large-scale molecular profiling and genotyping provide a unique opportunity to systematically compare the genetically predicted effects of therapeutic targets on the human metabolome. We firstly constructed genetic risk scores for 8 drug targets on the basis that they primarily modify low-density lipoprotein (LDL) cholesterol (HMGCR, PCKS9, and NPC1L1), high-density lipoprotein (HDL) cholesterol (CETP), or triglycerides (APOC3, ANGPTL3, ANGPTL4, and LPL). Conducting mendelian randomisation (MR) provided strong evidence of an effect of drug-based genetic scores on coronary artery disease (CAD) risk with the exception of ANGPTL3. We then systematically estimated the effects of each score on 249 metabolic traits derived using blood samples from an unprecedented sample size of up to

  • The genetics of a "femaleness/maleness" score in cardiometabolic traits in the UK biobank - Unknown journal (n.d.) · Unknown authors · PubMed 37277458

    ABSTRACT: We recently devised continuous "sex-scores" that sum up multiple quantitative traits, weighted by their respective sex-difference effect sizes, as an approach to estimating polyphenotypic "maleness/femaleness" within each binary sex. To identify the genetic architecture underlying these sex-scores, we conducted sex-specific genome-wide association studies (GWASs) in the UK Biobank cohort (females: n = 161,906; males: n = 141,980). As a control, we also conducted GWASs of sex-specific "sum-scores", simply aggregating the same traits, without weighting by sex differences. Among GWAS-identified genes, while sum-score genes were enriched for genes differentially expressed in the liver in both sexes, sex-score genes were enriched for genes differentially expressed

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