Expressive

rs1062577 - ESR1

Magnitude 2.2 · 2 studies on file

Reported associations

  • Gene-by-environment interactions modulate the infant gut microbiota in asthma and atopy. - The Journal of allergy and clinical immunology (2025) · Stickley SA, Fang ZY, Ambalavanan A, Zhang Y, Zacharias AM, Petersen C, Dai D, Azad MB, Brook JR, Mandhane PJ, Simons E, Moraes TJ, Surette MG, Turvey SE, Subbarao P, Duan Q · PubMed 40187613

    Gut microbiota has been associated with health and susceptibility to childhood diseases, including asthma and allergies. However, the genomic factors contributing to interindividual variations in gut microbiota remain poorly understood. We sought to integrate host genomics with early-life exposures to investigate main and interaction effects on gut microbiota during the first year of life. In addition, we identified gut microbes associated with childhood respiratory (asthma, wheeze) and atopic (atopic dermatitis, food/inhalant sensitization) outcomes. We leveraged microbiome data from infant stool at ages 3 months (N = 779) and 1 year (N = 770) from the CHILD Cohort Study. We identified microbial taxa and co-occurring network clusters associated with asthma and atopy by age 5 years. Genome

  • 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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