Expressive

rs114153232 - RALB - INHBB

Magnitude 2.0 · 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

  • Leveraging Polygenic Functional Enrichment to Improve GWAS Power. - American journal of human genetics (2019) · Kichaev G, Bhatia G, Loh PR, Gazal S, Burch K, Freund MK, Schoech A, Pasaniuc B, Price AL · PubMed 30595370

    Functional genomics data has the potential to increase GWAS power by identifying SNPs that have a higher prior probability of association. Here, we introduce a method that leverages polygenic functional enrichment to incorporate coding, conserved, regulatory, and LD-related genomic annotations into association analyses. We show via simulations with real genotypes that the method, functionally informed novel discovery of risk loci (FINDOR), correctly controls the false-positive rate at null loci and attains a 9%-38% increase in the number of independent associations detected at causal loci, depending on trait polygenicity and sample size. We applied FINDOR to 27 independent complex traits and diseases from the interim UK Biobank release (average N = 130K). Averaged across traits, we attaine

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