rs11152166 - CCBE1

Magnitude 2.8 · 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

  • Genome-wide association analysis accounting for environmental factors through propensity-score matching: application to stressful live events in major depressive disorder. - American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics (2014) · Power RA, Cohen-Woods S, Ng MY, Butler AW, Craddock N, Korszun A, Jones L, Jones I, Gill M, Rice JP, Maier W, Zobel A, Mors O, Placentino A, Rietschel M, Aitchison KJ, Tozzi F, Muglia P, Breen G, Farmer AE, McGuffin P, Lewis CM, Uher R · PubMed 23857890

    Stressful life events are an established trigger for depression and may contribute to the heterogeneity within genome-wide association analyses. With depression cases showing an excess of exposure to stressful events compared to controls, there is difficulty in distinguishing between "true" cases and a "normal" response to a stressful environment. This potential contamination of cases, and that from genetically at risk controls that have not yet experienced environmental triggers for onset, may reduce the power of studies to detect causal variants. In the RADIANT sample of 3,690 European individuals, we used propensity score matching to pair cases and controls on exposure to stressful life events. In 805 case-control pairs matched on stressful life event, we tested the influence of 457,670


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