Expressive

rs11250098 - XKR6

Magnitude 2.0 · 3 studies on file

Reported associations

  • Genetic overlap analysis of endometriosis and asthma identifies shared loci implicating sex hormones and thyroid signalling pathways. - Human reproduction (Oxford, England) (2022) · Adewuyi EO, Mehta D, Nyholt DR · PubMed 35472084

    Is there a shared genetic or causal association of endometriosis with asthma or what biological mechanisms may underlie their potential relationships? Our results confirm a significant but non-causal association of endometriosis with asthma implicating shared genetic susceptibility and biological pathways in the mechanisms of the disorders, and potentially, their co-occurrence. Some observational studies have reported a pattern of co-occurring relationship between endometriosis and asthma; however, there is conflicting evidence and the aetiology, as well as the underlying mechanisms of the relationship, remain unclear. We applied multiple statistical genetic approaches in the analysis of well-powered, genome-wide association study (GWAS) summary data to comprehensively assess the relations

  • 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

  • GWAS of 89,283 individuals identifies genetic variants associated with self-reporting of being a morning person - Unknown journal (n.d.) · Unknown authors · PubMed 26835600

    ABSTRACT: Circadian rhythms are a nearly universal feature of living organisms and affect almost every biological process. Our innate preference for mornings or evenings is determined by the phase of our circadian rhythms. We conduct a genome-wide association analysis of self-reported morningness, followed by analyses of biological pathways and related phenotypes. We identify 15 significantly associated loci, including seven near established circadian genes (rs12736689 near RGS16, P=7.0 × 10−18; rs9479402 near VIP, P=3.9 × 10−11; rs55694368 near PER2, P=2.6 × 10−9; rs35833281 near HCRTR2, P=3.7 × 10−9; rs11545787 near RASD1, P=1.4 × 10−8; rs11121022 near PER3, P=2.0 × 10−8; rs9565309 near FBXL3, P=3.5 × 10−8. Circadian and phototransduction pathways are enriched in our

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