rs10922907 - BARHL2 - LINC02609

Magnitude 2.2 · 8 studies on file

Reported associations

• A cross-population atlas of genetic associations for 220 human phenotypes. - Nature genetics (2021) · Sakaue S, Kanai M, Tanigawa Y, Karjalainen J, Kurki M, Koshiba S, Narita A, Konuma T, Yamamoto K, Akiyama M, Ishigaki K, Suzuki A, Suzuki K, Obara W, Yamaji K, Takahashi K, Asai S, Takahashi Y, Suzuki T, Shinozaki N, Yamaguchi H, Minami S, Murayama S, Yoshimori K, Nagayama S, Obata D, Higashiyama M, Masumoto A, Koretsune Y, Ito K, Terao C, Yamauchi T, Komuro I, Kadowaki T, Tamiya G, Yamamoto M, Nakamura Y, Kubo M, Murakami Y, Yamamoto K, Kamatani Y, Palotie A, Rivas MA, Daly MJ, Matsuda K, Okada Y · PubMed 34594039

  Current genome-wide association studies do not yet capture sufficient diversity in populations and scope of phenotypes. To expand an atlas of genetic associations in non-European populations, we conducted 220 deep-phenotype genome-wide association studies (diseases, biomarkers and medication usage) in BioBank Japan (n = 179,000), by incorporating past medical history and text-mining of electronic medical records. Meta-analyses with the UK Biobank and FinnGen (n = 628,000) identified ~5,000 new loci, which improved the resolution of the genomic map of human traits. This atlas elucidated the landscape of pleiotropy as represented by the major histocompatibility complex locus, where we conducted HLA fine-mapping. Finally, we performed statistical decomposition of matrices of phenome-wid

• Genetic Risk for Smoking: Disentangling Interplay Between Genes and Socioeconomic Status - Unknown journal (n.d.) · Unknown authors · PubMed 34855049

  ABSTRACT: This study aims to disentangle the contribution of genetic liability, educational attainment (EA), and their overlap and interaction in lifetime smoking. We conducted genome-wide association studies (GWASs) in UK Biobank (N = 394,718) to (i) capture variants for lifetime smoking, (ii) variants for EA, and (iii) variants that contribute to lifetime smoking independently from EA ('smoking-without-EA'). Based on the GWASs, three polygenic scores (PGSs) were created for individuals from the Netherlands Twin Register (NTR, N = 17,805) and the Netherlands Mental Health Survey and Incidence Study-2 (NEMESIS-2, N = 3090). We tested gene-environment (G × E) interactions between each PGS, neighborhood socioeconomic status (SES) and EA on lifetime smoking. To assess i

• Evidence for causal effects of lifetime smoking on risk for depression and schizophrenia: a Mendelian randomisation study - Unknown journal (n.d.) · Unknown authors · PubMed 31689377

  ABSTRACT: Background Smoking prevalence is higher amongst individuals with schizophrenia and depression compared with the general population. Mendelian randomisation (MR) can examine whether this association is causal using genetic variants identified in genome-wide association studies (GWAS). Methods We conducted two-sample MR to explore the bi-directional effects of smoking on schizophrenia and depression. For smoking behaviour, we used (1) smoking initiation GWAS from the GSCAN consortium and (2) we conducted our own GWAS of lifetime smoking behaviour (which captures smoking duration, heaviness and cessation) in a sample of 462690 individuals from the UK Biobank. We validated this instrument using positive control outcomes (e.g. lung cancer). For schizophrenia and depression we used GWA

• The Genetic and Neural Substrates of Externalizing Behavior - Unknown journal (n.d.) · Unknown authors · PubMed 36324656

  ABSTRACT: Background To gain more insight into the biological factors that mediate vulnerability to display externalizing behaviors, we leveraged genome-wide association study summary statistics on 13 externalizing phenotypes. Methods After data classification based on genetic resemblance, we performed multivariate genome-wide association meta-analyses and conducted extensive bioinformatic analyses, including genetic correlation assessment with other traits, Mendelian randomization, and gene set and gene expression analyses. Results The genetic data could be categorized into disruptive behavior (DB) and risk-taking behavior (RTB) factors, and subsequent genome-wide association meta-analyses provided association statistics for DB and RTB (Neff = 523,150 and 1,506,537, respectively), yieldi

• Gene discovery and polygenic prediction from a 1.1-million-person GWAS of educational attainment - Unknown journal (n.d.) · Unknown authors · PubMed 30038396

  ABSTRACT: We conduct a large-scale genetic association analysis of educational attainment in a sample of ~1.1 million individuals and identify 1,271 independent genome-wide-significant SNPs. For the SNPs taken together, we found evidence of heterogeneous effects across environments. The SNPs implicate genes involved in brain-development processes and neuron-to-neuron communication. In a separate analysis of the X chromosome, we identify 10 independent genome-wide-significant SNPs and estimate a SNP heritability of ~0.3% in both men and women, consistent with partial dosage compensation. A joint (multi-phenotype) analysis of educational attainment and three related cognitive phenotypes generates polygenic scores that explain 11-13% of the variance in educational attainment and 7-10% of

• Association studies of up to 1.2 million individuals yield new insights into the genetic etiology of tobacco and alcohol use - Unknown journal (n.d.) · Unknown authors · PubMed 30643251

  ABSTRACT: Tobacco and alcohol use are leading causes of mortality that influence risk for many complex diseases and disorders. They are heritable and etiologically related behaviors that have been resistant to gene discovery efforts. In sample sizes up to 1.2 million individuals, we discovered 566 genetic variants in 406 loci associated with multiple stages of tobacco use (initiation, cessation, and heaviness) as well as alcohol use, with 150 loci evidencing pleiotropic association. Smoking phenotypes were positively genetically correlated with many health conditions, whereas alcohol use was negatively correlated with these conditions, such that increased genetic risk for alcohol use is associated with lower disease risk. We report evidence for the involvement of many systems in tobacco an

• Identification of 371 genetic variants for age at first sex and birth linked to externalising behaviour - Unknown journal (n.d.) · Unknown authors · PubMed 34211149

  ABSTRACT: Age at first sexual intercourse (AFS) and age at first birth (AFB) have implications for health and evolutionary fitness. In this genome-wide association study (AFS, N=387,338; AFB, N=542,901), we identify 371 SNPs, 11 sex-specific, with a 5-6% polygenic score (PGS) prediction. Heritability of AFB shifted from 9% [CI=4-14] for women born in 1940 to 22% [CI=19-25] in 1965. Signals are driven by the genetics of reproductive biology and externalising behaviour, with key genes related to follicle stimulating hormone (FSHB), implantation (ESR1), infertility, and spermatid differentiation. Our findings suggest that Polycystic Ovarian Syndrome may lead to later AFB, linking with infertility. Late AFB is associated with parental longevity, and reduced incidence of Type 2 Diabetes (T2D) a

• Genome-wide association study of smoking trajectory and meta-analysis of smoking status in 842,000 individuals - Unknown journal (n.d.) · Unknown authors · PubMed 33082346

  ABSTRACT: Here we report a large genome-wide association study (GWAS) for longitudinal smoking phenotypes in 286,118 individuals from the Million Veteran Program (MVP) where we identified 18 loci for smoking trajectory of current versus never in European Americans, one locus in African Americans, and one in Hispanic Americans. Functional annotations prioritized several dozen genes where significant loci co-localized with either expression quantitative trait loci or chromatin interactions. The smoking trajectories were genetically correlated with 209 complex traits, for 33 of which smoking was either a causal or a consequential factor. We also performed European-ancestry meta-analyses for smoking status in the MVP and GWAS & Sequencing Consortium of Alcohol and Nicotine use (GSCAN) (Ntotal

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