rs11156429 - LIN28B-AS1

Magnitude 2.2 · 6 studies on file

Reported associations

  • Genome-wide association and longitudinal analyses reveal genetic loci linking pubertal height growth, pubertal timing and childhood adiposity. - Human molecular genetics (2014) · Cousminer DL, Berry DJ, Timpson NJ, Ang W, Thiering E, Byrne EM, Taal HR, Huikari V, Bradfield JP, Kerkhof M, Groen-Blokhuis MM, Kreiner-Møller E, Marinelli M, Holst C, Leinonen JT, Perry JR, Surakka I, Pietiläinen O, Kettunen J, Anttila V, Kaakinen M, Sovio U, Pouta A, Das S, Lagou V, Power C, Prokopenko I, Evans DM, Kemp JP, St Pourcain B, Ring S, Palotie A, Kajantie E, Osmond C, Lehtimäki T, Viikari JS, Kähönen M, Warrington NM, Lye SJ, Palmer LJ, Tiesler CM, Flexeder C, Montgomery GW, Medland SE, Hofman A, Hakonarson H, Guxens M, Bartels M, Salomaa V, Murabito JM, Kaprio J, Sørensen TI, Ballester F, Bisgaard H, Boomsma DI, Koppelman GH, Grant SF, Jaddoe VW, Martin NG, Heinrich J, Pennell CE, Raitakari OT, Eriksson JG, Smith GD, Hyppönen E, Järvelin MR, McCarthy MI, Ripatti S, Widén E · PubMed 23449627

    The pubertal height growth spurt is a distinctive feature of childhood growth reflecting both the central onset of puberty and local growth factors. Although little is known about the underlying genetics, growth variability during puberty correlates with adult risks for hormone-dependent cancer and adverse cardiometabolic health. The only gene so far associated with pubertal height growth, LIN28B, pleiotropically influences childhood growth, puberty and cancer progression, pointing to shared underlying mechanisms. To discover genetic loci influencing pubertal height and growth and to place them in context of overall growth and maturation, we performed genome-wide association meta-analyses in 18 737 European samples utilizing longitudinally collected height measurements. We found significan

  • Multi-ancestry genome-wide association study of major depression aids locus discovery, fine mapping, gene prioritization and causal inference - Unknown journal (n.d.) · Unknown authors · PubMed 38177345

    ABSTRACT: Most genome-wide association studies (GWAS) of major depression (MD) have been conducted in samples of European ancestry. Here we report a multi-ancestry GWAS of MD, adding data from 21 cohorts with 88,316 MD cases and 902,757 controls to previously reported data. This analysis used a range of measures to define MD and included samples of African (36% of effective sample size), East Asian (26%) and South Asian (6%) ancestry and Hispanic/Latin American participants (32%). The multi-ancestry GWAS identified 53 significantly associated novel loci. For loci from GWAS in European ancestry samples, fewer than expected were transferable to other ancestry groups. Fine mapping benefited from additional sample diversity. A transcriptome-wide association study identified 205 significantly a

  • Genome-wide physical activity interactions in adiposity ― A meta-analysis of 200,452 adults - Unknown journal (n.d.) · Unknown authors · PubMed 28448500

    ABSTRACT: Physical activity (PA) may modify the genetic effects that give rise to increased risk of obesity. To identify adiposity loci whose effects are modified by PA, we performed genome-wide interaction meta-analyses of BMI and BMI-adjusted waist circumference and waist-hip ratio from up to 200,452 adults of European (n = 180,423) or other ancestry (n = 20,029). We standardized PA by categorizing it into a dichotomous variable where, on average, 23% of participants were categorized as inactive and 77% as physically active. While we replicate the interaction with PA for the strongest known obesity-risk locus in the FTO gene, of which the effect is attenuated by ~30% in physically active individuals compared to inactive individuals, we do not identify additional loci that are sensitive t

  • Genomic analysis of male puberty timing highlights shared genetic basis with hair colour and lifespan - Unknown journal (n.d.) · Unknown authors · PubMed 32210231

    ABSTRACT: The timing of puberty is highly variable and is associated with long-term health outcomes. To date, understanding of the genetic control of puberty timing is based largely on studies in women. Here, we report a multi-trait genome-wide association study for male puberty timing with an effective sample size of 205,354 men. We find moderately strong genomic correlation in puberty timing between sexes (rg = 0.68) and identify 76 independent signals for male puberty timing. Implicated mechanisms include an unexpected link between puberty timing and natural hair colour, possibly reflecting common effects of pituitary hormones on puberty and pigmentation. Earlier male puberty timing is genetically correlated with several adverse health outcomes and Mendelian randomization analyses s

  • Genetic Susceptibility for Low Testosterone in Men and Its Implications in Biology and Screening: Data from the UK Biobank - Unknown journal (n.d.) · Unknown authors · PubMed 34337532

    ABSTRACT: Background Despite strong evidence of heritability, few studies have attempted to unveil the genetic underpinnings of testosterone levels. Objective To identify testosterone-associated loci in a large study and assess their biological and clinical implications. Design, setting, and participants The participants were men from the UK Biobank. A two-stage genome-wide association study (GWAS) was first used to identify/validate loci for low testosterone (LowT, <8 nmol/l) in 80% of men (N = 148 902). The cumulative effect of independent LowT risk loci was then evaluated in the remaining 20% of men. Outcome measurements and statistical analysis Associations of single nucleotide polymorphisms (SNPs) with LowT were tested using an additive model. Analyses of the expression quanti

  • The genetics of a "femaleness/maleness" score in cardiometabolic traits in the UK biobank - Unknown journal (n.d.) · Unknown authors · PubMed 37277458

    ABSTRACT: We recently devised continuous "sex-scores" that sum up multiple quantitative traits, weighted by their respective sex-difference effect sizes, as an approach to estimating polyphenotypic "maleness/femaleness" within each binary sex. To identify the genetic architecture underlying these sex-scores, we conducted sex-specific genome-wide association studies (GWASs) in the UK Biobank cohort (females: n = 161,906; males: n = 141,980). As a control, we also conducted GWASs of sex-specific "sum-scores", simply aggregating the same traits, without weighting by sex differences. Among GWAS-identified genes, while sum-score genes were enriched for genes differentially expressed in the liver in both sexes, sex-score genes were enriched for genes differentially expressed


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