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Erik Ingelsson

Researcher at Stanford University

Publications -  546
Citations -  99427

Erik Ingelsson is an academic researcher from Stanford University. The author has contributed to research in topics: Genome-wide association study & Population. The author has an hindex of 124, co-authored 538 publications receiving 85407 citations. Previous affiliations of Erik Ingelsson include Karolinska Institutet & Cardiovascular Institute of the South.

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The Trans-Ancestral Genomic Architecture of Glycaemic Traits

Ji Chen, +478 more
- 25 Jul 2020 - 
TL;DR: Genomic feature, gene-expression and gene-set analyses revealed distinct biological signatures for each trait, highlighting different underlying biological pathways, increasing understanding of diabetes pathophysiology by use of trans-ancestry studies for improved power and resolution.

Parent-of-origin specific allelic associations among 106 genomic loci for age at menarche

John R. B. Perry, +197 more
Journal ArticleDOI

Genome-wide meta-analysis uncovers novel loci influencing circulating leptin levels

Tuomas O. Kilpeläinen, +227 more
TL;DR: In this article, the authors performed a genome-wide association study (GWAS) of circulating leptin levels from 32,161 individuals and identified five loci robustly associated with leptin levels in/near LEP, SLC32A1, GCKR, CCNL1 and FTO.

Meta-analyses identify 13 loci associated with age at menopause and highlight DNA repair and immune pathways

Lisette Stolk, +179 more
TL;DR: A meta-analysis of genome-wide association studies in 38,968 women of European descent identified 13 loci newly associated with age at natural menopause, and candidate genes located at these newly associated loci include genes implicated in DNA repair and immune function.
Journal ArticleDOI

A Central Role for GRB10 in Regulation of Islet Function in Man.

Inga Prokopenko, +63 more
- 03 Apr 2014 - 
TL;DR: In this paper, the growth factor receptor-bound protein 10 (GRB10) gene was associated with reduced glucose-stimulated insulin secretion and increased risk of type 2 diabetes (T2D) if inherited from the father, but inexplicably reduced fasting glucose when inherited from a mother.