Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Genome-wide association studies (GWAS) have identified hundreds of genetic variants associated with complex traits and diseases. However, elucidating the causal genes underlying GWAS hits remains challenging. We applied the summary data-based Mendelian randomization (SMR) method to 28 GWAS summary datasets to identify genes whose expression levels were associated with traits and diseases due to pleiotropy or causality (the expression level of a gene and the trait are affected by the same causal variant at a locus). We identified 71 genes, of which 17 are novel associations (no GWAS hit within 1 Mb distance of the genes). We integrated all the results in an online database ( http://www.cnsgenomics/shiny/SMRdb/ ), providing important resources to prioritize genes for further follow-up, for example in functional studies.

Original publication

DOI

10.1186/s13073-016-0338-4

Type

Journal article

Journal

Genome medicine

Publication Date

08/2016

Volume

8

Addresses

Queensland Brain Institute, University of Queensland, Brisbane, Queensland, Australia.

Keywords

Humans, Inflammatory Bowel Diseases, Alzheimer Disease, Genetic Predisposition to Disease, Models, Statistical, Gene Expression Profiling, Gene Expression Regulation, Genotype, Quantitative Trait, Heritable, Phenotype, Quantitative Trait Loci, Genome, Human, Databases, Genetic, Coronary Artery Disease, Genome-Wide Association Study, Genetic Pleiotropy, Autism Spectrum Disorder