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Prioritising Causal Genes at Type 2 Diabetes Risk Loci
by
Grotz, Antje K.
, Thomsen, Soren K.
, Gloyn, Anna L.
in
Diabetes
/ Diabetes Mellitus, Type 2 - genetics
/ Gene loci
/ Genetic Loci
/ Genetic Predisposition to Disease
/ Genetic Testing
/ Genetic Variation
/ Genetics (AP Morris
/ Genetics (AP Morris, Section Editor)
/ Genome-Wide Association Study - methods
/ Humans
/ Medicine
/ Medicine & Public Health
/ Section Editor
/ Topical Collection on Genetics
2017
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Prioritising Causal Genes at Type 2 Diabetes Risk Loci
by
Grotz, Antje K.
, Thomsen, Soren K.
, Gloyn, Anna L.
in
Diabetes
/ Diabetes Mellitus, Type 2 - genetics
/ Gene loci
/ Genetic Loci
/ Genetic Predisposition to Disease
/ Genetic Testing
/ Genetic Variation
/ Genetics (AP Morris
/ Genetics (AP Morris, Section Editor)
/ Genome-Wide Association Study - methods
/ Humans
/ Medicine
/ Medicine & Public Health
/ Section Editor
/ Topical Collection on Genetics
2017
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Do you wish to request the book?
Prioritising Causal Genes at Type 2 Diabetes Risk Loci
by
Grotz, Antje K.
, Thomsen, Soren K.
, Gloyn, Anna L.
in
Diabetes
/ Diabetes Mellitus, Type 2 - genetics
/ Gene loci
/ Genetic Loci
/ Genetic Predisposition to Disease
/ Genetic Testing
/ Genetic Variation
/ Genetics (AP Morris
/ Genetics (AP Morris, Section Editor)
/ Genome-Wide Association Study - methods
/ Humans
/ Medicine
/ Medicine & Public Health
/ Section Editor
/ Topical Collection on Genetics
2017
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Journal Article
Prioritising Causal Genes at Type 2 Diabetes Risk Loci
2017
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Overview
Purpose of Review
Genome-wide association studies (GWAS) for type 2 diabetes (T2D) risk have identified a large number of genetic loci associated with disease susceptibility. However, progress moving from association signals through causal genes to functional understanding has so far been slow, hindering clinical translation. This review discusses the benefits and limitations of emerging, unbiased approaches for prioritising causal genes at T2D risk loci.
Recent Findings
Candidate causal genes can be identified by a number of different strategies that rely on genetic data, genomic annotations, and functional screening of selected genes. To overcome the limitations of each particular method, integration of multiple data sets is proving essential for establishing confidence in the prioritised genes. Previous studies have also highlighted the need to support these efforts through identification of causal variants and disease-relevant tissues.
Summary
Prioritisation of causal genes at T2D risk loci by integrating complementary lines of evidence promises to accelerate our understanding of disease pathology and promote translation into new therapeutics.
Publisher
Springer US,Springer Nature B.V
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