We are analyzing https://link.springer.com/article/10.1007/s11892-017-0908-x.

Title:
Mechanisms of Type 2 Diabetes Risk Loci | Current Diabetes Reports
Description:
Purpose of Review Deciphering the mechanisms of type 2 diabetes (T2DM) risk loci can greatly inform on disease pathology. This review discusses current knowledge of mechanisms through which genetic variants influence T2DM risk and considerations for future studies. Recent Findings Over 100 T2DM risk loci to date have been identified. Candidate causal variants at risk loci map predominantly to non-coding sequence. Physiological, epigenomic and gene expression data suggest that variants at many known T2DM risk loci affect pancreatic islet regulation, although variants at other loci also affect protein function and regulatory processes in adipose, pre-adipose, liver, skeletal muscle and brain. The effects of T2DM variants on regulatory activity in these tissues appear largely, but not exclusively, due to altered transcription factor binding. Putative target genes of T2DM variants have been defined at an increasing number of loci and some, such as FTO, may entail several genes and multiple tissues. Gene networks in islets and adipocytes have been implicated in T2DM risk, although the molecular pathways of risk genes remain largely undefined. Summary Efforts to fully define the mechanisms of T2DM risk loci are just beginning. Continued identification of risk mechanisms will benefit from combining genetic fine-mapping with detailed phenotypic association data, high-throughput epigenomics data from diabetes-relevant tissue, functional screening of candidate genes and genome editing of cellular and animal models.
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Keywords {🔍}

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Topics {✒️}

genome-wide trans-ancestry meta-analysis int/mediacentre/factsheets/fs312/en/ allele-specific transcriptional activity trans-ethnic fine-mapping studies reveal cell-type-specific expression pancreas-specific tcf7l2-null mice altered cis-regulatory elements genome-wide association identifies month download article/chapter human transcription factors combining genetic fine-mapping leveraging functional-annotation data statistical fine-mapping studies high-throughput epigenomics data genome-wide approach accounting phenome-wide association studies large-scale association analysis genome-wide association studies multitissue gene regulation body mass index characterize protein-dna interactions full article pdf transcription factor complexes fogarty mp mammalian genomes identified van de bunt genetic fine mapping transancestral fine-mapping open access resource cis-regulatory landscapes small effect variants manning fox je genetic regulatory signature lymphoid gene enhancers affect protein function klf14 locus related diabetes risk loci genome-wide associations ciliary gene vicinal expression qtl mapping van de geijn genetic association studies privacy choices/manage cookies t2dm risk loci diabetes risk locus human pancreatic islets muylti-ethnic samples pancreatic beta cell genome editing techniques locke ae

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         description:Deciphering the mechanisms of type 2 diabetes (T2DM) risk loci can greatly inform on disease pathology. This review discusses current knowledge of mechanisms through which genetic variants influence T2DM risk and considerations for future studies. Over 100 T2DM risk loci to date have been identified. Candidate causal variants at risk loci map predominantly to non-coding sequence. Physiological, epigenomic and gene expression data suggest that variants at many known T2DM risk loci affect pancreatic islet regulation, although variants at other loci also affect protein function and regulatory processes in adipose, pre-adipose, liver, skeletal muscle and brain. The effects of T2DM variants on regulatory activity in these tissues appear largely, but not exclusively, due to altered transcription factor binding. Putative target genes of T2DM variants have been defined at an increasing number of loci and some, such as FTO, may entail several genes and multiple tissues. Gene networks in islets and adipocytes have been implicated in T2DM risk, although the molecular pathways of risk genes remain largely undefined. Efforts to fully define the mechanisms of T2DM risk loci are just beginning. Continued identification of risk mechanisms will benefit from combining genetic fine-mapping with detailed phenotypic association data, high-throughput epigenomics data from diabetes-relevant tissue, functional screening of candidate genes and genome editing of cellular and animal models.
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