ArticleDiabetologia2013
In vitro scan for enhancers at the TCF7L2 locus.
Article in Diabetologia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
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- A double-negative prostate cancer subtype is vulnerable to SWI/SNF-targeting degrader molecules.bioRxiv : the preprint server for biology · 2025Article
- The Role ofDiabetes · 2021Review
- Admixture mapping and fine-mapping of type 2 diabetes susceptibility loci in African American women.Journal of human genetics · 2018Article
- The rs7903146 Variant in theDiabetes care · 2017Article
- Efficient Integrative Multi-SNP Association Analysis via Deterministic Approximation of Posteriors.American journal of human genetics · 2016Article
- Evidence of non-pancreatic beta cell-dependent roles of Tcf7l2 in the regulation of glucose metabolism in mice.Human molecular genetics · 2015Article
- Characterization of the transcriptional machinery bound across the widely presumed type 2 diabetes causal variant, rs7903146, within TCF7L2.European journal of human genetics : EJHG · 2015Article
- Redundant enhancers and causal variants in the TCF7L2 gene.European journal of human genetics : EJHG · 2014Article
- Cross-sectional and longitudinal replication analyses of genome-wide association loci of type 2 diabetes in Han Chinese.PloS one · 2014Article
- Enhancers: five essential questions.Nature reviews. Genetics · 2013Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
aims/hypothesisRecent functional characterisations of genome-wide association study (GWAS) loci suggest that cis-regulatory variation may be a common paradigm for complex disease susceptibility. Several studies point to a similar mechanism at the transcription factor 7-like 2 (TCF7L2) GWAS locus for type 2 diabetes. To address this possibility, we carried out an in vitro scan of this diabetes-associated locus to fine-map cis-regulatory sequences within this genomic interval.
methodsA systematic cell-based enhancer strategy was employed to interrogate all sequences within the 92 kb type-2-diabetes-association interval for cis-regulatory activity in a panel of cell lines (HCT-116, Neuro-2a, C2C12, U2OS, MIN6 and HepG2). We further evaluated chromatin state at a subset of these regions in HCT-116 and U2OS cells and examined allelic-specific enhancer properties at the type-2-diabetes-associated single nucleotide polymorphism (SNP) rs7903146.
resultsIn total, we assigned cis-regulatory activity to approximately 30% (9/28) of constructs tested. Notably, a subset of enhancers was active across multiple cell lines and overlapped with key epigenetic markers suggestive of cis-regulatory sequences. We further replicated the allelic-specific properties for SNP rs7903146 in pancreatic beta cells and additionally demonstrate identical allelic-specific enhancer effects in other cell lines.
conclusionsThese results provide a detailed map of cis-regulatory elements within the TCF7L2 GWAS locus and support the hypothesis of cis-regulatory variation leading to type 2 diabetes predisposition. The detection of allelic-specific effects for SNP rs7903146 in multiple cell lines further alludes to the likelihood of a peripheral defect in disease aetiology.
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