Capture Hi-C identifies the chromatin interactome of colorectal cancer risk loci.
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Multiple regulatory elements distant from their targets on the linear genome can influence the expression of a single gene through chromatin looping. Chromosome conformation capture implemented in Hi-C allows for genome-wide agnostic characterization of chromatin contacts. However, detection of functional enhancer-promoter interactions is precluded by its effective resolution that is determined by both restriction fragmentation and sensitivity of the experiment. Here we develop a capture Hi-C (cHi-C) approach to allow an agnostic characterization of these physical interactions on a genome-wide scale. Single-nucleotide polymorphisms associated with complex diseases often reside within regulatory elements and exert effects through long-range regulation of gene expression. Applying this cHi-C approach to 14 colorectal cancer risk loci allows us to identify key long-range chromatin interactions in cis and trans involving these loci.
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Cell Line, Tumor
Chromosomes, Human, Pair 8
Genetic Predisposition to Disease
In Situ Hybridization, Fluorescence
Statistics as Topic
Molecular Sequence Annotation
Functional Genetic Epidemiology
Computational Pathology & Integrated Genomics
Molecular & Population Genetics
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Nature Communications, 2015, 6 pp. 6178 - ?