Abstract
A recent study used CRISPR/Cas9 to reveal long-range looping between disease-related genes and their regulatory elements that is mediated by the CCCTC-binding factor (CTCF) in prostate cancer.
Highlights
Extensive studies are currently devoted to understanding the three-dimensional (3D) architecture of genomes, including the formation and function of chromatin loops, topologically associated domains (TADs) and transcriptional activity-based A and B compartments
The major architectural protein CCCT C-binding factor (CTCF) is an 11 zinc-finger DNAbinding protein that associates with the cohesin complex and orchestrates long range interactions between remote enhancers and their target gene promoters to modulate gene transcription
Whether this regulation is direct or indirect and involving an insulator function is an open question. In this issue of Genome Biology, Guo et al [2] describe how prostate cancer (PCa) risk loci that they identified in genome-wide association studies (GWAS) participate in CTCF-mediated chromatin loops and function to repress the expression of the encircled genes
Summary
Extensive studies are currently devoted to understanding the three-dimensional (3D) architecture of genomes, including the formation and function of chromatin loops, topologically associated domains (TADs) and transcriptional activity-based A and B compartments. In this issue of Genome Biology, Guo et al [2] describe how prostate cancer (PCa) risk loci that they identified in GWAS participate in CTCF-mediated chromatin loops and function to repress the expression of the encircled genes.
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