Authors
Dimitre R Simeonov, Benjamin G Gowen, Mandy Boontanrart, Theodore L Roth, John D Gagnon, Maxwell R Mumbach, Ansuman T Satpathy, Youjin Lee, Nicolas L Bray, Alice Y Chan, Dmytro S Lituiev, Michelle L Nguyen, Rachel E Gate, Meena Subramaniam, Zhongmei Li, Jonathan M Woo, Therese Mitros, Graham J Ray, Gemma L Curie, Nicki Naddaf, Julia S Chu, Hong Ma, Eric Boyer, Frederic Van Gool, Hailiang Huang, Ruize Liu, Victoria R Tobin, Kathrin Schumann, Mark J Daly, Kyle K Farh, K Mark Ansel, Chun J Ye, William J Greenleaf, Mark S Anderson, Jeffrey A Bluestone, Howard Y Chang, Jacob E Corn, Alexander Marson
Publication date
2017/9/7
Journal
Nature
Volume
549
Issue
7670
Pages
111-115
Publisher
Nature Publishing Group UK
Description
The majority of genetic variants associated with common human diseases map to enhancers, non-coding elements that shape cell-type-specific transcriptional programs and responses to extracellular cues,,. Systematic mapping of functional enhancers and their biological contexts is required to understand the mechanisms by which variation in non-coding genetic sequences contributes to disease. Functional enhancers can be mapped by genomic sequence disruption,,, but this approach is limited to the subset of enhancers that are necessary in the particular cellular context being studied. We hypothesized that recruitment of a strong transcriptional activator to an enhancer would be sufficient to drive target gene expression, even if that enhancer was not currently active in the assayed cells. Here we describe a discovery platform that can identify stimulus-responsive enhancers for a target gene independent of …
Scholar articles
DR Simeonov, BG Gowen, M Boontanrart, TL Roth… - Nature, 2017