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Jason Wright

Researcher at Broad Institute

Publications -  21
Citations -  10480

Jason Wright is an academic researcher from Broad Institute. The author has contributed to research in topics: Gene & CRISPR. The author has an hindex of 14, co-authored 21 publications receiving 8441 citations. Previous affiliations of Jason Wright include Massachusetts Institute of Technology & Dartmouth College.

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Genome engineering using the CRISPR-Cas9 system

TL;DR: A set of tools for Cas9-mediated genome editing via nonhomologous end joining (NHEJ) or homology-directed repair (HDR) in mammalian cells, as well as generation of modified cell lines for downstream functional studies are described.
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Breast cancer risk–associated SNPs modulate the affinity of chromatin for FOXA1 and alter gene expression

TL;DR: The results show that breast cancer risk–associated SNPs are enriched in the cistromes of FOXA1 and ESR1 and the epigenome of histone H3 lysine 4 monomethylation in a cancer- and cell type–specific manner.
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Genome-scale activation screen identifies a lncRNA locus regulating a gene neighbourhood

TL;DR: A genome-scale CRISPR-Cas9 activation screen that targets more than 10,000 lncRNA transcriptional start sites to identify noncoding loci that influence a phenotype of interest found 11 lncRNAs that, upon recruitment of an activator, mediate resistance to BRAF inhibitors in human melanoma cells.
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Upregulation of c-MYC in cis through a Large Chromatin Loop Linked to a Cancer Risk-Associated Single-Nucleotide Polymorphism in Colorectal Cancer Cells

TL;DR: The findings of these studies support a mechanism for intergenic SNPs that can promote cancer through the regulation of distal genes by utilizing preexisting large chromatin loops.
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High-resolution interrogation of functional elements in the noncoding genome

TL;DR: A CRISPR screen using ~18,000 single guide RNAs targeting >700 kilobases surrounding the genes NF1, NF2, and CUL3, which are involved in BRAF inhibitor resistance in melanoma, finds that noncoding locations that modulate drug resistance also harbor predictive hallmarks ofnoncoding function.