dc.contributor.author | Reczek, Colleen R | |
dc.contributor.author | Birsoy, Kıvanç | |
dc.contributor.author | Kong, Hyewon | |
dc.contributor.author | Martínez-Reyes, Inmaculada | |
dc.contributor.author | Gao, Peng | |
dc.contributor.author | Chandel, Navdeep S | |
dc.contributor.author | Wang, Tim | |
dc.contributor.author | Sabatini, David | |
dc.date.accessioned | 2018-07-03T19:03:49Z | |
dc.date.available | 2018-07-03T19:03:49Z | |
dc.date.issued | 2017-10 | |
dc.date.submitted | 2016-12 | |
dc.identifier.issn | 1552-4450 | |
dc.identifier.issn | 1552-4469 | |
dc.identifier.uri | http://hdl.handle.net/1721.1/116772 | |
dc.description.abstract | Paraquat, a herbicide linked to Parkinson's disease, generates reactive oxygen species (ROS), which causes cell death. Because the source of paraquat-induced ROS production remains unknown, we conducted a CRISPR-based positive-selection screen to identify metabolic genes essential for paraquat-induced cell death. Our screen uncovered three genes, POR (cytochrome P450 oxidoreductase), ATP7A (copper transporter), and SLC45A4 (sucrose transporter), required for paraquat-induced cell death. Furthermore, our results revealed POR as the source of paraquat-induced ROS production. Thus, our study highlights the use of functional genomic screens for uncovering redox biology. | en_US |
dc.publisher | Nature Publishing Group | en_US |
dc.relation.isversionof | http://dx.doi.org/10.1038/NCHEMBIO.2499 | en_US |
dc.rights | Creative Commons Attribution-Noncommercial-Share Alike | en_US |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/4.0/ | en_US |
dc.source | PMC | en_US |
dc.title | A CRISPR screen identifies a pathway required for paraquat-induced cell death | en_US |
dc.type | Article | en_US |
dc.identifier.citation | Reczek, Colleen R, Kıvanç Birsoy, Hyewon Kong, Inmaculada Martínez-Reyes, Tim Wang, Peng Gao, David M Sabatini, and Navdeep S Chandel. “A CRISPR Screen Identifies a Pathway Required for Paraquat-Induced Cell Death.” Nature Chemical Biology 13, 12 (October 2017): 1274–1279 © 2017 Nature America, Inc., part of Springer Nature | en_US |
dc.contributor.department | Koch Institute for Integrative Cancer Research at MIT | en_US |
dc.contributor.mitauthor | Wang, Tim | |
dc.contributor.mitauthor | Sabatini, David | |
dc.relation.journal | Nature Chemical Biology | en_US |
dc.eprint.version | Author's final manuscript | en_US |
dc.type.uri | http://purl.org/eprint/type/JournalArticle | en_US |
eprint.status | http://purl.org/eprint/status/PeerReviewed | en_US |
dc.date.updated | 2018-07-03T18:11:02Z | |
dspace.orderedauthors | Reczek, Colleen R; Birsoy, Kıvanç; Kong, Hyewon; Martínez-Reyes, Inmaculada; Wang, Tim; Gao, Peng; Sabatini, David M; Chandel, Navdeep S | en_US |
dspace.embargo.terms | N | en_US |
dc.identifier.orcid | https://orcid.org/0000-0002-4227-5163 | |
dc.identifier.orcid | https://orcid.org/0000-0002-1446-7256 | |
mit.license | OPEN_ACCESS_POLICY | en_US |