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dc.contributor.authorChevrier, Nicolas
dc.contributor.authorMertins, Philipp
dc.contributor.authorArtyomov, Maxim N.
dc.contributor.authorShalek, Alex K.
dc.contributor.authorIannacone, Matteo
dc.contributor.authorCiaccio, Mark F.
dc.contributor.authorGat-Viks, Irit
dc.contributor.authorTonti, Elena
dc.contributor.authorDeGrace, Marciela M.
dc.contributor.authorClauser, Karl R.
dc.contributor.authorGarber, Manuel
dc.contributor.authorEisenhaure, Thomas
dc.contributor.authorYosef, Nir
dc.contributor.authorRobinson, Jacob
dc.contributor.authorSutton, Amy
dc.contributor.authorAndersen, Mette S.
dc.contributor.authorRoot, David E.
dc.contributor.authorvon Andrian, Ulrich
dc.contributor.authorJones, Richard Bradley
dc.contributor.authorPark, Hongkun
dc.contributor.authorCarr, Steven A.
dc.contributor.authorRegev, Aviv
dc.contributor.authorAmit, Ido
dc.contributor.authorHacohen, Nir
dc.date.accessioned2014-03-14T18:23:27Z
dc.date.available2014-03-14T18:23:27Z
dc.date.issued2011-11
dc.date.submitted2011-04
dc.identifier.issn00928674
dc.identifier.issn1097-4172
dc.identifier.urihttp://hdl.handle.net/1721.1/85646
dc.description.abstractDeciphering the signaling networks that underlie normal and disease processes remains a major challenge. Here, we report the discovery of signaling components involved in the Toll-like receptor (TLR) response of immune dendritic cells (DCs), including a previously unkown pathway shared across mammalian antiviral responses. By combining transcriptional profiling, genetic and small-molecule perturbations, and phosphoproteomics, we uncover 35 signaling regulators, including 16 known regulators, involved in TLR signaling. In particular, we find that Polo-like kinases (Plk) 2 and 4 are essential components of antiviral pathways in vitro and in vivo and activate a signaling branch involving a dozen proteins, among which is Tnfaip2, a gene associated with autoimmune diseases but whose role was unknown. Our study illustrates the power of combining systematic measurements and perturbations to elucidate complex signaling circuits and discover potential therapeutic targets.en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Grant P50 HG006193)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.). Pioneer Awarden_US
dc.description.sponsorshipBurroughs Wellcome Fund (Career Award at the Scientific Interface)en_US
dc.description.sponsorshipAlfred P. Sloan Foundationen_US
dc.description.sponsorshipHoward Hughes Medical Instituteen_US
dc.language.isoen_US
dc.publisherElsevieren_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.cell.2011.10.022en_US
dc.rightsArticle is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.en_US
dc.sourceElsevier Open Archiveen_US
dc.titleSystematic Discovery of TLR Signaling Components Delineates Viral-Sensing Circuitsen_US
dc.typeArticleen_US
dc.identifier.citationChevrier, Nicolas, Philipp Mertins, Maxim N. Artyomov, Alex K. Shalek, Matteo Iannacone, Mark F. Ciaccio, Irit Gat-Viks, et al. “Systematic Discovery of TLR Signaling Components Delineates Viral-Sensing Circuits.” Cell 147, no. 4 (November 2011): 853-867. Copyright © 2011 Elsevier Inc.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.mitauthorRegev, Aviven_US
dc.relation.journalCellen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsChevrier, Nicolas; Mertins, Philipp; Artyomov, Maxim N.; Shalek, Alex K.; Iannacone, Matteo; Ciaccio, Mark F.; Gat-Viks, Irit; Tonti, Elena; DeGrace, Marciela M.; Clauser, Karl R.; Garber, Manuel; Eisenhaure, Thomas M.; Yosef, Nir; Robinson, Jacob; Sutton, Amy; Andersen, Mette S.; Root, David E.; von Andrian, Ulrich; Jones, Richard B.; Park, Hongkun; Carr, Steven A.; Regev, Aviv; Amit, Ido; Hacohen, Niren_US
dc.identifier.orcidhttps://orcid.org/0000-0001-8567-2049
mit.licensePUBLISHER_POLICYen_US


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