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dc.contributor.authorKim, Dennis H
dc.date.accessioned2018-07-27T20:09:43Z
dc.date.available2018-07-27T20:09:43Z
dc.date.issued2016-08
dc.identifier.issn1097-2765
dc.identifier.issn1097-4164
dc.identifier.urihttp://hdl.handle.net/1721.1/117179
dc.description.abstractMaintenance of cellular homeostasis is a fundamental aspect of stress-responsive signal transduction pathways. Specific signaling pathways are often considered, and certainly most often studied, in the context of responses to a specific endogenous or environmental stressor, but there are also fundamental questions that remain regarding how information about stress pathways with potentially overlapping inputs and/or outputs is optimally integrated and transduced by the cellular circuitry. In the current issue of Molecular Cell, Hourihan et al. (2016), combining molecular genetic and biochemical analysis in Caenorhabditis elegans and in mammalian cell systems, identify a mechanism by which IRE1, a principal regulator of the endoplasmic reticulum (ER) Unfolded Protein Response (UPR) (Walter and Ron, 2011), also regulates a response to reactive oxygen species (ROS). Signaling through IRE1 to promote ER homeostasis and the response to oxidative stress appears to be mutually exclusive—that is, signaling one response turns off the other, and vice versa.en_US
dc.language.isoen_US
dc.publisherElsevieren_US
dc.relation.isversionofhttps://doi.org/10.1016/j.molcel.2016.08.003en_US
dc.rightsCreative Commons Attribution-NonCommercial-NoDerivs Licenseen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en_US
dc.sourceProf. Kim via Courtney Crummetten_US
dc.titleIRE1 sulfenylation by reactive oxygen species coordinates cellular stress signalingen_US
dc.typeArticleen_US
dc.identifier.citationKim, Dennis H. “IRE1 Sulfenylation by Reactive Oxygen Species Coordinates Cellular Stress Signaling.” Molecular Cell, vol. 63, no. 4, Aug. 2016, pp. 541–42.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.approverKim, Dennisen_US
dc.contributor.mitauthorKim, Dennis H
dc.relation.journalMolecular Cellen_US
dc.eprint.versionAuthor's final manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsKim, Dennis H.en_US
dspace.embargo.termsNen_US
dc.identifier.orcidhttps://orcid.org/0000-0002-4109-5152
mit.licensePUBLISHER_CCen_US


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