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dc.contributor.author Mandl, József
dc.contributor.author Mészáros, Tamás
dc.contributor.author Bánhegyi, Gábor
dc.contributor.author Csala, Miklós
dc.date.accessioned 2017-06-13T08:41:22Z
dc.date.available 2017-06-13T08:41:22Z
dc.date.issued 2013
dc.identifier 84874547702
dc.identifier.citation pagination=384-393; journalVolume=27; journalIssueNumber=3; journalTitle=MOLECULAR ENDOCRINOLOGY;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/2555
dc.identifier.uri doi:10.1210/me.2012-1317
dc.description.abstract Endoplasmic reticulum (ER) stress is a regulatory mechanism that allows cells to adapt to a series of metabolic, redox, and other environmental changes. The role of ER stress was first identified in the maintenance of proteostasis. It has since been shown that ER stress is also critical to the regulation of lipid homeostasis, membrane turnover, and autophagy. ER stress initiates an intrinsic signaling network, the unfolded protein response, one component of the multifold and complex cellular signaling process system, which leads to major changes in the profiles of transcription factors. The unfolded protein response affects several other signaling routes through direct connections and also by indirect means. It directly influences hormone formation and life/death decisions at a cellular level; this relationship also involves connections to nutrient and environmental sensing-biotransformation processes. In conclusion, ER stress represents an integrated complex organelle response that makes an essential contribution to the maintenance of intracellular homeostasis. © 2013 by The Endocrine Society.
dc.relation.ispartof urn:issn:0888-8809
dc.title Minireview: Endoplasmic reticulum stress: Control in protein, lipid, and signal homeostasis
dc.type Journal Article
dc.date.updated 2015-11-23T14:16:34Z
dc.language.rfc3066 en
dc.identifier.mtmt 2226968
dc.identifier.wos 000315455300002
dc.identifier.pubmed 23349523
dc.contributor.department SE/AOK/I/Orvosi Vegytani, Molekuláris Biológiai és Patobiokémiai Intézet
dc.contributor.institution Semmelweis Egyetem


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