Please use this identifier to cite or link to this item: https://doi.org/10.1002/jcp.24341
DC FieldValue
dc.titleLinking membrane dynamics and trafficking to autophagy and the unfolded protein response
dc.contributor.authorChua, C.E.L.
dc.contributor.authorTang, B.L.
dc.date.accessioned2014-11-25T09:46:20Z
dc.date.available2014-11-25T09:46:20Z
dc.date.issued2013-08
dc.identifier.citationChua, C.E.L., Tang, B.L. (2013-08). Linking membrane dynamics and trafficking to autophagy and the unfolded protein response. Journal of Cellular Physiology 228 (8) : 1638-1640. ScholarBank@NUS Repository. https://doi.org/10.1002/jcp.24341
dc.identifier.issn00219541
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/108450
dc.description.abstractCellular stressors typically induce two protective counter-responses-autophagy and the unfolded protein response (UPR). It is conceivable that these two endoplasmic reticulum (ER) membrane-based processes would intersect/interact somehow with the constitutive housekeeping process of exocytic membrane traffic from the ER. How exactly might this occur? Recent evidence indicates that a conserved Rab protein, Rab1/Ypt1p, has functional roles in UPR and autophagy. This molecular switch and its associated effectors may therefore serve to link up a network of cellular responses to stress through changes in membrane dynamics and protein turnover. The notion provides further explanations as to why elevation of Rab1/Ypt1p levels could counter the cytotoxicity of α-synuclein, and a similar mode of protection may well be at work against other stresses. © 2013 Wiley Periodicals, Inc.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1002/jcp.24341
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentBIOCHEMISTRY
dc.description.doi10.1002/jcp.24341
dc.description.sourcetitleJournal of Cellular Physiology
dc.description.volume228
dc.description.issue8
dc.description.page1638-1640
dc.description.codenJCLLA
dc.identifier.isiut000318165300002
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