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Article: KDEL receptors assist dengue virus exit from the endoplasmic reticulum

TitleKDEL receptors assist dengue virus exit from the endoplasmic reticulum
Authors
Issue Date2015
PublisherElsevier (Cell Press): OAJ. The Journal's web site is located at http://cell.com/cell-reports
Citation
Cell Reports, 2015, v. 10 n. 9, p. 1496-1507 How to Cite?
AbstractMembrane receptors at the surface of target cells are key host factors for virion entry; however, it is unknown whether trafficking and secretion of progeny virus requires host intracellular receptors. In this study, we demonstrate that dengue virus (DENV) interacts with KDEL receptors (KDELR), which cycle between the ER and Golgi apparatus, for vesicular transport from ER to Golgi. Depletion of KDELR by siRNA reduced egress of both DENV progeny and recombinant subviral particles (RSPs). Coimmunoprecipitation of KDELR with dengue structural protein prM required three positively charged residues at the N terminus, whose mutation disrupted protein interaction and inhibited RSP transport from the ER to the Golgi. Finally, siRNA depletion of class II Arfs, which results in KDELR accumulation in the Golgi, phenocopied results obtained with mutagenized prME and KDELR knockdown. Our results have uncovered a function for KDELR as an internal receptor involved in DENV trafficking.
Persistent Identifierhttp://hdl.handle.net/10722/209403

 

DC FieldValueLanguage
dc.contributor.authorLi, Men_US
dc.contributor.authorGrandadam, Men_US
dc.contributor.authorKwok, KTHen_US
dc.contributor.authorLagache, Ten_US
dc.contributor.authorSiu, YLen_US
dc.contributor.authorZhang, Jen_US
dc.contributor.authorSayteng, Ken_US
dc.contributor.authorKudelko, MAen_US
dc.contributor.authorQin, CFen_US
dc.contributor.authorOlivo-Marin, JCen_US
dc.contributor.authorBruzzone, Ren_US
dc.contributor.authorWang, Pen_US
dc.date.accessioned2015-04-17T05:15:44Z-
dc.date.available2015-04-17T05:15:44Z-
dc.date.issued2015en_US
dc.identifier.citationCell Reports, 2015, v. 10 n. 9, p. 1496-1507en_US
dc.identifier.urihttp://hdl.handle.net/10722/209403-
dc.description.abstractMembrane receptors at the surface of target cells are key host factors for virion entry; however, it is unknown whether trafficking and secretion of progeny virus requires host intracellular receptors. In this study, we demonstrate that dengue virus (DENV) interacts with KDEL receptors (KDELR), which cycle between the ER and Golgi apparatus, for vesicular transport from ER to Golgi. Depletion of KDELR by siRNA reduced egress of both DENV progeny and recombinant subviral particles (RSPs). Coimmunoprecipitation of KDELR with dengue structural protein prM required three positively charged residues at the N terminus, whose mutation disrupted protein interaction and inhibited RSP transport from the ER to the Golgi. Finally, siRNA depletion of class II Arfs, which results in KDELR accumulation in the Golgi, phenocopied results obtained with mutagenized prME and KDELR knockdown. Our results have uncovered a function for KDELR as an internal receptor involved in DENV trafficking.en_US
dc.languageengen_US
dc.publisherElsevier (Cell Press): OAJ. The Journal's web site is located at http://cell.com/cell-reports-
dc.relation.ispartofCell Reportsen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleKDEL receptors assist dengue virus exit from the endoplasmic reticulumen_US
dc.typeArticleen_US
dc.identifier.emailLi, M: myli2014@hku.hken_US
dc.identifier.emailKwok, KTH: kwokth@hku.hken_US
dc.identifier.emailSiu, YL: ylsiu@hkucc.hku.hken_US
dc.identifier.emailZhang, J: tamizjs@hku.hken_US
dc.identifier.emailKudelko, MA: kudelko@hku.hken_US
dc.identifier.emailBruzzone, R: bruzzone@hkucc.hku.hken_US
dc.identifier.emailWang, P: pgwang@hkucc.hku.hken_US
dc.identifier.authorityBruzzone, R=rp01442en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1016/j.celrep.2015.02.021en_US
dc.identifier.hkuros242754en_US
dc.identifier.volume10en_US
dc.identifier.issue9en_US
dc.identifier.spage1496en_US
dc.identifier.epage1507en_US

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