Insulin promotes Rip11 accumulation at the plasma membrane by inhibiting a dynamin- and PI3-kinase-dependent, but Akt-independent, internalisation event

dc.contributor.authorBoal, Frédéric
dc.contributor.authorHodgson, Lorna R.
dc.contributor.authorReed, Sam E.
dc.contributor.authorYarwood, Sophie E.
dc.contributor.authorJust, Victoria J.
dc.contributor.authorStephens, David J.
dc.contributor.authorMcCaffrey, Mary W.
dc.contributor.authorTavaré, Jeremy M.
dc.contributor.funderBiotechnology and Biological Sciences Research Councilen
dc.contributor.funderOpen Society Instituteen
dc.contributor.funderMedical Research Councilen
dc.contributor.funderWellcome Trusten
dc.contributor.funderDiabetes UKen
dc.contributor.funderScience Foundation Irelanden
dc.date.accessioned2019-10-26T07:22:06Z
dc.date.available2019-10-26T07:22:06Z
dc.date.issued2015-10-26
dc.description.abstractRip11 is a Rab11 effector protein that has been shown to be important in controlling the trafficking of several intracellular cargoes, including the fatty acid transporter FAT/CD36, V-ATPase and the glucose transporter GLUT4. We have previously demonstrated that Rip11 translocates to the plasma membrane in response to insulin and here we examine the basis of this regulated phenomenon in more detail. We show that Rip11 rapidly recycles between the cell interior and surface, and that the ability of insulin to increase the appearance of Rip11 at the cell surface involves an inhibition of Rip11 internalisation from the plasma membrane. By contrast the hormone has no effect on the rate of Rip11 translocation towards the plasma membrane. The ability of insulin to inhibit Rip11 internalisation requires dynamin and class I PI3-kinases, but is independent of the activation of the protein kinase Akt; characteristics which are very similar to the mechanism by which insulin inhibits GLUT4 endocytosis.en
dc.description.sponsorshipMedical Research Council (G0900177); Diabetes UK (08/0003712)en
dc.description.statusPeer revieweden
dc.description.versionPublished Versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.citationBoal, F., Hodgson, L. R., Reed, S. E., Yarwood, S. E., Just, V. J., Stephens, D. J., McCaffrey, M. W. and Tavaré, J. M. (2016), 'Insulin promotes Rip11 accumulation at the plasma membrane by inhibiting a dynamin- and PI3-kinase-dependent, but Akt-independent, internalisation event', Cellular Signalling, 28(1), pp. 74-82. DOI: 10.1016/j.cellsig.2015.10.014en
dc.identifier.doi10.1016/j.cellsig.2015.10.014en
dc.identifier.eissn1873-3913
dc.identifier.endpage82en
dc.identifier.issn0898-6568
dc.identifier.issued1en
dc.identifier.journaltitleCellular Signallingen
dc.identifier.startpage74en
dc.identifier.urihttps://hdl.handle.net/10468/8883
dc.identifier.volume28en
dc.language.isoenen
dc.publisherElsevieren
dc.relation.projectinfo:eu-repo/grantAgreement/SFI/SFI Principal Investigator Programme (PI)/09/IN.1/B2629/IE/Functional analysis of the Rab11 and Rab14 GTPases and their associated proteins in eukaryotic membrane trafficking with potential identification of targets for therapeutic intervention in the treatment of human disease/en
dc.relation.urihttps://www.sciencedirect.com/science/article/pii/S0898656815003071?via%3Dihub
dc.rights©2015 Published by Elsevier Inc. This is an open access article under the CC BY license. (http://creativecommons.org/licenses/by/4.0/)en
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectInsulinen
dc.subjectRip11en
dc.subjectRaben
dc.subjectRecyclingen
dc.subjectEndocytosisen
dc.titleInsulin promotes Rip11 accumulation at the plasma membrane by inhibiting a dynamin- and PI3-kinase-dependent, but Akt-independent, internalisation eventen
dc.typeArticle (peer-reviewed)en
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