Hide metadata

dc.date.accessioned2018-01-15T13:26:36Z
dc.date.available2018-01-15T13:26:36Z
dc.date.created2017-12-19T11:48:10Z
dc.date.issued2017
dc.identifier.citationKjos, Ingrid Distefano, Marita Borg Sætre, Frank Ove Repnik, Urska Holland, Petter Jones, Arwyn T Engedal, Nikolai Simonsen, Anne Bakke, Oddmund Progida, Cinzia . Rab7b modulates autophagic flux by interacting with Atg4B. EMBO Reports. 2017
dc.identifier.urihttp://hdl.handle.net/10852/59609
dc.description.abstractAutophagy (macroautophagy) is a highly conserved eukaryotic degradation pathway in which cytosolic components and organelles are sequestered by specialized autophagic membranes and degraded through the lysosomal system. The autophagic pathway maintains basal cellular homeostasis and helps cells adapt during stress; thus, defects in autophagy can cause detrimental effects. It is therefore crucial that autophagy is properly regulated. In this study, we show that the cysteine protease Atg4B, a key enzyme in autophagy that cleaves LC3, is an interactor of the small GTPase Rab7b. Indeed, Atg4B interacts and co‐localizes with Rab7b on vesicles. Depletion of Rab7b increases autophagic flux as indicated by the increased size of autophagic structures as well as the magnitude of macroautophagic sequestration and degradation. Importantly, we demonstrate that Rab7b regulates LC3 processing by modulating Atg4B activity. Taken together, our findings reveal Rab7b as a novel negative regulator of autophagy through its interaction with Atg4B.en_US
dc.languageEN
dc.language.isoenen_US
dc.publisherNature Publishing Group
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/
dc.titleRab7b modulates autophagic flux by interacting with Atg4Ben_US
dc.typeJournal articleen_US
dc.creator.authorKjos, Ingrid
dc.creator.authorDistefano, Marita Borg
dc.creator.authorSætre, Frank Ove
dc.creator.authorRepnik, Urska
dc.creator.authorHolland, Petter
dc.creator.authorJones, Arwyn T
dc.creator.authorEngedal, Nikolai
dc.creator.authorSimonsen, Anne
dc.creator.authorBakke, Oddmund
dc.creator.authorProgida, Cinzia
cristin.unitcode185,15,0,0
cristin.unitnameDet matematisk-naturvitenskapelige fakultet
cristin.ispublishedtrue
cristin.fulltextpostprint
cristin.qualitycode2
dc.identifier.cristin1529568
dc.identifier.bibliographiccitationinfo:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=EMBO Reports&rft.volume=&rft.spage=&rft.date=2017
dc.identifier.jtitleEMBO Reports
dc.identifier.volume18
dc.identifier.startpage1727
dc.identifier.endpage1739
dc.identifier.doihttp://dx.doi.org/10.15252/embr.201744069
dc.identifier.urnURN:NBN:no-62281
dc.type.documentTidsskriftartikkelen_US
dc.type.peerreviewedPeer reviewed
dc.source.issn1469-221X
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/59609/5/1727.full.pdf
dc.type.versionPublishedVersion
dc.relation.projectNFR/239903; 230779;179573
dc.relation.projectKF/5760850; 4604944


Files in this item

Appears in the following Collection

Hide metadata

Attribution-NonCommercial-NoDerivatives 4.0 International
This item's license is: Attribution-NonCommercial-NoDerivatives 4.0 International