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dc.contributor.advisorSvenning, Steingrim
dc.contributor.advisorLamark, Trond
dc.contributor.advisorJohansen, Terje
dc.contributor.authorNæss, Morten Svendsen
dc.date.accessioned2019-11-04T09:08:37Z
dc.date.available2019-11-04T09:08:37Z
dc.date.issued2017-11-02
dc.description.abstractAutophagy is a conserved catabolic pathway for the lysosomal degradation of cytoplasmic components. Autophagy can be both selective and unselective. Selective autophagy receptor proteins are involved in mediating the degradation of specific substrates. Among these receptors we find the evolutionary related proteins p62 and NBR1, which are both involved in autophagic degradation of different ubiquitinated substrates. The p62 protein is known to shuttle between the nucleus and cytoplasm dependent on nuclear localization (NLS) and nuclear export sequences (NES). Here, we find that NBR1 harbors two active NES motifs. We also find that the subcellular distribution of NBR1 is dependent on its aggregation status and we map the location of the different domains responsible for aggregation of NBR1.en_US
dc.identifier.urihttps://hdl.handle.net/10037/16585
dc.language.isoengen_US
dc.publisherUiT Norges arktiske universiteten_US
dc.publisherUiT The Arctic University of Norwayen_US
dc.rights.accessRightsopenAccessen_US
dc.rights.holderCopyright 2017 The Author(s)
dc.rights.urihttps://creativecommons.org/licenses/by-nc-sa/3.0en_US
dc.rightsAttribution-NonCommercial-ShareAlike 3.0 Unported (CC BY-NC-SA 3.0)en_US
dc.subject.courseIDMED-3910
dc.subjectVDP::Medisinske Fag: 700::Basale medisinske, odontologiske og veterinærmedisinske fag: 710::Medisinsk molekylærbiologi: 711en_US
dc.subjectVDP::Medical disciplines: 700::Basic medical, dental and veterinary science disciplines: 710::Medical molecular biology: 711en_US
dc.titleMapping of Nuclear Export Signals and domains mediating aggregation of NBR1en_US
dc.typeMaster thesisen_US
dc.typeMastergradsoppgaveen_US


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Attribution-NonCommercial-ShareAlike 3.0 Unported (CC BY-NC-SA 3.0)
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-ShareAlike 3.0 Unported (CC BY-NC-SA 3.0)