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dc.contributor.authorTakalo Mari
dc.contributor.authorNatunen Teemu
dc.contributor.authorLeskelä Stina
dc.contributor.authorPaldanius Kaisa MA
dc.contributor.authorSoininen Hilkka
dc.contributor.authorHiltunen MIkko
dc.contributor.authorHaapasalo Annakaisa
dc.date.accessioned2020-01-13T09:31:20Z
dc.date.available2020-01-13T09:31:20Z
dc.date.issued2017
dc.identifier.urihttps://erepo.uef.fi/handle/123456789/7920
dc.description.abstractAmple evidence links ubiquilins to the pathogenesis of various neurodegenerative disorders. Ubiquilin-1 (also called PLIC-1) is associated to the pathogenesis of Alzheimer’s disease (AD) both genetically and functionally as indicated by investigations in different in vitro and in vivo models and human brain. Previous studies by us and others have identified ubiquilin-1 as a central regulator of the metabolism, subcellular localization, trafficking, as well as accumulation and degradation of various neurodegenerative disease-linked proteins, including the AD-associated β-amyloid precursor protein (APP) and presenilins. Our recent report reveals a previously uncharacterized relationship between ubiquilin-1 and AD-associated β-site cleaving enzyme 1 (BACE1), the rate-limiting enzyme in the generation of the β-amyloid (Aβ) peptides, in cell-based model systems in vitro as well as in the brains of AD model mice in vivo and human patients. Our data suggest that ubiquilin-1 controls BACE1 levels and localization to the late endosomal compartment, the preferred cellular site for Aβ generation. Therefore, the observed decreased levels of ubiquilin-1 in AD brain may result in altered APP processing and Aβ accumulation. Here, we provide a short review on the links between ubiquilin-1 and mechanisms of AD and some other neurodegenerative diseases and then summarize the data in our recent report regarding the newly observed interrelationship between ubiquilin-1 and BACE1.
dc.relation.ispartofseriesJournal of Alzheimers Disease & Parkinsonism
dc.relation.urihttp://dx.doi.org/10.4172/2161-0460.1000365
dc.rightsCC BY http://creativecommons.org/licenses/by/4.0/
dc.subjectAlzheimer’s disease
dc.subjectubiquilin-1
dc.subjectBACE1
dc.subjectbeta-amyloid
dc.subjectubiquitin-proteasome system
dc.subjectautophagosome-lysosome pathway
dc.subjectneurodegeneration
dc.titleNew Implications for the Role for Ubiquilin-1 in Molecular Mechanisms of Alzheimer's Disease: Interrelationship with BACE1
dc.description.versionpublished version
dc.contributor.departmentA.I. Virtanen -instituutti
dc.contributor.departmentSchool of Medicine / Clinical Medicine,School of Medicine / Biomedicine
uef.solecris.id51862334en
dc.type.publicationTieteelliset aikakauslehtiartikkelit
dc.rights.accessrights© Authors
dc.relation.doi10.4172/2161-0460.1000365
dc.description.reviewstatuspeerReviewed
dc.relation.articlenumber1000365
dc.relation.issn2161-0460
dc.relation.issue5
dc.relation.volume7
dc.rights.accesslevelopenAccess
dc.type.okmA2
uef.solecris.openaccessEi


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