Cell-Permeable Parkin Proteins Suppress Parkinson Disease-Associated Phenotypes in Cultured Cells and Animals
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Duong, Tam | - |
dc.contributor.author | Kim, Jaetaek | - |
dc.contributor.author | Ruley, H. Earl | - |
dc.contributor.author | Jo, Daewoong | - |
dc.date.available | 2019-03-08T21:40:02Z | - |
dc.date.issued | 2014-07 | - |
dc.identifier.issn | 1932-6203 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/12046 | - |
dc.description.abstract | Parkinson's disease (PD) is a neurodegenerative disorder of complex etiology characterized by the selective loss of dopaminergic neurons, particularly in the substantia nigra. Parkin, a tightly regulated E3 ubiquitin ligase, promotes the survival of dopaminergic neurons in both PD and Parkinsonian syndromes induced by acute exposures to neurotoxic agents. The present study assessed the potential of cell-permeable parkin (CP-Parkin) as a neuroprotective agent. Cellular uptake and tissue penetration of recombinant, enzymatically active parkin was markedly enhanced by the addition of a hydrophobic macromolecule transduction domain (MTD). The resulting CP-Parkin proteins (HPM13 and PM10) suppressed dopaminergic neuronal toxicity in cells and mice exposed to 6-hydroxydopamine (6-OHDH) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). These included enhanced survival and dopamine expression in cultured CATH. a and SH-SY5Y neuronal cells; and protection against MPTP-induced damage in mice, notably preservation of tyrosine hydroxylase-positive cells with enhanced dopamine expression in the striatum and midbrain, and preservation of gross motor function. These results demonstrate that CP-Parkin proteins can compensate for intrinsic limitations in the parkin response and provide a therapeutic strategy to augment parkin activity in vivo. | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | PUBLIC LIBRARY SCIENCE | - |
dc.title | Cell-Permeable Parkin Proteins Suppress Parkinson Disease-Associated Phenotypes in Cultured Cells and Animals | - |
dc.type | Article | - |
dc.identifier.doi | 10.1371/journal.pone.0102517 | - |
dc.identifier.bibliographicCitation | PLOS ONE, v.9, no.7 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000339618600089 | - |
dc.identifier.scopusid | 2-s2.0-84904261988 | - |
dc.citation.number | 7 | - |
dc.citation.title | PLOS ONE | - |
dc.citation.volume | 9 | - |
dc.type.docType | Article | - |
dc.publisher.location | 미국 | - |
dc.subject.keywordPlus | PROTECTS DOPAMINERGIC-NEURONS | - |
dc.subject.keywordPlus | UBIQUITIN LIGASE ACTIVITY | - |
dc.subject.keywordPlus | NUCLEAR IMPORT INHIBITOR | - |
dc.subject.keywordPlus | MOUSE MODEL | - |
dc.subject.keywordPlus | ANTITUMOR-ACTIVITY | - |
dc.subject.keywordPlus | MOLECULAR-MECHANISMS | - |
dc.subject.keywordPlus | INDUCED TOXICITY | - |
dc.subject.keywordPlus | ALPHA-SYNUCLEIN | - |
dc.subject.keywordPlus | L-DOPA | - |
dc.subject.keywordPlus | DELIVERY | - |
dc.relation.journalResearchArea | Science & Technology - Other Topics | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
84, Heukseok-ro, Dongjak-gu, Seoul, Republic of Korea (06974)02-820-6194
COPYRIGHT 2019 Chung-Ang University All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.