Direct Interaction of alpha-Synuclein and AKT Regulates IGF-1 Signaling: Implication of Parkinson Disease
DC Field | Value | Language |
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dc.contributor.author | Chung, Ji-Yun | - |
dc.contributor.author | Lee, Su-Jin | - |
dc.contributor.author | Lee, Sun-Hye | - |
dc.contributor.author | Jung, Youn Sang | - |
dc.contributor.author | Ha, Nam-Chul | - |
dc.contributor.author | Seol, Wongi | - |
dc.contributor.author | Park, Bum-Joon | - |
dc.date.accessioned | 2023-03-08T22:30:17Z | - |
dc.date.available | 2023-03-08T22:30:17Z | - |
dc.date.issued | 2011-06 | - |
dc.identifier.issn | 1424-862X | - |
dc.identifier.issn | 1424-8638 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/65019 | - |
dc.description.abstract | Genetic mutation of alpha-synuclein (alpha-SYN) is clearly verified as the causal factor of human and mouse Parkinson's disease. However, biological function of alpha-SYN has not been clearly demonstrated until now. In this investigation, we reveal that alpha-SYN is a co-regulator of growth factor-induced AKT activation. Elimination of SYN reduces the IGF-1-mediated AKT activation. Similarly, mutant SYN suppresses the IGF-1-induced AKT activation. Wild-type SYN can interact with AKT and enhance the solubility and plasma localization of AKT in response to IGF-1, whereas mutant alpha-SYNs do not interact with AKT. In addition, elevated expression of SYN blocks the AKT activation. We also find that si-RNA against alpha-SYN abolished the protective effect of IGF-1 against DNA damage-induced apoptosis. Our result strongly indicates that Parkinson's disease, induced by alpha-SYN mutation, is evoked by deregulation of the AKT-signaling cascade. Copyright (C) 2011 S. Karger AG, Basel | - |
dc.format.extent | 11 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | KARGER | - |
dc.title | Direct Interaction of alpha-Synuclein and AKT Regulates IGF-1 Signaling: Implication of Parkinson Disease | - |
dc.type | Article | - |
dc.identifier.doi | 10.1159/000325028 | - |
dc.identifier.bibliographicCitation | NEUROSIGNALS, v.19, no.2, pp 86 - 96 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000291160200003 | - |
dc.identifier.scopusid | 2-s2.0-79958115666 | - |
dc.citation.endPage | 96 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 86 | - |
dc.citation.title | NEUROSIGNALS | - |
dc.citation.volume | 19 | - |
dc.type.docType | Article | - |
dc.publisher.location | 스위스 | - |
dc.subject.keywordAuthor | alpha-Synuclein | - |
dc.subject.keywordAuthor | AKT | - |
dc.subject.keywordAuthor | Parkinson's disease | - |
dc.subject.keywordAuthor | IGF-1 signaling | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | SYNPHILIN-1 | - |
dc.subject.keywordPlus | MUTATIONS | - |
dc.subject.keywordPlus | PROTECTS | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Biophysics | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalResearchArea | Neurosciences & Neurology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biophysics | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Neurosciences | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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