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Cited 60 time in webofscience Cited 64 time in scopus
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dc.contributor.authorSong S.-
dc.contributor.authorJang S.-
dc.contributor.authorPark J.-
dc.contributor.authorBang S.-
dc.contributor.authorChoi S.-
dc.contributor.authorKwon K.-Y.-
dc.contributor.authorZhuang X.-
dc.contributor.authorKim E.-
dc.contributor.authorChung J.-
dc.date.accessioned2021-11-15T02:51:57Z-
dc.date.available2021-11-15T02:51:57Z-
dc.date.created2021-11-15-
dc.date.issued2013-02-22-
dc.identifier.issn0021-9258-
dc.identifier.urihttps://oasis.postech.ac.kr/handle/2014.oak/107479-
dc.description.abstractBackground: Mutations in PINK1 cause recessive Parkinson disease. Results: PINK1 mutations in the kinase domain hamper Parkin translocation to mitochondria, and their analogous mutations in Drosophila cannot rescue PINK1-null phenotypes. Conclusion: PINK1 kinase activity is essential for its function and for regulating Parkin functions in mitochondria. Significance: Understanding the roles of PINK1 mutations will be helpful for deciphering the pathogenic mechanism of PINK1-linked Parkinson disease. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.-
dc.languageEnglish-
dc.publisherAmerican Society for Biochemistry and Molecular Biology Inc.-
dc.relation.isPartOfJournal of Biological Chemistry-
dc.titleCharacterization of PINK1 (PTEN-induced putative kinase 1) mutations associated with parkinson disease in mammalian cells and drosophila-
dc.typeArticle-
dc.identifier.doi10.1074/jbc.M112.430801-
dc.type.rimsART-
dc.identifier.bibliographicCitationJournal of Biological Chemistry, v.288, no.8, pp.5660 - 5672-
dc.identifier.wosid000315342500039-
dc.citation.endPage5672-
dc.citation.number8-
dc.citation.startPage5660-
dc.citation.titleJournal of Biological Chemistry-
dc.citation.volume288-
dc.contributor.affiliatedAuthorChoi S.-
dc.identifier.scopusid2-s2.0-84874322054-
dc.description.journalClass1-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.type.docTypeArticle-
dc.subject.keywordPlusEARLY-ONSET PARKINSONISM-
dc.subject.keywordPlusMITOCHONDRIAL DYSFUNCTION-
dc.subject.keywordPlusDOPAMINERGIC-NEURONS-
dc.subject.keywordPlusPROTEASOME-
dc.subject.keywordPlusPATHWAY-
dc.subject.keywordPlusPHOSPHORYLATION-
dc.subject.keywordPlusDEGRADATION-
dc.subject.keywordPlusRECRUITMENT-
dc.subject.keywordPlusPATHOLOGY-
dc.subject.keywordPlusMEMBRANE-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-

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