Roles of PINK1, mTORC2, and mitochondria in preserving brain tumor-forming stem cells in a noncanonical Notch signaling pathway

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dc.contributor.authorKyu-Sun Lee-
dc.contributor.authorZ Wu-
dc.contributor.authorY Song-
dc.contributor.authorS S Mitra-
dc.contributor.authorA H Feroze-
dc.contributor.authorS H Cheshier-
dc.contributor.authorB Lu-
dc.date.accessioned2017-04-19T09:49:42Z-
dc.date.available2017-04-19T09:49:42Z-
dc.date.issued2013-
dc.identifier.issn0890-9369-
dc.identifier.uri10.1101/gad.225169.113ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11776-
dc.description.abstractThe self-renewal versus differentiation choice of Drosophila and mammalian neural stem cells (NSCs) requires Notch (N) signaling. How N regulates NSC behavior is not well understood. Here we show that canonical N signaling cooperates with a noncanonical N signaling pathway to mediate N-directed NSC regulation. In the noncanonical pathway, N interacts with PTEN-induced kinase 1 (PINK1) to influence mitochondrial function, activating mechanistic target of rapamycin complex 2 (mTORC2)/AKT signaling. Importantly, attenuating noncanonical N signaling preferentially impaired the maintenance of Drosophila and human cancer stem cell-like tumor-forming cells. Our results emphasize the importance of mitochondria to N and NSC biology, with important implications for diseases associated with aberrant N signaling.-
dc.publisherCold Spring Harbor Lab Press, Publications Dept-
dc.titleRoles of PINK1, mTORC2, and mitochondria in preserving brain tumor-forming stem cells in a noncanonical Notch signaling pathway-
dc.title.alternativeRoles of PINK1, mTORC2, and mitochondria in preserving brain tumor-forming stem cells in a noncanonical Notch signaling pathway-
dc.typeArticle-
dc.citation.titleGenes & Development-
dc.citation.number24-
dc.citation.endPage2647-
dc.citation.startPage2642-
dc.citation.volume27-
dc.contributor.affiliatedAuthorKyu-Sun Lee-
dc.contributor.alternativeName이규선-
dc.contributor.alternativeNameWu-
dc.contributor.alternativeNameSong-
dc.contributor.alternativeNameMitra-
dc.contributor.alternativeNameFeroze-
dc.contributor.alternativeNameCheshier-
dc.contributor.alternativeNameLu-
dc.identifier.bibliographicCitationGenes & Development, vol. 27, no. 24, pp. 2642-2647-
dc.identifier.doi10.1101/gad.225169.113-
dc.subject.keywordCancer stem cells-
dc.subject.keywordMitochondria-
dc.subject.keywordmTORC2/AKT signaling-
dc.subject.keywordNeural stem cells-
dc.subject.keywordNotch-
dc.subject.keywordPINK1-
dc.subject.localcancer stem cell-
dc.subject.localCancer stem cell (CSC)-
dc.subject.localCancer stem cell-
dc.subject.localCancer stem cells-
dc.subject.localCancer Stem Cells-
dc.subject.localMitochondria-
dc.subject.localmitochondria-
dc.subject.localmTORC2/AKT signaling-
dc.subject.localneural stem cell-
dc.subject.localNeural stem cell-
dc.subject.localNeural stem cells-
dc.subject.localNeural stem cells (NSCs)-
dc.subject.localNotch-
dc.subject.localPINK1-
dc.description.journalClassY-
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