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dc.contributor.authorKim, Jin-Hwan
dc.contributor.authorChoi, Tae Gyu
dc.contributor.authorPark, Seolhui
dc.contributor.authorYun, Hyeong Rok
dc.contributor.authorNguyen, Ngoc Ngo Yen
dc.contributor.authorJo, Yong Hwa
dc.contributor.authorJang, Miran
dc.contributor.authorKim, Jieun
dc.contributor.authorKim, Joungmok
dc.contributor.authorKang, Insug
dc.contributor.authorHa, Joohun
dc.contributor.authorMurphy, Michael P
dc.contributor.authorTang, Dean G
dc.contributor.authorKim, Sung Soo
dc.date.accessioned2018-11-22T00:32:58Z
dc.date.available2018-11-22T00:32:58Z
dc.date.issued2018-11
dc.identifier.issn1476-5403
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/285681
dc.description.abstractMuscle differentiation is a crucial process controlling muscle development and homeostasis. Mitochondrial reactive oxygen species (mtROS) rapidly increase and function as critical cell signaling intermediates during the muscle differentiation. However, it has not yet been elucidated how they control myogenic signaling. Autophagy, a lysosome-mediated degradation pathway, is importantly recognized as intracellular remodeling mechanism of cellular organelles during muscle differentiation. Here, we demonstrated that the mtROS stimulated phosphatidylinositol 3 kinase/AKT/mammalian target of rapamycin (mTOR) cascade, and the activated mTORC1 subsequently induced autophagic signaling via phosphorylation of uncoordinated-51-like kinase 1 (ULK1) at serine 317 and upregulation of Atg proteins to prompt muscle differentiation. Treatment with MitoQ or rapamycin impaired both phosphorylation of ULK1 and expression of Atg proteins. Therefore, we propose a novel regulatory paradigm in which mtROS are required to initiate autophagic reconstruction of cellular organization through mTOR activation in muscle differentiation.
dc.description.sponsorshipThis study was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (NRF-2016R1D1A1B03933763 to TGC, and NRF-2011-0030072, NRF-2017R1A2B2007870, and NRF-2018R1A6A1A03025124 to SSK).
dc.languageeng
dc.publisherSpringer Nature
dc.titleMitochondrial ROS-derived PTEN oxidation activates PI3K pathway for mTOR-induced myogenic autophagy.
dc.typeArticle
prism.publicationNameCell Death & Differentiation
dc.identifier.doi10.17863/CAM.33033
dcterms.dateAccepted2018-07-02
rioxxterms.versionofrecord10.1038/s41418-018-0165-9
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2018-07-02
dc.contributor.orcidMurphy, Mike [0000-0003-1115-9618]
dc.identifier.eissn1476-5403
rioxxterms.typeJournal Article/Review
pubs.funder-project-idMedical Research Council (MC_UU_00015/3)
cam.issuedOnline2018-07-24
rioxxterms.freetoread.startdate2019-07-24


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