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dc.contributor.authorChang, Tsun-Kaien_US
dc.contributor.authorShravage, Bhupendra V.en_US
dc.contributor.authorHayes, Sebastian D.en_US
dc.contributor.authorPowers, Christine M.en_US
dc.contributor.authorSimin, Rachel T.en_US
dc.contributor.authorHarper, J. Wadeen_US
dc.contributor.authorBaehrecke, Eric H.en_US
dc.date.accessioned2014-04-11T14:12:09Z
dc.date.issued2013en_US
dc.identifier.citationChang, Tsun-Kai, Bhupendra V. Shravage, Sebastian D. Hayes, Christine M. Powers, Rachel T. Simin, J. Wade Harper, and Eric H. Baehrecke. 2013. “Uba1 functions in Atg7- and Atg3-independent autophagy.” Nature cell biology 15 (9): 1067-1078. doi:10.1038/ncb2804. http://dx.doi.org/10.1038/ncb2804.en
dc.identifier.issn1465-7392en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:12064440
dc.description.abstractAutophagy is a conserved process that delivers components of the cytoplasm to lysosomes for degradation. The E1 and E2 enzymes encoded by Atg7 and Atg3 are thought to be essential for autophagy involving the ubiquitin-like protein Atg8. Here, we describe an Atg7- and Atg3-independent autophagy pathway that facilitates programmed reduction of cell size during intestine cell death. Although multiple components of the core autophagy pathways, including Atg8, are required for autophagy and cells to shrink in the midgut of the intestine, loss of either Atg7 or Atg3 function does not influence these cellular processes. Rather, Uba1, the E1 used in ubiquitination, is required for autophagy and reduction of cell size. Our data reveal that distinct autophagy programs are used by different cells within an animal, and disclose an unappreciated role for ubiquitin activation in autophagy.en
dc.language.isoen_USen
dc.relation.isversionofdoi:10.1038/ncb2804en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3762904/pdf/en
dash.licenseLAAen_US
dc.titleUba1 functions in Atg7- and Atg3-independent autophagyen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalNature cell biologyen
dc.date.available2014-04-11T14:12:09Z
dc.identifier.doi10.1038/ncb2804*


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