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dc.contributor.authorWang, Lu
dc.contributor.authorXu, Caiyue
dc.contributor.authorJohansen, Terje
dc.contributor.authorBerger, Shelley L.
dc.contributor.authorDou, Zhixun
dc.description.abstractMacroautophagic/autophagic degradation of nuclear components (or nuclear autophagy) is a poorly understood area in autophagy research. We previously reported the nuclear lamina protein LMNB1 (lamin B1) as a nuclear autophagy substrate in primary human cells, stimulating the investigation of nuclear autophagy in the mammalian system. We recently reported the sirtuin protein SIRT1 as a new selective substrate of nuclear autophagy in senescence and aging. Upon senescence of primary human cells, SIRT1 degradation is mediated by a direct nuclear SIRT1-LC3 interaction, followed by nucleus-to-cytoplasm shuttling of SIRT1 and autophagosome-lysosome degradation. In vivo, SIRT1 is downregulated by lysosomes in hematopoietic and immune organs upon natural aging in mice and in aged human T cells. Our study identified another substrate of nuclear autophagy and suggests a new strategy to promote SIRT1-mediated health benefits by suppressing its autophagic degradation.en_US
dc.identifier.citationWang, Xu, Johansen, Berger, Dou. SIRT1 - a new mammalian substrate of nuclear autophagy. Autophagy. 2020en_US
dc.identifier.cristinIDFRIDAID 1893565
dc.publisherTaylor and Francis Groupen_US
dc.rights.holderCopyright 2020 The Author(s)en_US
dc.rightsAttribution 4.0 International (CC BY 4.0)en_US
dc.titleSIRT1 - a new mammalian substrate of nuclear autophagyen_US
dc.typeJournal articleen_US
dc.typePeer revieweden_US

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Attribution 4.0 International (CC BY 4.0)
Except where otherwise noted, this item's license is described as Attribution 4.0 International (CC BY 4.0)