Regulation of TFEB and V-ATPases by mTORC1
EMBO Journal, ISSN: 0261-4189, Vol: 30, Issue: 16, Page: 3242-3258
2011
- 389Citations
- 406Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations389
- Citation Indexes389
- 389
- CrossRef360
- Captures406
- Readers406
- 406
Article Description
Mammalian target of rapamycin (mTOR) complex 1 (mTORC1) is an important, highly conserved, regulator of cell growth. Ancient among the signals that regulate mTORC1 are nutrients. Amino acids direct mTORC1 to the surface of the late endosome/lysosome, where mTORC1 becomes receptive to other inputs. However, the interplay between endosomes and mTORC1 is poorly understood. Here, we report the discovery of a network that links mTORC1 to a critical component of the late endosome/lysosome, the V-ATPase. In an unbiased screen, we found that mTORC1 regulated the expression of, among other lysosomal genes, the V-ATPases. mTORC1 regulates V-ATPase expression both in cells and in mice. V-ATPase regulation by mTORC1 involves a transcription factor translocated in renal cancer, TFEB. TFEB is required for the expression of a large subset of mTORC1 responsive genes. mTORC1 coordinately regulates TFEB phosphorylation and nuclear localization and in a manner dependent on both TFEB and V-ATPases, mTORC1 promotes endocytosis. These data uncover a regulatory network linking an oncogenic transcription factor that is a master regulator of lysosomal biogenesis, TFEB, to mTORC1 and endocytosis. © 2011 European Molecular Biology Organization.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=80052841665&origin=inward; http://dx.doi.org/10.1038/emboj.2011.257; http://www.ncbi.nlm.nih.gov/pubmed/21804531; http://emboj.embopress.org/cgi/doi/10.1038/emboj.2011.257; https://dx.doi.org/10.1038/emboj.2011.257; https://www.embopress.org/doi/full/10.1038/emboj.2011.257
Springer Science and Business Media LLC
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