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Cited by 277

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Regulation of Autophagy by the p300 Acetyltransferase

Lee, In Hye, Finkel, Toren·2009·Journal of Biological Chemistry
DOI 10.1074/jbc.m807135200
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Abstract

Autophagy is a regulated process of intracellular catabolism required for normal cellular maintenance, as well as serving as an adaptive response under various stress conditions, including starvation. The molecular regulation of autophagy in mammalian cells remains incompletely understood. Here we demonstrate a role for protein acetylation in the execution and regulation of autophagy. In particular, we demonstrate that the p300 acetyltransferase can regulate the acetylation of various known components of the autophagy machinery. Knockdown of p300 reduces acetylation of Atg5, Atg7, Atg8, and Atg12, although overexpressed p300 increases the acetylation of these same proteins. Furthermore, p300 and Atg7 colocalize within cells, and the two proteins physically interact. The interaction between p300 and Atg7 is dependent on nutrient availability. Finally, we demonstrate that knockdown of p300 can stimulate autophagy, whereas overexpression of p300 inhibits starvation-induced autophagy. These results demonstrate a role for protein acetylation and particularly p300 in the regulation of autophagy under conditions of limited nutrient availability.

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Crossref · 10.1074/jbc.m807135200

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6 of 6 references verified0 citation errors · 0 not checkable

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  • Modulation of the amount of S-nitrosylated proteins by changes in activity or expression of ADH5/GSNOR has no major effects on nonselective autophagy, whereas it affects recognition of damaged mitochondria for selective mitophagy.

    “Conversely, the modulation of the amount of S-nitrosylated proteins triggered by changes in the activity or expression of the denitrosylase ADH5/GSNOR (alcohol dehydrogenase 5 [class III], chi polypeptide), seems to have no major effects on nonselective autophagy, whereas there is an effect on the recognition of damaged mitochondria to be targeted for selective mitophagy [1005, 1006].”

    From Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1 (2021) · cites this paper as [1005]

Citations

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Flagged first, then by citations

Research works printed but not linked: 11

  1. Sarbassov, 2005, Curr. Opin. Cell Biol., 17, 596, 10.1016/j.ceb.2005.09.009 · DOI
  2. Lee, 2008, Proc. Natl. Acad. Sci. U. S. A., 105, 3374, 10.1073/pnas.0712145105 · DOI
  3. Bjorkoy, 2005, J. Cell Biol., 171, 603, 10.1083/jcb.200507002 · DOI · Paper page
  4. Shintani, 2004, Science, 306, 990, 10.1126/science.1099993 · DOI
  5. Mavrakis, 2006, Hum. Mol. Genet., 15, 2962, 10.1093/hmg/ddl239 · DOI
  6. Klionsky, 2007, Autophagy, 4, 151, 10.4161/auto.5338 · DOI · Paper page
  7. Bishop, 2008, Nat. Rev. Genet., 8, 835, 10.1038/nrg2188 · DOI
  8. Melendez, 2003, Science, 301, 1387, 10.1126/science.1087782 · DOI · Paper page
  9. Bergamini, 2007, Ann. N. Y. Acad. Sci., 1114, 69, 10.1196/annals.1396.020 · DOI
  10. Toth, 2008, Autophagy, 4, 330, 10.4161/auto.5618 · DOI
  11. Komatsu, 2006, Nature, 441, 819, 10.1038/nature04723 · DOI · Paper page

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Metadata

Authors
Lee, I. H., & Finkel, T.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2009-03
Volume
284
Issue
10
Pages
6322-6328
ISSN
0021-9258
DOI
10.1074/jbc.m807135200
Cited by
277
References
6
Language
en
Licence

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