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- W2059280539 abstract "Normal cells reach senescence after a specific time and number of divisions, leading ultimately to cell death. Although escape from this fate may be a requisite step in neoplastic transformation, the mechanisms governing senescent cell death have not been well investigated. We show here, using normal human epidermal keratinocytes, that no apoptotic markers appear with senescence. In contrast, the expression of several proteins involved in the regulation of macroautophagy, notably Beclin-1 and Bcl-2, was found to change with senescence. The corpses occurring at the senescence growth plateau displayed a large central area delimited by the cytokeratin network that contained a huge quantity of autophagic vacuoles, the damaged nucleus, and most mitochondria. 3-methyladenine, an inhibitor of autophagosome formation, but not the caspase inhibitor zVAD, prevented senescent cell death. We conclude that senescent cells do not die by apoptosis, but as a result of high macroautophagic activity that targets the primary vital cell components." @default.
- W2059280539 created "2016-06-24" @default.
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- W2059280539 date "2009-02-01" @default.
- W2059280539 modified "2023-09-30" @default.
- W2059280539 title "Senescent Keratinocytes Die by Autophagic Programmed Cell Death" @default.
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- W2059280539 doi "https://doi.org/10.2353/ajpath.2009.080332" @default.
- W2059280539 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2630552" @default.
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