Aberrant signaling and senescence associated protein degradation

Aberrant signaling and senescence associated protein degradation Senescent cells accumulate with age and contribute to pathologies associated to old age. The senescent program can be induced by pro-cancer stimuli or is developmentally controlled. In cells forced to senesce by expression of oncogenes or short telomeres, aberrant activation of the ERK/MAP kinase signaling pathway leads to selective protein degradation by the ubiquitin proteasome system. The proteins affected by this process control key cellular processes known to be defective in senescent cells. We discuss the evidence supporting a general role for aberrant signaling and senescence associated protein degradation for organismal aging. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Experimental Gerontology Elsevier

Aberrant signaling and senescence associated protein degradation

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Publisher
Elsevier
Copyright
Copyright © 2017 Elsevier Ltd
ISSN
0531-5565
eISSN
1873-6815
D.O.I.
10.1016/j.exger.2017.06.016
Publisher site
See Article on Publisher Site

Abstract

Senescent cells accumulate with age and contribute to pathologies associated to old age. The senescent program can be induced by pro-cancer stimuli or is developmentally controlled. In cells forced to senesce by expression of oncogenes or short telomeres, aberrant activation of the ERK/MAP kinase signaling pathway leads to selective protein degradation by the ubiquitin proteasome system. The proteins affected by this process control key cellular processes known to be defective in senescent cells. We discuss the evidence supporting a general role for aberrant signaling and senescence associated protein degradation for organismal aging.

Journal

Experimental GerontologyElsevier

Published: Jul 1, 2018

References

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