Abstract
Be quiet and you'll keep young: does mTOR underlie p53 action in protecting against senescence by favoring quiescence?
Highlights
Commentary on: O Leontieva and M Blagosklonny
Cell cycle arrest requires inhibition of cyclin-dependent kinases (CDK), that drive division by both activating diverse regulators involved in replication and mitosis and by inactivating pRb pocket protein family members
Clearly involved [4], the role of p53 in quiescence is probably not essential, as this cell cycle arrest is mostly mediated by p27Kip1 (p27), a CDK inhibitor whose levels are not controlled by p53 [5]
Summary
Commentary on: O Leontieva and M Blagosklonny. DNA damaging agents and p53 do not cause senescence in quiescent cells, while consecutive re‐activation of mTOR is associated with conversion to senescence. Confluence and the absence of mitogens or nutrients induce quiescence, while cell ageing, inappropriate signaling or irreparable DNA damage lead to senescence, which is characterized by a large and flat cell morphology and expression of specific biomarkers.
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