CELL BIOLOGY. GATA get a hold on senescence.
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A transcription factor's abundance connects autophagy to cellular senescence and a secretory phenotype [Also see Research Article by Kang et al. ]
Cellular senescence is a state of “permanent” arrest of the cell division cycle. It is associated with hyperactivated secretion of proinflammatory factors and with a range of pathophysiological processes such as wound healing, aging, and cancer ( 1 ). The processes that control the senescence-associated secretory phenotype (SASP) are not well defined. One candidate effector mechanism is macroautophagy (herein referred to as autophagy), a major intracellular degradation system, but whether it promotes or inhibits senescence is disputed ( 2 ). On page 1503 of this issue, Kang et al. begin to unravel this paradox and provide new insights into the mechanisms by which the SASP is controlled ( 3 ).
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1095-9203
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Cancer Research UK (15890)
