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MDM2 acts as a timer reporting the length of mitosis
Abstract Delays in mitosis trigger p53-dependent arrest in G1 of the following cell cycle, enabling cells to respond to changes that would otherwise promote chromosome instability and aneuploidy. We find that MDM2, the p53 ubiquitin ligase, is a key component of the timer mechanism triggering G1 arrest in response to prolonged mitosis. This timer function arises because MDM2 has a short half-life and ongoing protein synthesis is therefore necessary to maintain its steady-state concentration.
MDM2 acts as a timer reporting the length of mitosis
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Membrane Traffic: Trans-Golgi Tethers Leave a Surprisingly Small GAP
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