Human GTSE1 (G2 and S phase-expressed 1) is a cell cycle-regulated protein with increased expression during S and G2 phases of the cell cycle. We have previously reported that hGTSE1 is a microtubule-localized protein that becomes stabilized upon DNA-damage, and a cell cycle-specific inhibitor of the p53 pathway. Recently we describe a new function of hGTSE1 as a physiological regulator of the cyclin-dependent kinase inhibitor p21 levels independently of p53. In the present work we unravel the functional consequence of hGTSE1-mediated p21 modulation, that is reflected in the cellular response to stress particularly in the G2 checkpoint and apoptosis. Indeed, hGTSE1 was able to modulate cellular response upon different apoptotic insults such as DNA-damage and microtubule poisons through p21 regulation, this effect being potentially important in drug resistance phenotype acquisition.

hGTSE1 protein unveils new pathways that regulate apoptosis and cell motility(2010 Oct 22).

hGTSE1 protein unveils new pathways that regulate apoptosis and cell motility

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2010-10-22

Abstract

Human GTSE1 (G2 and S phase-expressed 1) is a cell cycle-regulated protein with increased expression during S and G2 phases of the cell cycle. We have previously reported that hGTSE1 is a microtubule-localized protein that becomes stabilized upon DNA-damage, and a cell cycle-specific inhibitor of the p53 pathway. Recently we describe a new function of hGTSE1 as a physiological regulator of the cyclin-dependent kinase inhibitor p21 levels independently of p53. In the present work we unravel the functional consequence of hGTSE1-mediated p21 modulation, that is reflected in the cellular response to stress particularly in the G2 checkpoint and apoptosis. Indeed, hGTSE1 was able to modulate cellular response upon different apoptotic insults such as DNA-damage and microtubule poisons through p21 regulation, this effect being potentially important in drug resistance phenotype acquisition.
22-ott-2010
Scolz, Massimiliano
Schneider, Claudio
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11767/4131
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