Regulation of protein synthesis by inducible wild-type p53 in human lung carcinoma cells

FEBS Letters
Vivienne J TillerayM J Clemens

Abstract

Activation of an over-expressed mutant form of the tumour suppressor protein p53 has been shown to inhibit protein synthesis. To determine whether this effect is due only to high level expression or the mutant nature of the protein, we have used a doxycycline-inducible lung carcinoma cell line capable of expressing wild-type p53. We now show that levels of wild-type p53 similar to those expressed endogenously also inhibit protein synthesis. The mechanism involves dephosphorylation and accumulation of the translational inhibitor 4E-BP1, and increased association of 4E-BP1 with initiation factor eIF4E. The inhibition of translation is not a consequence of p53-mediated apoptosis.

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Citations

May 7, 2009·Proceedings of the National Academy of Sciences of the United States of America·Cheol-Hee YoonYong-Soo Bae
Mar 10, 2010·Proceedings of the National Academy of Sciences of the United States of America·Ian G CannellMartin Bushell
Jan 16, 2008·Molecular and Cellular Biology·Kyle W Sherrill, Richard E Lloyd
Sep 11, 2007·Experimental Cell Research·David PiñeiroM Elena Martín
Nov 21, 2007·Biology of the Cell·Constantina ConstantinouMichael J Clemens

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