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EMBO reports 7, 4, 404–410 (2006)
doi:10.1038/sj.embor.7400623
AOP Published online: 20 January 2006
Two internal ribosome entry sites mediate the translation of p53 isoforms
Partho Sarothi Ray†, Richa Grover & Saumitra Das
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Department of Microbiology and Cell Biology, Indian Institute of Science, Sir C.V. Raman Avenue, Bangalore-560012, India
To whom correspondence should be addressed
Saumitra Das Tel: +91 80 2293 2886; Fax: +91 80 2360 2697; E-mail: sdas@mcbl.iisc.ernet.in
† Present address: Department of Cell Biology, The Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
Received 22 September 2005; Accepted 5 December 2005; Published online 20 January 2006.
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Abstract
The p53 tumour suppressor protein has a crucial role in cell-cycle arrest and apoptosis. Previous reports show that the p53 messenger RNA is translated to produce an amino-terminal-deleted isoform ( N-p53) from an internal initiation codon, which acts as a dominant-negative inhibitor of full-length p53. Here, we show that two internal ribosome entry sites (IRESs) mediate the translation of both full-length and N-p53 isoforms. The IRES directing the translation of full-length p53 is in the 5'-untranslated region of the mRNA, whereas the IRES mediating the translation of N-p53 extends into the protein-coding region. The two IRESs show distinct cell-cycle phase-dependent activity, with the IRES for full-length p53 being active at the G2–M transition and the IRES for N-p53 showing highest activity at the G1–S transition. These results indicate a novel translational control of p53 gene expression and activity.
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