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Journal of Biochemistry Advance Access published online on March 23, 2007
Journal of Biochemistry, doi:10.1093/jb/mvm076
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© 2007 The Japanese Biochemical Society

p53 stabilization can be uncoupled from its role in transcriptional activation by loss of PTTG1/securin.

Juan A. Bernal1,2 and Agustín Hernández1,*

1 Centro Andaluz de Biología y Medicina Regenerativa (C.S.I.C.) Avda. Americo Vespucio s/n 41092 Seville, Spain
2 Pressent address: CR UK Dept of Oncology, Hutchison / MRC Research Centre, Hills Road, Cambridge CB2 2XZ, UK

* Corresponding author,Centro Andaluz de Biología y Medicina Regenerativa (C.S.I.C.) Avda. Americo Vespucio s/n 41092 Seville, Spain. E-mail: ahernan{at}cica.es

Received March 1, 2007; Accepted March 6, 2007


  Abstract

HCT116 cells devoid of PTTG1/securin (sec-/- HCT116) show a stabilized yet transcriptionally latent form of p53 protein in the absence of DNA damage. Ser15, Ser20 phosphorylation and other posttranscriptional modifications of p53 resolved by 2D gel electrophoresis are comparable to that observed in sec+/+ HCT116 cells. The difference in degradation was also shown to be independent of the ubiquitin system but reliant on calpains. However, the p53-mediated checkpoint response is active only after genotoxic stress in sec-/- HCT116 cells. These findings point to the calpain pathway as a key player to maintain steady state levels of p53 in resting cells without affecting its activity.

Key Words: calpains, gene regulation, p53 tumor suppressor, protein stability, PTTG1/Securin


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