Skip Navigation


Journal of Biochemistry Advance Access originally published online on March 23, 2007
Journal of Biochemistry 2007 141(5):737-745; doi:10.1093/jb/mvm076
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
141/5/737    most recent
mvm076v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Bernal, J. A.
Right arrow Articles by Hernández, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bernal, J. A.
Right arrow Articles by Hernández, A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2007 The Japanese Biochemical Society.

p53 Stabilization can be Uncoupled from its Role in Transcriptional Activation by Loss of PTTG1/Securin

Juan A. Bernal* and Agustín Hernández{dagger}

Centro Andaluz de Biología Molecular y Medicina Regenerativa (C.S.I.C.) Avda. Americo Vespucio s/n 41092 Seville, Spain

{dagger}To whom correspondence should be addressed. Tel: +34 954 468004, Fax: +34 954 461664, 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 post-transcriptional 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 tumour suppressor, protein stability, PTTG1/Securin

Abbreviations: ATM, ataxia telangectasia mutated; ATR, ataxia telangectasia related; cdk, cyclin-dependent kinase; CHX, cyclohexymide; Dox, doxorubicin; LLnL, N-acetyl-L-Leucyl-L-leucyl-L-norleucinal; NP40, nonidet P40; PMSF, phenylmethylsulfonylfluoride

*Present address: CR UK Dept of Oncology, Hutchison/MRC Research Centre, Hills Road, Cambridge CB2 2XZ, UK


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Ann OncolHome page
H. Gogas, A. M. M. Eggermont, A. Hauschild, P. Hersey, P. Mohr, D. Schadendorf, A. Spatz, and R. Dummer
Biomarkers in melanoma
Ann. Onc., August 1, 2009; 20(suppl_6): vi8 - vi13.
[Abstract] [Full Text] [PDF]

Home page
 Endocr Relat CancerHome page
F. Salehi, K. Kovacs, B. W Scheithauer, R. V Lloyd, and M. Cusimano
Pituitary tumor-transforming gene in endocrine and other neoplasms: a review and update
Endocr. Relat. Cancer, September 1, 2008; 15(3): 721 - 743.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.