Skip Navigation



Nucleic Acids Research Advance Access published online on October 16, 2007
Nucleic Acids Research, doi:10.1093/nar/gkm744
This Article
Right arrow Full Text Freely available
Right arrow Print PDF (215K) Freely available
Right arrow Screen PDF (198K) Freely available
Right arrowOA All Versions of this Article:
35/22/7475    most recent
gkm744v1
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 Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Rodier, F.
Right arrow Articles by Bhaumik, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rodier, F.
Right arrow Articles by Bhaumik, D.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Survey and Summary

Two faces of p53: aging and tumor suppression

Francis Rodier1,2, Judith Campisi1,2 and Dipa Bhaumik1,*

1Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945 and 2Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, CA 94720, USA

* To whom correspondence should be addressed. Tel: +1 415 209 2042; Fax: 415-209-22232; Email: dbhaumik{at}buckinstitute.org

Received July 12, 2007. Revised September 5, 2007. Accepted September 5, 2007.

The p53 tumor suppressor protein, often termed guardian of the genome, integrates diverse physiological signals in mammalian cells. In response to stress signals, perhaps the best studied of which is the response to DNA damage, p53 becomes functionally active and triggers either a transient cell cycle arrest, cell death (apoptosis) or permanent cell cycle arrest (cellular senescence). Both apoptosis and cellular senescence are potent tumor suppressor mechanisms that irreversibly prevent damaged cells from undergoing neoplastic transformation. However, both processes can also deplete renewable tissues of proliferation-competent progenitor or stem cells. Such depletion, in turn, can compromise the structure and function of tissues, which is a hallmark of aging. Moreover, whereas apoptotic cells are by definition eliminated from tissues, senescent cells can persist, acquire altered functions, and thus alter tissue microenvironments in ways that can promote both cancer and aging phenotypes. Recent evidence suggests that increased p53 activity can, at least under some circumstances, promote organismal aging. Here, we discuss the role of p53 as a key regulator of the DNA damage responses, and discuss how p53 integrates the outcome of the DNA damage response to optimally balance tumor suppression and longevity.


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
 Am. J. Physiol. Heart Circ. Physiol.Home page
R. N. Re and J. L. Cook
Senescence, apoptosis, and stem cell biology: the rationale for an expanded view of intracrine action
Am J Physiol Heart Circ Physiol, September 1, 2009; 297(3): H893 - H901.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
J. Yan, D. Menendez, X.-P. Yang, M. A. Resnick, and A. M. Jetten
A Regulatory Loop Composed of RAP80-HDM2-p53 Provides RAP80-enhanced p53 Degradation by HDM2 in Response to DNA Damage
J. Biol. Chem., July 17, 2009; 284(29): 19280 - 19289.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
U. K. Mukhopadhyay, R. Eves, L. Jia, P. Mooney, and A. S. Mak
p53 Suppresses Src-Induced Podosome and Rosette Formation and Cellular Invasiveness through the Upregulation of Caldesmon
Mol. Cell. Biol., June 1, 2009; 29(11): 3088 - 3098.
[Abstract] [Full Text] [PDF]

Home page
 GeneticsHome page
H. Zetterberg, M. Bath, M. Zetterberg, P. Bernhardt, and O. Hammarsten
The Szilard Hypothesis on the Nature of Aging Revisited
Genetics, May 1, 2009; 182(1): 3 - 9.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
K. Yamasaki, S. Kawasaki, R. D. Young, H. Fukuoka, H. Tanioka, M. Nakatsukasa, A. J. Quantock, and S. Kinoshita
Genomic Aberrations and Cellular Heterogeneity in SV40-Immortalized Human Corneal Epithelial Cells
Invest. Ophthalmol. Vis. Sci., February 1, 2009; 50(2): 604 - 613.
[Abstract] [Full Text] [PDF]

Home page
 BioinformaticsHome page
J. Namkung, K. Kim, S. Yi, W. Chung, M.-S. Kwon, and T. Park
New evaluation measures for multifactor dimensionality reduction classifiers in gene-gene interaction analysis
Bioinformatics, February 1, 2009; 25(3): 338 - 345.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
K. Hasan Md., C. Cheung, Z. Kaul, N. Shah, S. Sakaushi, K. Sugimoto, S. Oka, S. C. Kaul, and R. Wadhwa
CARF Is a Vital Dual Regulator of Cellular Senescence and Apoptosis
J. Biol. Chem., January 16, 2009; 284(3): 1664 - 1672.
[Abstract] [Full Text] [PDF]

Home page
 Nucleic Acids ResHome page
M. A. A. Castro, R. J. S. Dalmolin, J. C. F. Moreira, J. C. M. Mombach, and R. M. C. de Almeida
Evolutionary origins of human apoptosis and genome-stability gene networks
Nucleic Acids Res., November 1, 2008; 36(19): 6269 - 6283.
[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.