Carcinogenesis Advance Access published online on July 1, 2004
Carcinogenesis, doi:10.1093/carcin/bgh212
© 2004 by Oxford University Press
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 YCR P53 Research Group, Department of Biology, University of York, York, YO10 5DD, UK
* To whom correspondence should be addressed. E-mail: sja13{at}york.ac.uk.
The tumour suppressor p53 has an essential role in maintaining the genomic integrity of the mammalian cell. This is achieved in part through its function as a transcription factor enabling it to induce either growth arrest or apoptosis in response to cellular stress. Changes in gene expression commonly require localised chromatin remodelling and p53 is known to interact in vivo with a variety of transcriptional co-activators and co-repressors with intrinsic histone modifying activities. Here we examine the links between p53 and chromatin structures associated with (i) transcriptional regulation of gene expression, (ii) with DNA repair as part of the process of nucleotide excision repair, and (iii) with histone modifications which impact upon chromosomal condensation and ploidy.
Revised June 2, 2004
Accepted June 6, 2004
COMMENTARY
Remodelling chromatin on a global scale: a novel protective function of p53
![]()
Abstract ![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
A. Samanta, B. Li, X. Song, K. Bembas, G. Zhang, M. Katsumata, S. J. Saouaf, Q. Wang, W. W. Hancock, Y. Shen, et al. TGF-{beta} and IL-6 signals modulate chromatin binding and promoter occupancy by acetylated FOXP3 PNAS, September 16, 2008; 105(37): 14023 - 14027. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. J. Krieg, E. M. Hammond, and A. J. Giaccia Functional Analysis of p53 Binding under Differential Stresses. Mol. Cell. Biol., October 1, 2006; 26(19): 7030 - 7045. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. H. Dashwood Xenobiotic Metabolism Relevance to Cancer J. Nutr., October 1, 2006; 136(10): 2681S - 2682S. [Full Text] [PDF] |
||||
![]() |
T. Kobayashi, T. Wang, M. Maezawa, M. Kobayashi, S. Ohnishi, K. Hatanaka, S. Hige, Y. Shimizu, M. Kato, M. Asaka, et al. Overexpression of the Oncoprotein Prothymosin {alpha} Triggers a p53 Response that Involves p53 Acetylation. Cancer Res., March 15, 2006; 66(6): 3137 - 3144. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. H. Dashwood, M. C. Myzak, and E. Ho Dietary HDAC inhibitors: time to rethink weak ligands in cancer chemoprevention? Carcinogenesis, February 1, 2006; 27(2): 344 - 349. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Hublitz, N. Kunowska, U. P. Mayer, J. M. Muller, K. Heyne, N. Yin, C. Fritzsche, C. Poli, L. Miguet, I. W. Schupp, et al. NIR is a novel INHAT repressor that modulates the transcriptional activity of p53 Genes & Dev., December 1, 2005; 19(23): 2912 - 2924. [Abstract] [Full Text] [PDF] |
||||





