Gene-specific mechanisms of p53 transcriptional control and prospects for cancer therapy
✍ Scribed by Lois Resnick-Silverman; James J. Manfredi
- Publisher
- John Wiley and Sons
- Year
- 2006
- Tongue
- English
- Weight
- 186 KB
- Volume
- 99
- Category
- Article
- ISSN
- 0730-2312
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
The regulation of gene‐specific activation is critical to the tumor suppressor function by p53. p53 is a well‐characterized transcription factor that responds to DNA damage and other genotoxic stresses by the activation of downstream targets that are involved with repair, differentiation, senescence, growth arrest, and apoptosis. Sequence‐specific binding to DNA, conformation, post‐translational modifications, cofactor binding, stability, and subcellular localization all influence the performance of p53. The purpose of this review is to define features that play a key role in gene‐specific activation and to show that these are often incapacitated in cancer cells. Using such knowledge to design selective strategies for the restoration of p53 wild‐type function in cancer cells represents a promising cancer therapy. J. Cell. Biochem. 99: 679–689, 2006. © 2006 Wiley‐Liss, Inc.
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