期刊
JOURNAL OF PATHOLOGY
卷 205, 期 2, 页码 206-220出版社
WILEY
DOI: 10.1002/path.1704
关键词
p53 regulators; p53 mediators; knockout; knockin
资金
- NATIONAL CANCER INSTITUTE [P01CA071907, P01CA034936, R01CA047296, R29CA047296, R01CA063230] Funding Source: NIH RePORTER
- NCI NIH HHS [CA47296, CA63230, CA071907, CA34936] Funding Source: Medline
Mouse models have provided important insight into the in vivo significance of upstream and downstream signals that regulate the p53 tumour suppressor. One important lesson learned from these models is that negative regulators of p53 are critical in vivo modulators of p53 activity. Additionally, upstream regulators of p53 activity, such as p19(Arf) and Atm, are themselves critical tumour modifiers/suppressors. The presence of multiple positive regulators of p53 and numerous downstream targets indicates a redundancy that ensures activation of the p53 pathway. Importantly, p53 plays a prominent role as a tumour suppressor in vivo by virtue of its ability both to block cell cycle progression and to induce cell death. Finally, different p53 mutants have different properties in vivo. Three missense mutations have been generated at the p53 locus and all three exhibit unique differences in their ability to contribute to the tumour phenotype. Clearly, determining the levels of p53 inhibitors, and the typing of p53 mutations in human tumours should be performed to determine the best avenue for treatment. Copyright (C) 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley Sons, Ltd.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据