p53 isoforms Δ133p53 and p53β are endogenous regulators of replicative cellular senescence

被引：0
|
作者：
Kaori Fujita
Abdul M. Mondal
Izumi Horikawa
Giang H. Nguyen
Kensuke Kumamoto
Jane J. Sohn
Elise D. Bowman
Ewy A. Mathe
Aaron J. Schetter
Sharon R. Pine
Helen Ji
Borivoj Vojtesek
Jean-Christophe Bourdon
David P. Lane
Curtis C. Harris
机构：
[1] Laboratory of Human Carcinogenesis,Department of Surgery and Molecular Oncology
[2] Center for Cancer Research,undefined
[3] National Cancer Institute,undefined
[4] National Institutes of Health,undefined
[5] Howard Hughes Medical Institute-National Institutes of Health Research Scholars Program,undefined
[6] 1 Cloister Court,undefined
[7] Building 60,undefined
[8] Masaryk Memorial Cancer Institute,undefined
[9] Zluty Kopec 7,undefined
[10] 65653 Brno,undefined
[11] University of Dundee,undefined
[12] Ninewells Hospital,undefined
[13] Inserm-European Associated Laboratory,undefined
[14] Institute of Molecular and Cell Biology,undefined
[15] 61 Biopolis Drive,undefined
[16] Proteos,undefined
来源：
Nature Cell Biology | 2009年 / 11卷
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摘要：
p53-mediated replicative cellular senescence is a barrier to tumorigenesis. The p53 isoforms p53β and Δ133p53 are respectively induced and downregulated during replicative senescence. Elevated p53β and reduced Δ133p53 levels are observed in colon adenomas with senescent phenotypes, whereas the opposite is found in colon carcinomas that might have escaped from the senescence barrier.
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页码：1135 / 1142
页数：7
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