Targets for Transcriptional Activation by Wild-type p53: Endogenous Retroviral LTR, Immunoglobulin-like Promoter, and an Internal Promoter of the mdm2 Gene

Yaacov Barak(Weizmann Institute of Science), Angelo Lupo(Weizmann Institute of Science), Ayelet Zauberman(Weizmann Institute of Science), T. Juven(Weizmann Institute of Science), Ronit Aloni-Grinstein(Weizmann Institute of Science), Eyal Gottlieb(Weizmann Institute of Science), Varda Rotter(Weizmann Institute of Science), Moshe Oren(Weizmann Institute of Science)
Cold Spring Harbor Symposia on Quantitative Biology
January 1, 1994
Cited by 8

Abstract

The p53 protein is the product of a tumor suppressor gene which is subject to an extremely high frequency of structural alterations in human cancer (for review, see Hollstein et al. 1991; Levine et al. 1991; Oren 1992; Donehower and Bradley 1993; Harris and Hollstein 1993; Berns 1994). The main selective advantage of such alterations is probably the elimination of the tumor suppressor functions of the wild-type (wt) p53 protein. However, at least some of the p53 point mutations commonly encountered in tumor cells may also entail an oncogenic gain of function (Wolf et al. 1984; Chen et al. 1990; Michalovitz et al. 1991; Dittmer et al. 1993).


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