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Accessible Unlicensed Requires Authentication Published by De Gruyter May 20, 2009

The do's and don'ts of p53 isoforms

Reiner U. Jänicke, Vilma Graupner, Wilfried Budach and Frank Essmann
From the journal

Abstract

Upon DNA damage and other stresses, the transcription factor p53 elicits numerous responses including DNA repair, cell cycle arrest and apoptosis, properties that make p53 the prototype tumor suppressor. In addition, p53 also transactivates genes whose products act in an anti-apoptotic manner providing strong evidence that p53 exhibits both tumor suppressive and tumorigenic functions. Although several events were postulated to contribute to the p53-mediated decision process, the precise mechanism(s) that governs p53 activities is still elusive. Recently, it was found that the p53 gene allows expression of at least nine different isoforms that arise from multiple splicing events and the usage of alternative promoters. Several of these isoforms were shown to critically interfere with the function of the full-length p53 mainly by acting in a dominant-negative manner. However, an isoform-dependent selective activation of p53 target genes was also observed. Furthermore, certain p53 isoforms are aberrantly expressed in various tumors strongly implying their involvement in tumorigenic events. Thus, p53 isoforms may represent crucial determinants in p53-mediated decision processes whose precise functions (their do's and don'ts) are only beginning to emerge.


Corresponding author

Received: 2009-3-11
Accepted: 2009-4-28
Published Online: 2009-05-20
Published in Print: 2009-10-01

©2009 by Walter de Gruyter Berlin New York