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Distinct p53 Transcriptional Programs Dictate Acute DNA-Damage Responses and Tumor Suppression
Journal article   Open access   Peer reviewed

Distinct p53 Transcriptional Programs Dictate Acute DNA-Damage Responses and Tumor Suppression

Colleen A. Brady, Dadi Jiang, Stephano S. Mello, Thomas M. Johnson, Lesley A. Jarvis, Margaret M. Kozak, Daniela Kenzelmann Broz, Shashwati Basak, Eunice J. Park, Margaret E. McLaughlin, …
Cell, Vol.145(4), pp.571-583
05/13/2011
DOI: 10.1016/j.cell.2011.03.035
PMCID: PMC3259909
PMID: 21565614
url
https://doi.org/10.1016/j.cell.2011.03.035View
Published (Version of record) Open Access

Abstract

The molecular basis for p53-mediated tumor suppression remains unclear. Here, to elucidate mechanisms of p53 tumor suppression, we use knockin mice expressing an allelic series of p53 transcriptional activation mutants. Microarray analysis reveals that one mutant, p53(25,26), is severely compromised for transactivation of most p53 target genes, and, moreover, p53(25,26) cannot induce G(1)-arrest or apoptosis in response to acute DNA damage. Surprisingly, p(5325,26) retains robust activity in senescence and tumor suppression, indicating that efficient transactivation of the majority of known p53 targets is dispensable for these pathways. In contrast, the transactivation-dead p53(25,26,53,54) mutant cannot induce senescence or inhibit tumorigenesis, like p53 nullizygosity. Thus, p53 transactivation is essential for tumor suppression but, intriguingly, in association with a small set of novel p53 target genes. Together, our studies distinguish the p53 transcriptional programs involved in acute DNA-damage responses and tumor suppression-a critical goal for designing therapeutics that block p53-dependent side effects of chemotherapy without compromising p53 tumor suppression.
Biochemistry & Molecular Biology Cell Biology Life Sciences & Biomedicine Science & Technology

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