p53 Oligomerization Domain Mutants: A New Class of Mutants That Retain "License to Kill"
- PMID: 37139723
- DOI: 10.1158/2159-8290.CD-23-0200
p53 Oligomerization Domain Mutants: A New Class of Mutants That Retain "License to Kill"
Abstract
In this issue of Cancer Discovery, companion articles from the Prives and Lozano groups describe functional analyses of a common dimeric mutant of p53 found in Li-Fraumeni disease and sporadic cancer: A347D (AD). The authors show that the AD mutant is completely defective for canonical p53 transcriptional function, but interestingly retains some tumor suppressor function, which they show is manifested as "neomorphic" activities in transcription and the control of mitochondrial metabolism. See related article by Gencel-Augusto et al., p. 1230 (7). See related article by Choe et al., p. 1250 (6).
©2023 American Association for Cancer Research.
Comment on
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Li-Fraumeni Syndrome-Associated Dimer-Forming Mutant p53 Promotes Transactivation-Independent Mitochondrial Cell Death.Cancer Discov. 2023 May 4;13(5):1250-1273. doi: 10.1158/2159-8290.CD-22-0882. Cancer Discov. 2023. PMID: 37067901 Free PMC article.
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Dimeric p53 Mutant Elicits Unique Tumor-Suppressive Activities through an Altered Metabolic Program.Cancer Discov. 2023 May 4;13(5):1230-1249. doi: 10.1158/2159-8290.CD-22-0872. Cancer Discov. 2023. PMID: 37067911 Free PMC article.
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