SNPing away at mutant p53 activities

Genes & Development
Guadalupe J Ortiz, Guillermina Lozano

Abstract

A delicate balance in the levels of proteins that regulate the p53 tumor suppressor pathway exists such that subtle changes alter p53 tumor suppressor activity and cancer risk. Many single-nucleotide polymorphisms (SNPs) in the p53 pathway alter p53 transcriptional activity and are associated with cancer risk. In addition, some SNPs influence the gain-of-function (GOF) activities of mutant p53 through unknown mechanisms. In this issue of Genes & Development, Basu and colleagues (pp. 230-243) provide direct evidence that the presence of an R72 polymorphism enhances the GOF invasive and metastatic properties of mutant p53 by regulating interactions with PGC-1α, an important regulator of mitochondrial biogenesis and oxidative phosphorylation. The study culminates with evidence that R72 is associated with worse outcomes in human breast cancer.

References

Jul 19, 2011·Genes & Development·Søren F Schmidt, Susanne Mandrup
Feb 4, 2014·Human Mutation·Christine M Eischen, Guillermina Lozano
Apr 3, 2016·Cold Spring Harbor Perspectives in Medicine·Subhasree Basu, Maureen E Murphy
Nov 4, 2017·Cell Death and Differentiation·Michael P Kim, Guillermina Lozano
Feb 22, 2018·Genes & Development·Subhasree BasuMaureen E Murphy
Jan 1, 2018·Cell Death and Differentiation·Michael P Kim, Guillermina Lozano

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Citations

Dec 12, 2018·Aging·Piervito LoprioreIvano Amelio

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