Mutant p53: one name, many proteins.

By William A. Freed-Pastor, Carol Prives. Genes & Development, 2012

1,212 citations recorded by the source corpus.

There is now strong evidence that mutation not only abrogates p53 tumor-suppressive functions, but in some instances can also endow mutant proteins with novel activities. Such neomorphic p53 proteins are capable of dramatically altering tumor cell behavior, primarily through their interactions with other cellular proteins and regulation of cancer cell transcriptional programs. Different missense mutations in p53 may confer unique activities and thereby offer insight into the mutagenic events that drive tumor progression. Here we review mechanisms by which mutant p53 exerts its cellular effects, with a particular focus on the burgeoning mutant p53 transcriptome, and discuss the biological and clinical consequences of mutant p53 gain of function.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/8e48ef2a89ed135d125c99acba5711e210907e9d

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Citations in the corpus

p53 Proteoforms and Intrinsic Disorder: An Illustration of the Protein Structure–Function Continuum Concept (2016, background): “In a recent review article discussing the roles of various p53 mutations in modulating the structure and function of this protein, it was pointed out that “While many groups choose to use the generic term “mutant p53” to designate any tumor-derived p53 mutant, it is important to recognize that not a”
Targeting p53 pathways: mechanisms, structures and advances in therapy (2023, background): “198 The major type of mutation in TP53 is a missense mutation, a single amino acid substitution and the DNA binding domain (DBD) is the most common mutated region 199,200 (Fig.”