Journal
ANNUAL REVIEW OF BIOCHEMISTRY
Volume 77, Issue -, Pages 557-582Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev.biochem.77.060806.091238
Keywords
drug design; intrinsic disorder; multidomain protein; oncogenic mutation; transcription factor
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The tumor suppressor protein p53 induces or represses the expression of a variety of target genes involved in cell cycle control, senescence, and apoptosis in response to oncogenic or other cellular stress signals. It exerts its function as guardian of the genome through an intricate interplay of independently folded and intrinsically disordered functional domains. In this review, we provide insights into the structural complexity of p53, the molecular mechanisms of its inactivation in cancer, and therapeutic strategies for the pharmacological rescue of p53 function in tumors. p53 emerges as a paradigm for a more general understanding of the structural organization of modular proteins and the effects of disease-causing mutations.
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