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|Abstract:||Tumor protein p53 (TP53) is the most commonly mutated gene in human cancer. The majority of mutations are missense, and generate a defective protein that is druggable. Yet, for decades, the small-molecule restoration of wild-type (WT) p53 function in mutant p53 tumors (so-called p53 mutant ‘reactivation’) has been elusive to researchers. The p53 protein requires the binding of a single zinc ion for proper folding, and impairing zinc binding is a major mechanism for loss of function in missense mutant p53. Here, we describe recent work defining a new class of drugs termed zinc metallochaperones that restore WT p53 structure and function by restoring Zn2+ to Zn2+-deficient mutant p53.|
|Citation:||Blanden, Adam R, Yu, Xin, Loh, Stewart N, Levine, Arnold J, Carpizo, Darren R. (2015). Reactivating mutant p53 using small molecules as zinc metallochaperones: awakening a sleeping giant in cancer. Drug Discovery Today, 20 (11), 1391 - 1397. doi:10.1016/j.drudis.2015.07.006|
|Pages:||1391 - 1397|
|Type of Material:||Journal Article|
|Journal/Proceeding Title:||Drug Discovery Today|
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