Article
Protein mimetic amyloid inhibitor potently abrogates cancer-associated mutant p53 aggregation and restores tumor suppressor function.
Nature communications - 25 Jun 2021
Palanikumar L, Karpauskaite Laura, Al-Sayegh Mohamed, Chehade Ibrahim, Alam Maheen, Hassan Sarah, Maity Debabrata, Ali Liaqat, Kalmouni Mona, Hunashal Yamanappa, Ahmed Jemil, Houhou Tatiana, Karapetyan Shake, Falls Zackary, Samudrala Ram, Pasricha Renu, Esposito Gennaro, Afzal Ahmed J, Hamilton Andrew D, Kumar Sunil, Magzoub Mazin
Abstract excerpt
Missense mutations in p53 are severely deleterious and occur in over 50% of all human cancers. The majority of these mutations are located in the inherently unstable DNA-binding domain (DBD), many of which destabilize the domain further and expose its aggregation-prone hydrophobic core, prompting self-assembly of mutant p53 into inactive cytosolic amyloid-like aggregates. Screening an oligopyridylamide library,...
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