The oncogenicity of tumor-derived mutant p53 is enhanced by the recruitment of PLK3

The mechanisms of how gain-of-function (GOF) mutant p53 drives carcinogenesis are unclear. Here, the authors show that a GOF mutant p53 requires its transactivation capability to induce mouse lung tumors and this is dependent on PLK3 phosphorylation of GOF mutant p53.

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Detalles Bibliográficos
Autores principales: Catherine A. Vaughan, Shilpa Singh, Mark A. Subler, Jolene J. Windle, Kazushi Inoue, Elizabeth A. Fry, Raghavendra Pillappa, Steven R. Grossman, Brad Windle, W. Andrew Yeudall, Swati Palit Deb, Sumitra Deb
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/54a056e3c31c4f638609e87d39e9e921
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Sumario:The mechanisms of how gain-of-function (GOF) mutant p53 drives carcinogenesis are unclear. Here, the authors show that a GOF mutant p53 requires its transactivation capability to induce mouse lung tumors and this is dependent on PLK3 phosphorylation of GOF mutant p53.