PRMT5-dependent p53 escape in tumorigenesis

Extensive studies have characterized mutational disruption of p53 signaling in human cancers. However, the mechanism for bypass of p53 function in tumors retaining wild-type p53 has remained ambiguous. Recent studies suggest that PRMT5, which is frequently elevated in human cancers, cooperates with...

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Detalles Bibliográficos
Autores principales: Li, Yan, Diehl, J. Alan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2015
Materias:
Research Perspective
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4580063/
https://www.ncbi.nlm.nih.gov/pubmed/26425661
Descripción
Sumario:Extensive studies have characterized mutational disruption of p53 signaling in human cancers. However, the mechanism for bypass of p53 function in tumors retaining wild-type p53 has remained ambiguous. Recent studies suggest that PRMT5, which is frequently elevated in human cancers, cooperates with oncogenic cyclin D1 and leaves marks on p53 by way of arginine methylation, promoting the bypass of wild-type p53, and in doing so, evade apoptosis.

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