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Cell Cycle ; 23(4): 339-352, 2024 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-38557443

RESUMEN

REV7 is an abundant, multifunctional protein that is a known factor in cell cycle regulation and in several key DNA repair pathways including Trans-Lesion Synthesis (TLS), the Fanconi Anemia (FA) pathway, and DNA Double-Strand Break (DSB) repair pathway choice. Thus far, no direct role has been studied for REV7 in the DNA damage response (DDR) signaling pathway. Here we describe a novel function for REV7 in DSB-induced p53 signaling. We show that REV7 binds directly to p53 to block ATM-dependent p53 Ser15 phosphorylation. We also report that REV7 is involved in the destabilization of p53. These findings affirm REV7's participation in fundamental cell cycle and DNA repair pathways. Furthermore, they highlight REV7 as a critical factor for the integration of multiple processes that determine viability and genome stability.


Asunto(s)
Proteínas de la Ataxia Telangiectasia Mutada , Daño del ADN , Transducción de Señal , Proteína p53 Supresora de Tumor , Proteínas de la Ataxia Telangiectasia Mutada/metabolismo , Proteína p53 Supresora de Tumor/metabolismo , Proteína p53 Supresora de Tumor/genética , Humanos , Fosforilación , Roturas del ADN de Doble Cadena , Unión Proteica , Reparación del ADN , Proteínas de Unión al ADN/metabolismo , Proteínas de Unión al ADN/genética , Línea Celular Tumoral
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