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Enlace de ATM con la regulación del ciclo celular por la proteína kinasa Chk2
S Matsuoka1, M Huang, S J Elledge
1Howard Hughes Medical Institute, Verna and Marrs McLean Department of Biochemistry, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Science (New York, N.Y.)
|December 4, 1998
Resumen
La quinasa del punto de control 2 (Chk2) se activa por el daño del ADN y el estrés de replicación, funcionando en la regulación del ciclo celular. Se fosforila Cdc25C, evitando potencialmente la entrada de la mitosis, similar a Chk1.
Área de la Ciencia:
- Biología celular Biología celular.
- Biología Molecular Biología Molecular
- Genética La genética.
Sus antecedentes:
- La progresión del ciclo celular está estrictamente regulada para mantener la estabilidad genómica.
- Los daños en el ADN y los bloqueos de replicación desencadenan puntos de control para evitar la división celular.
- Los reguladores clave controlan la progresión del ciclo celular en respuesta al estrés celular.
Objetivo del estudio:
- Identificar y caracterizar Chk2, una nueva proteína quinasa involucrada en el daño del ADN y puntos de control de replicación.
- Investigar el mecanismo de activación y los objetivos aguas abajo de Chk2.
Principales métodos:
- Identificación de Chk2 como un homólogo de las quinasas de punto de control de levadura.
- Análisis de la fosforilación y activación de Chk2 en respuesta a daños en el ADN y bloqueos de replicación.
- Ensayos de quinasa in vitro para determinar la especificidad del sustrato de Chk2.
Principales resultados:
- Chk2 fue rápidamente fosforilada y activada por los bloqueos de replicación y el daño al ADN.
- La activación de Chk2 por daño en el ADN depende de la ataxia telangiectasia mutada (ATM).
- Chk2 fosforila Cdc25C en la serina-216, un sitio inhibidor conocido.
Conclusiones:
- Chk2 es un componente crítico del daño del ADN de los mamíferos y las vías de los puntos de control de replicación.
- La activación de Chk2 conduce a la fosforilación de Cdc25C, lo que contribuye a la detención del ciclo celular.
- Chk1 y Chk2 pueden cooperar para regular Cdc25C y prevenir la entrada mitótica bajo condiciones de estrés.
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