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Papel de la PP2A/B56delta fosfatasa en la regulación de la liberación de 14-3-3 de Cdc25 para controlar la mitosis
Seth S Margolis1, Jennifer A Perry, Craig M Forester
1Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA.
Cell
|November 18, 2006
Resumen
Los puntos de control del daño en el ADN regulan la división celular mediante el control del activador mitótico Cdc25. Este estudio revela cómo las interacciones de la PP2A/B56delta fosfatasa y la proteína 14-3-3 activan Cdc25 para promover la progresión del ciclo celular.
Área de la Ciencia:
- Biología celular Biología celular.
- Biología Molecular Biología Molecular
- La bioquímica es la bioquímica.
Sus antecedentes:
- Los puntos de control de respuesta al ADN son cruciales para prevenir la progresión del ciclo celular después del daño del ADN.
- El activador mitótico Cdc25 está regulado por la fosforilación inhibidora y la unión a la proteína 14-3-3.
- La entrada mitótica requiere la eliminación de las proteínas 14-3-3 y la desfosforilación de Cdc25 en Ser287.
Objetivo del estudio:
- Investigar el papel de la PP2A/B56delta fosfatasa en el control del punto de control de respuesta al ADN de Cdc25.
- Para dilucidar el mecanismo por el cual Cdc25 se activa para promover la entrada mitótica.
Principales métodos:
- Investigó la desfosforilación de Cdc25 por el PP2A/B56delta.
- Se analizó el papel de la fosforilación de T138 en la unión 14-3-3 a Cdc25.
- Examinó la formación de "sumideros" 14-3-3 utilizando proteínas de filamento intermedias.
Principales resultados:
- Los puntos de control que responden al ADN activan PP2A/B56delta para desfosforilar Cdc25 en T138, distinto de Ser287.
- La fosforilación T138 es necesaria pero no suficiente para la liberación 14-3-3 de Cdc25.
- Un "sumidero" 14-3-3 formado por proteínas de filamento intermedias y una afinidad reducida Cdc25-14-3-3 contribuyen a la activación de Cdc25.
Conclusiones:
- PP2A/B56delta es un efector clave de los puntos de control de respuesta al ADN en la regulación de Cdc25.
- Un nuevo mecanismo que involucra "sumideros" 14-3-3 y una afinidad proteica alterada controla la activación de Cdc25 y la entrada mitótica.
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