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Interacción de c-Abl y p73alfa y su colaboración para inducir la apoptosis
1Department of Molecular Genetics, The Weizmann Institute of Science, Rehovot, Israel.
Nature
|July 3, 1999
Resumen
El estudio revela que el supresor tumoral p73alpha requiere la quinasa c-Abl para su función apoptótica. El daño en el ADN activa esta vía de señalización pro-apoptótica p73 y c-Abl.
Área de la Ciencia:
- Biología Molecular Biología Molecular
- Biología celular Biología celular.
- Oncología Oncología.
Sus antecedentes:
- c-Abl (una tirosina quinasa no receptora) se activa por el daño del ADN, lo que lleva a la detención del ciclo celular o la apoptosis.
- p73, un supresor de tumores de la familia p53, también induce la apoptosis.
Objetivo del estudio:
- Para investigar la relación entre p73 y c-Abl en la apoptosis.
- Para dilucidar el mecanismo de la apoptosis mediada por p73.
Principales métodos:
- Investigó la interacción entre p73 y c-Abl.
- Evaluó la actividad de la quinasa de c-Abl en p73.
- Utilizamos la irradiación gamma para inducir daño en el ADN y observar cambios en la fosforilación.
Principales resultados:
- La actividad apoptótica de p73alpha es dependiente del c-Abl.competente funcional y con kinasa.
- p73 y c-Abl se asocian a través de un motivo PxxP en p73 y el dominio SH3 de c-Abl.
- c-Abl fosforilados p73, con un aumento de la fosforilación observada después de la irradiación gamma e in vivo.
Conclusiones:
- Se define una nueva vía de señalización pro-apoptótica que involucra a p73 y c-Abl.
- La actividad de la c-Abl quinasa es crucial para la apoptosis mediada por p73.
- La radiación ionizante mejora la fosforilación de p73 por c-Abl.
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