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BAX y BAK proapoptóticos: una puerta de entrada necesaria para la disfunción mitocondrial y la muerte
1Howard Hughes Medical Institute, Departments of Pathology and Medicine, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
Science (New York, N.Y.)
|April 28, 2001
Resumen
La activación de las proteínas BAX o BAK es esencial para iniciar la disfunción mitocondrial y la muerte celular. Las células que carecen de BAX y BAK resisten múltiples estímulos apoptóticos, destacando su papel crítico en la apoptosis.
Área de la Ciencia:
- Biología celular Biología celular.
- Biología Molecular Biología Molecular
- La bioquímica es la bioquímica.
Sus antecedentes:
- La disfunción mitocondrial es un evento clave en la apoptosis, pero el desencadenante inicial sigue sin estar claro.
- La proteína tBID solo BH3 activa el BAX o BAK proapoptótico, lo que lleva a la liberación del citocromo c.
- El papel preciso de BAX y BAK en el inicio de la apoptosis mitocondrial in vivo no se entiende completamente.
Objetivo del estudio:
- Para determinar el evento inicial crítico para la disfunción mitocondrial durante la apoptosis.
- Investigar el papel esencial de BAX y BAK en la apoptosis inducida por tBID y otros estímulos de muerte.
- Para dilucidar el mecanismo de entrada para la permeabilización de la membrana externa mitocondrial.
Principales métodos:
- Utilizó modelos de células knockout que carecen de Bax y / o Bak.
- Inducción de la apoptosis utilizando varios estímulos, incluidos tBID, estaurosporina, radiación UV y agentes de estrés ER.
- Evaluar la liberación del citocromo c y la viabilidad celular para medir la apoptosis.
Principales resultados:
- Las células que carecían tanto de Bax como de Bak eran completamente resistentes a la liberación del citocromo c inducida por tBID y a la apoptosis.
- Las células doblemente deficientes mostraron resistencia a múltiples estímulos apoptóticos, incluidas la estaurosporina, los rayos UV, la privación del factor de crecimiento, la etoposida, la tapsigargina y la tunicamicina.
- Una sola deficiencia en Bax o Bak no confería una resistencia completa.
Conclusiones:
- La activación de BAX o BAK es una puerta esencial para la disfunción mitocondrial en la apoptosis.
- BAX y BAK actúan como un punto de convergencia crítico para diversos estímulos apoptóticos que conducen a la muerte celular.
- Estos hallazgos aclaran el papel central de BAX/BAK en el inicio de la apoptosis mitocondrial in vivo.
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