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BAD y glucokinasa residen en un complejo mitocondrial que integra la glucólisis y la apoptosis
Nika N Danial1, Colette F Gramm, Luca Scorrano
1Howard Hughes Medical Institute, Dana-Faber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.
Nature
|August 22, 2003
Resumen
El estudio revela que BAD, una proteína que regula la muerte celular, también juega un papel crucial en el metabolismo de la glucosa al formar un complejo con la glucokinasa en las mitocondrias. Este hallazgo vincula las vías de apoptosis y glucólisis.
Área de la Ciencia:
- Biología celular Biología celular.
- Las vías metabólicas.
- La función mitocondrial es la función mitocondrial.
Sus antecedentes:
- La glicólisis y la apoptosis son críticas para la supervivencia celular, pero generalmente se consideran vías independientes.
- BAD, una proteína pro-apoptótica, está regulada por la fosforilación en respuesta a los factores de crecimiento.
Objetivo del estudio:
- Para investigar el papel potencial de BAD en la fisiología mitocondrial.
- Para explorar la integración de BAD en las vías metabólicas.
Principales métodos:
- Análisis proteómico de las mitocondrias hepáticas.
- Estudios genéticos con hepatocitos deficientes y ratones.
- Evaluación de la respiración mitocondrial y la homeostasis de la glucosa.
Principales resultados:
- BAD forma un complejo holoenzimático en las mitocondrias con la proteína quinasa A, la proteína fosfatasa 1, WAVE-1 y la glucoquinasa.
- Una deficiencia grave interrumpe este complejo, deteriorando la actividad de la glucokinasa basada en las mitocondrias y la respiración inducida por la glucosa.
- El estado de fosforilación de BAD regula la actividad de la glucokinasa, y su ausencia o mutación no fosforilable causa intolerancia a la glucosa.
Conclusiones:
- BAD integra el metabolismo de la glucosa y las vías de la apoptosis.
- BAD juega un papel inesperado en la regulación de la actividad mitocondrial de la glucokinasa y la homeostasis de la glucosa.
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