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El Cdc42 activado secuestra c-Cbl y evita la degradación de los receptores del FEAG
Wen Jin Wu1, Shine Tu, Richard A Cerione
1Department of Molecular Medicine, Veterinary Medical Center, Baker Laboratory, Cornell University, Ithaca, NY 14853, USA.
Cell
|September 25, 2003
Resumen
La activación de Cdc42 impide que el receptor EGF se ubiquitine por c-Cbl, un paso clave en la regulación del crecimiento celular. La desregulación conduce a una señalización sostenida y a la transformación celular.
Área de la Ciencia:
- Biología celular Biología celular.
- La señalización molecular.
- Investigación de la investigación del cáncer.
Sus antecedentes:
- Cdc42, una proteína relacionada con Ras, regula el crecimiento celular y está implicada en la transformación celular.
- La señalización del factor de crecimiento epidérmico (EGF) involucra al receptor EGF y la c-Cbl ubiquitin ligasa.
- La regulación aberrante de estas vías puede conducir a una proliferación celular incontrolada.
Objetivo del estudio:
- Investigar el papel de Cdc42 en la regulación de la actividad de los receptores del FEAG.
- Aclarar el mecanismo molecular por el cual Cdc42 influye en la ubiquitinación del receptor EGF.
- Para entender cómo la desregulación del Cdc42 contribuye a la transformación celular.
Principales métodos:
- Investigó la interacción entre Cdc42 activado y p85Cool-1/beta-Pix.
- Se evaluó el efecto de Cdc42 en la unión de c-Cbl al receptor del FEAG.
- Utilizado Cdc42 constitutivamente activo (Cdc42(F28L)) para estudiar los efectos de señalización sostenida.
Principales resultados:
- El Cdc42 activado se une a p85Cool-1/beta-Pix, inhibiendo la ubiquitinación del receptor del EGF por c-Cbl.
- Esta inhibición impide la regulación negativa del receptor del FEA.
- El Cdc42 constitutivamente activo conduce a una señalización sostenida del receptor EGF y la activación de ERK, promoviendo la transformación celular.
Conclusiones:
- Cdc42 juega un papel crítico en el tiempo de las interacciones EGF receptor-c-Cbl.
- Cdc42 actúa como un factor protector para el receptor del FEAG contra la degradación mediada por c-Cbl.
- La alteración de este eje regulador por Cdc42 contribuye a la oncogénesis.
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