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El receptor del factor de crecimiento epidérmico está regulado a la baja por una proteína de 10.400 MW codificada por
C R Carlin1, A E Tollefson, H A Brady
1Institute for Molecular Virology, St. Louis University Medical Center, Missouri 63110.
Cell
|April 7, 1989
Resumen
Los adenovirus humanos regulan a la baja los receptores del factor de crecimiento epidérmico (EGF-R) durante la infección. Una proteína viral específica induce la internalización y degradación del EGF-R, lo que sugiere un nuevo mecanismo de interacción.
Área de la Ciencia:
- Biología celular Biología celular.
- Virología Virología.
- Biología Molecular Biología Molecular
Sus antecedentes:
- La señalización del factor de crecimiento epidérmico (EGF) implica la internalización del receptor (EGF-R) y la degradación lisosómica.
- Las infecciones virales pueden modular los procesos de las células huésped, incluido el tráfico de receptores.
Objetivo del estudio:
- Investigar el mecanismo de regulación a la baja del receptor del factor de crecimiento epidérmico (EGF-R) durante la infección por adenovirus humano.
- Para identificar el gen viral responsable de la modulación del EGF-R.
Principales métodos:
- Utilizó mutantes de deleción de los adenovirus humanos del grupo C.
- Analizó el efecto de los productos genéticos virales en los niveles de FEAG-R y el tráfico.
- Se realizó un análisis de homología de secuencia entre la proteína viral y el EGF-R.
Principales resultados:
- Los adenovirus humanos del grupo C inducen una regulación a la baja del EGF-R en las células infectadas.
- La unidad de transcripción E3 codifica una proteína 10.4K responsable de la internalización y degradación del EGF-R.
- La proteína 10.4K comparte similitud de secuencia con EGF-R, lo que sugiere la formación de heterooligómeros.
Conclusiones:
- Un nuevo mecanismo para la regulación a la baja del EGF-R durante la infección por adenovirus implica una proteína viral E3.
- La proteína viral 10.4K probablemente interactúa con el EGF-R para mediar su degradación.
- Esta interacción puede implicar la formación de heterooligómeros entre la proteína viral y el receptor huésped.
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