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Smad3 y Smad4 cooperan con c-Jun/c-Fos para mediar la transcripción inducida por TGF-beta
1Department of Growth and Development, Program in Cell Biology, University of California at San Francisco, 94143-0640, USA.
Nature
|September 11, 1998
Resumen
Las proteínas Smad3 y Smad4 activan la transcripción génica a través de los sitios de unión AP1, interactuando con los factores Smad y AP-1. Esto revela una convergencia de las vías de señalización Smad y MAPK/JNK.
Área de la Ciencia:
- Biología Molecular Biología Molecular
- La señalización celular de las células.
- Regulación genética Reglamento genético.
Sus antecedentes:
- Las proteínas Smad median la señalización transformadora del factor de crecimiento beta (TGF-beta).
- La señalización de TGF-beta regula la transcripción génica a través de los complejos Smad.
- Los factores de transcripción AP-1 (c-Jun, c-Fos) se unen a los elementos sensibles al TPA (TREs).
Objetivo del estudio:
- Para investigar la interacción de las proteínas Smad con las TREs.
- Para determinar si las proteínas Smad pueden activar la transcripción independientemente de los factores AP-1.
- Para dilucidar el mecanismo de la transcripción inducida por TGF-beta que involucra a los factores Smad y AP-1.
Principales métodos:
- Ensayos de interacción directa entre Smad3 y TREs.
- Análisis de la activación de la transcripción inducible por TGF-beta.
- Investigación de las interacciones proteína-proteína (Smad3, Smad4, c-Jun, c-Fos).
Principales resultados:
- Smad3 interactúa directamente con las TREs.
- Smad3 y Smad4 activan la transcripción inducible por TGF-beta de TREs sin c-Jun/c-Fos.
- Smad3 y Smad4 cooperan con c-Jun/c-Fos para la transcripción inducida por TGF-beta a través de nuevas interacciones.
Conclusiones:
- La señalización Smad y la señalización MAPK/JNK convergen en los sitios promotores de unión AP1.
- Las interacciones funcionales y físicas entre Smad3-Smad4 y c-Jun-c-Fos median la activación transcripcional del TGF-beta.
- Este estudio revela un nuevo mecanismo para la expresión génica regulada por TGF-beta.
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