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Mecanismos de sinergia transcripcional entre distintos elementos potenciadores inducibles por el virus
1Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, Massachusetts 02138.
Cell
|September 10, 1993
Resumen
La proteína del grupo de alta movilidad HMG I(Y) es crucial para la regulación del gen de interferón-beta. Mejora la actividad de los elementos inducibles al virus PRDII y PRDIV facilitando las interacciones entre los factores de transcripción NF-kappa B y activando el factor de transcripción 2 (ATF-2).
Área de la Ciencia:
- Biología Molecular Biología Molecular
- Regulación genética Reglamento genético.
- Inmunología Inmunología.
Sus antecedentes:
- El promotor del gen interferón-beta humano contiene elementos reguladores inducibles por el virus.
- La actividad del dominio regulador positivo II (PRDII) requiere la proteína del grupo de alta movilidad HMG I(Y) y el factor de transcripción NF-kappa B.
Objetivo del estudio:
- Investigar el papel de HMG I(Y) en la actividad de PRDIV, un elemento regulador que tiene sinergias con PRDII.
- Para aclarar los mecanismos moleculares por los cuales HMG I(Y) contribuye a la sinergia transcripcional.
Principales métodos:
- Ensayos de desplazamiento de movilidad electroforética (EMSA) para estudiar las interacciones proteína-ADN.
- Los ensayos de coinmunoprecipitación analizan las interacciones proteína-proteína.
- Análisis de la actividad del elemento regulador en respuesta a la inducción viral.
Principales resultados:
- HMG I(Y) es esencial para la actividad PRDIV, trabajando en sinergia con PRDII.
- HMG I(Y) promueve la unión del factor de transcripción activador 2 (ATF-2) y el ensamblaje de complejos inducibles que contienen ATF-2 y c-Jun.
- HMG I(Y) interactúa directamente con el cierre de la leucina / región básica de ATF-2, y ATF-2 interactúa con NF-kappa B.
Conclusiones:
- HMG I(Y) juega un papel estructural crítico en el establecimiento de la sinergia transcripcional entre PRDII y PRDIV.
- HMG I(Y) facilita la interacción entre NF-kappa B y ATF-2, promoviendo así sus actividades y/o vinculando.
- Este mecanismo es vital para la expresión inducible por el virus del gen del interferón beta.
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