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A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3
Published on: January 24, 2016
Requisito para la actividad de la MAP quinasa (ERK2) en la expresión génica estimulada por interferón alfa e
M David1, E Petricoin, C Benjamin
1Division of Cytokine Biology, Center for Biologics Evaluation and Research, Bethesda, MD 20892, USA.
Science (New York, N.Y.)
|September 22, 1995
Resumen
La proteína quinasa activada por mitógeno (MAPK) interactúa con los receptores de interferón, regulando la activación temprana de los genes. Este descubrimiento revela el MAPK.
Área de la Ciencia:
- Inmunología Inmunología.
- Biología Molecular Biología Molecular
- La señalización celular de las células.
Sus antecedentes:
- Los interferones (IFN) activan los genes de respuesta temprana a través de la fosforilación de la proteína STAT.
- Los mecanismos precisos que regulan la señalización IFN requieren una mayor aclaración.
Objetivo del estudio:
- Para investigar el papel de la proteína quinasa activada por mitógeno (MAPK) en la señalización del interferón alfa/beta (IFN-α/β).
- Para determinar si el MAPK modula la vía Jak-STAT en respuesta a las IFN.
Principales métodos:
- Estudios in vitro e in vivo de interacción entre el MAPK (ERK2) y el receptor IFN-α/β.
- Tratamiento celular con IFN-β para evaluar la fosforilación de MAPK y Stat1α y la coinmunoprecipitación.
- Análisis de la transcripción inducida por IFN-β utilizando la expresión de MAPK dominante negativo.
Principales resultados:
- Se encontró que la proteína quinasa activada por mitógeno (MAPK), específicamente ERK2, interactúa con el receptor IFN-α/β.
- El tratamiento con IFN-β indujo la fosforilación de la tirosina y la activación de MAPK.
- MAPK y Stat1α co-inmunoprecipitados después de la estimulación de IFN-β.
- La inhibición de la señalización de MAPK con construcciones dominantes negativas bloqueó la transcripción inducida por IFN-β.
Conclusiones:
- MAPK juega un papel regulador en las vías de señalización de IFN-α e IFN-β.
- MAPK modifica la cascada Jak-STAT, influyendo en la activación de los genes de respuesta temprana por los IFN.
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