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La modificación redox de la actina nuclear por MICAL-2 regula la señalización de las SRF

Mark R Lundquist¹, Andrew J Storaska², Ting-Chun Liu³

¹Department of Pharmacology, Weill Cornell Medical College, Cornell University, New York, NY 10065, USA.

|January 21, 2014

Resumen

MICAL-2 regula el factor de respuesta sérica (SRF) y la transcripción del gen del factor de transcripción A (MRTF-A) relacionado con la miocardina mediante la alteración de los niveles de actina nuclear. Esta proteína se dirige a la despolimerización de la actina nuclear, lo que afecta a la importación nuclear de MRTF-A y a la actividad de SRF/MRTF-A.

Área de la Ciencia:

Biología Molecular Biología Molecular
La señalización celular.
El Reglamento de transcripción.

Sus antecedentes:

El factor de respuesta sérica (SRF) y el factor de transcripción relacionado con la miocardina-A (MRTF-A) forman complejos para mediar la transcripción génica en respuesta a las vías de señalización.
Los niveles nucleares de MRTF-A dictan la formación del complejo SRF/MRTF-A y la actividad transcripcional.
La G-actina nuclear regula la exportación nuclear de MRTF-A, pero las vías que controlan la actina nuclear aún no están claras.

Objetivo del estudio:

Investigar el papel de MICAL-2 en la regulación de la transcripción génica dependiente de SRF/MRTF-A.
Para aclarar el mecanismo por el cual MICAL-2 influye en la dinámica de la actina nuclear.
Para identificar MICAL-2 como un objetivo potencial para la intervención terapéutica.

Principales métodos:

Investigó el efecto de MICAL-2 en la transcripción dependiente de SRF/MRTF-A inducida por el factor de crecimiento nervioso y el suero.
Se evaluó el impacto de MICAL-2 en la polimerización y despolimerización de la actina nuclear.
Examinó la relación entre MICAL-2 y el inhibidor de molécula pequeña CCG-1423.3.

Principales resultados:

MICAL-2 media en la transcripción de genes dependientes de SRF/MRTF-A.
MICAL-2 induce la despolimerización redox-dependiente de la actina nuclear, reduciendo así la G-actina nuclear.
La reducción de la G-actina nuclear conduce a un aumento del MRTF-A nuclear y a una mayor formación de complejos SRF/MRTF-A.
MICAL-2 ha sido identificado como un objetivo del inhibidor de SRF/MRTF-A CCG-1423.3.

Conclusiones:

MICAL-2 actúa como un regulador clave de la transcripción dependiente de SRF/MRTF-A.
La modificación redox de la actina nuclear por MICAL-2 sirve como un interruptor regulador para la actividad SRF/MRTF-A.
Estos hallazgos destacan MICAL-2 como un objetivo terapéutico potencial para las enfermedades que implican la desregulación SRF / MRTF-A.

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