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γCaMKII transporta Ca2+/CaM al núcleo para desencadenar la fosforilación de CREB y la expresión génica

Huan Ma¹, Rachel D Groth², Samuel M Cohen¹

¹Department of Neuroscience and Physiology, Neuroscience Institute, NYU Langone Medical Center, New York, NY 10016, USA.

|October 11, 2014

Resumen

Los investigadores descubrieron una nueva vía celular para la comunicación neuronal a larga distancia. Una proteína lanzadera transporta señales de calcio al núcleo, cruciales para la plasticidad neuronal e implicadas en trastornos neuropsiquiátricos.

Área de la Ciencia:

La neurociencia es la neurociencia.
Biología Molecular Biología Molecular
La señalización celular de las células.

Sus antecedentes:

La fosforilación CREB dependiente de la actividad es vital para la plasticidad neuronal a largo plazo.
La señalización local en los canales CaV1 inicia estos eventos, pero los mecanismos de transporte nuclear no están claros.

Objetivo del estudio:

Para dilucidar el mecanismo de la comunicación intracelular de larga distancia para la plasticidad neuronal.
Para identificar la proteína de transporte responsable del transporte de Ca2+/calmodulina (CaM) hacia el núcleo.

Principales métodos:

Investigó el transporte de Ca2+/CaM utilizando ensayos bioquímicos y imágenes celulares.
Se examinaron las funciones de gamma-CaMKII (γCaMKII), beta-CaMKII (βCaMKII) y calcineurina (CaN) en la vía de señalización.

Principales resultados:

Identificó γCaMKII como la proteína de transporte para Ca2+/CaM desde la superficie celular hasta el núcleo.
Se demostró que βCaMKII fosforila γCaMKII, protegiendo la señal Ca2+/CaM, y CaN desencadena su translocación nuclear.
Se ha demostrado que el Ca2+/CaM nuclear activa el CaMKK y el CaMKIV, lo que lleva a la fosforilación del CREB.

Conclusiones:

Un nuevo mecanismo que involucra a γCaMKII como una lanzadera Ca(2+) / CaM resuelve las vías de señalización al núcleo.
Esta vía es crítica para la plasticidad neuronal y su desregulación está relacionada con trastornos neuropsiquiátricos.

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