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La duración de la acción nuclear de NF-kappaB está regulada por la acetilación reversible
1Gladstone Institute of Virology and Immunology, Department of Medicine, University of California, San Francisco, CA 94141, USA.
Science (New York, N.Y.)
|September 5, 2001
Resumen
La terminación de la actividad del factor nuclear kappa B (NF-kappaB) está controlada por la acetilación y la desacetilación de RelA. La histona desacetilasa 3 (HDAC3) desacetila la RelA, lo que permite su regreso al citoplasma y la reposición de los complejos inhibidores.
Área de la Ciencia:
- Biología Molecular Biología Molecular
- La señalización celular.
- La epigenética es la epigenética.
Sus antecedentes:
- El factor nuclear kappa B (NF-kappaB) es un factor de transcripción crucial que regula las respuestas inmunes e inflamatorias.
- La activación de NF-kappaB requiere fosforilación y degradación de sus inhibidores, las proteínas de IkappaB, que conducen a la translocación nuclear.
- Los mecanismos que ponen fin a la actividad nuclear de NF-kappaB y su secuestro citoplasmático no se comprenden completamente.
Objetivo del estudio:
- Para dilucidar los eventos moleculares que regulan la terminación de la acción nuclear NF-kappaB.
- Investigar el papel de las modificaciones post-traducionales de las subunidades de NF-kappaB en la regulación de su actividad.
- Para identificar las proteínas clave involucradas en la desactivación y la re-secuestro citoplasmático de NF-kappaB.
Principales métodos:
- Estudió la acetilación inducible de la subunidad RelA de NF-kappaB.
- Interacciones investigadas entre RelA acetilado / desacetilado e IkappaBalpha.
- Examinó el papel de la histona desacetilasa 3 (HDAC3) en la desacetilación de RelA.
- Utilizada vía dependiente del mantenimiento de la región cromosómica-1 (CRM-1) para el análisis de exportación nuclear.
Principales resultados:
- Se ha demostrado la acetilación inducible de la subunidad RelA de NF-kappaB.
- Se demostró que la RelA acetilada exhibe una interacción débil con IkappaBalpha.
- Identificó HDAC3 como la enzima responsable de la desacetilación de la RelA.
- Se reveló que la desacetilación mediada por HDAC3 promueve la unión de RelA a IkappaBalpha y la subsiguiente exportación nuclear a través de CRM-1.
Conclusiones:
- La desacetilación de RelA por HDAC3 actúa como un interruptor molecular intranuclear que controla la duración de la respuesta transcripcional de NF-kappaB.
- Este proceso facilita la reposición de los complejos NF-kappaB-IkappaBalpha del citoplasma, restableciendo el NF-kappaB latente.
- Los hallazgos proporcionan información crítica sobre la regulación dinámica de la terminación de la señalización NF-kappaB.
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