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Analysis of Cell Cycle Position in Mammalian Cells
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Fosforilación de la proteína del retinoblastoma por una proteína viral con función de quinasa dependiente de la
Adam J Hume1, Jonathan S Finkel, Jeremy P Kamil
1Institute for Molecular Virology and McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI 53706, USA.
Science (New York, N.Y.)
|May 10, 2008
Resumen
La proteína del citomegalovirus humano UL97 imita las cinasas dependientes de ciclina (CDK) celulares mediante la fosforilación de los reguladores clave del ciclo celular. Esta proteína viral impulsa la progresión del ciclo celular y elude la inhibición normal de la CDK, ayudando a la replicación viral.
Área de la Ciencia:
- Virología Virología.
- Biología celular Biología celular.
- Biología Molecular Biología Molecular
Sus antecedentes:
- Los virus son parásitos intracelulares obligados que manipulan los procesos celulares del huésped para la replicación.
- Las proteínas virales pueden imitar las funciones celulares, a menudo carecen de características reguladoras normales.
- El citomegalovirus humano (HCMV) es un patógeno humano significativo.
Objetivo del estudio:
- Para investigar las actividades enzimáticas de la proteína HCMV UL97.
- Para determinar si UL97 posee funciones similares a las de los complejos celulares de cinasa dependiente de ciclina (CDK).
- Para entender cómo UL97 interactúa con la regulación del ciclo celular huésped.
Principales métodos:
- Evaluación de la actividad de fosforilación de UL97 en el supresor de tumores del retinoblastoma.
- Evaluar la capacidad de UL97 para estimular la progresión del ciclo celular en células de mamíferos.
- Prueba de la capacidad de UL97 para rescatar la proliferación en levaduras que carecen de actividad CDK.
- Analizando UL97 para los residuos de CDK conservados y la inhibición por p21.
Principales resultados:
- UL97 fosforilado e inactivado el supresor del tumor del retinoblastoma.
- UL97 estimuló la progresión del ciclo celular en las células de mamíferos.
- UL97 rescató la proliferación en Saccharomyces cerevisiae que carece de actividad CDK.
- UL97 no fue inhibido por el inhibidor de CDK p21 y carecía de residuos reguladores clave que se encuentran en las CDK.
Conclusiones:
- La proteína HCMV UL97 funciona como una cinasa dependiente de la ciclina viral (CDK).
- UL97 posee actividad de kinasa similar a la CDK, impulsando la progresión del ciclo celular del huésped.
- UL97 es resistente a los mecanismos de control de las CDK celulares, incluida la inhibición de p21, lo que facilita la replicación viral.
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