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Oligopeptide Competition Assay for Phosphorylation Site Determination
Published on: May 18, 2017
El éster de forbol y el diacilglicerol inducen la fosforilación de proteínas en la tirosina
Nature
|December 1, 1983
Resumen
El promotor tumoral 12-O-tetradecanoil-forbol-13-acetato (TPA) activa la proteína quinasa C. El TPA también induce la fosforilación de tirosina de una proteína 42K, lo que sugiere un papel en el TPA.
Área de la Ciencia:
- Biología celular Biología celular.
- La bioquímica es la bioquímica.
- Oncología Oncología.
Sus antecedentes:
- El 12-O-tetradecanoil-forbol-13-acetato (TPA) es un potente promotor de tumores in vivo.
- El TPA activa la proteína quinasa C (PKC) in vitro, imitando la acción del diacilglicerol.
- La PKC fosforila los sustratos en los residuos de serina y treonina.
Objetivo del estudio:
- Investigar el mecanismo de los efectos del TPA en los fibroblastos cultivados.
- Para determinar si el TPA media sus efectos a través de la fosforilación de la tirosina.
- Para examinar el estado de fosforilación de un polipéptido 42K específico en respuesta al TPA.
Principales métodos:
- Tratamiento de fibroblastos cultivados con TPA.
- Análisis de la fosforilación de proteínas en los residuos de tirosina.
- Investigación del efecto del diacilglicerol agregado de forma exógena.
Principales resultados:
- El tratamiento con TPA conduce a un aumento de la fosforilación de tirosina de un polipéptido de un peso molecular de 42.000 (42K).
- Este polipéptido de 42K también se fosforila en tirosina en respuesta a factores de crecimiento como EGF, PDGF y MSA.
- El diacilglicerol agregado exógenamente también estimula la fosforilación de tirosina de esta proteína 42K.
Conclusiones:
- Los efectos promotores de tumores del TPA pueden implicar la inducción de la fosforilación de la tirosina.
- El polipéptido 42K es un sustrato común para la fosforilación de tirosina inducida por TPA, factores de crecimiento y diacilglicerol.
- Este hallazgo vincula la activación de PKC inducida por TPA con las vías de señalización de la tirosina quinasa.
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