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Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
Published on: October 17, 2015
Complejos precursores de la proteína amiloide de Alzheimer con la proteína GTP-unidora del cerebro G(o)
I Nishimoto1, T Okamoto, Y Matsuura
1Fourth Department of Internal Medicine, University of Tokyo School of Medicine, Japan.
Nature
|March 4, 1993
Resumen
La enfermedad de Alzheimer implica cambios en la proteína precursora amiloide (APP, por sus siglas en inglés). Este estudio revela que la APP actúa como un receptor, formando un complejo con la proteína G, lo que sugiere que la señalización anormal de la APP-G contribuye a la patogénesis de la enfermedad de Alzheimer.
Área de la Ciencia:
- La neurociencia es la neurociencia.
- Biología Molecular Biología Molecular
- La bioquímica es la bioquímica.
Sus antecedentes:
- La enfermedad de Alzheimer se caracteriza por depósitos de proteína beta amiloide / A4, derivados de su proteína precursora (APP).
- Las alteraciones estructurales en la APP están relacionadas con la patogénesis de la enfermedad de Alzheimer, pero los mecanismos subyacentes siguen sin estar claros.
- APP posee una estructura parecida a un receptor, pero su función receptora específica no se ha demostrado previamente.
Objetivo del estudio:
- Para investigar la función potencial del receptor de la APP.
- Para determinar si APP interactúa con las proteínas de señalización conocidas en el cerebro.
- Para aclarar el papel de las interacciones APP-proteína en la enfermedad de Alzheimer.
Principales métodos:
- Investigó la interacción entre APP y las proteínas de unión a GTP en el tejido cerebral.
- Identificó la secuencia específica APP responsable de la formación de complejos proteicos.
- Se evaluó el efecto de GTP-gamma S en la interacción de la proteína APP-G.
Principales resultados:
- La proteína precursora de amiloide (APP) forma un complejo con la proteína de unión al GTP G.
- Una secuencia citoplasmática específica de APP (His 657-Lys 676) media la unión y la activación de G.
- La proteína G ((o), cuando se une a GTP-gamma S, pierde su capacidad de asociarse con APP.
Conclusiones:
- La APP funciona como un receptor acoplado a la proteína G (o).
- La señalización anormal de APP-G está implicada en los procesos patológicos de la enfermedad de Alzheimer.
- Este hallazgo proporciona un nuevo mecanismo molecular para la patogénesis de la enfermedad de Alzheimer.
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