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Modo dual de la transducción de la señal por el factor de crecimiento de los fibroblastos ácidos añadido externamente
A Wiedłocha1, P O Falnes, I H Madshus
1Institute for Cancer Research, Norwegian Radium Hospital, Montebello, Oslo.
Cell
|March 25, 1994
Resumen
La proteína de fusión del factor de crecimiento de los fibroblastos ácidos (aFGF) estimuló la síntesis de ADN en células que carecían de receptores aFGF. La entrada en el núcleo celular fue crucial para que aFGF promoviera la síntesis de ADN, lo que indica vías de señalización duales.
Área de la Ciencia:
- Biología celular Biología celular.
- Biología Molecular Biología Molecular
- La bioquímica es la bioquímica.
Sus antecedentes:
- El factor de crecimiento de fibroblastos ácidos (aFGF) es un regulador clave de la proliferación celular y la supervivencia.
- La toxina de difteria (DT) es una toxina potente que entra en las células a través de la endocitosis mediada por receptores.
- Comprender las vías de señalización del factor de crecimiento es crucial para desarrollar terapias dirigidas.
Objetivo del estudio:
- Investigar los mecanismos de señalización de aFGF, en particular el papel de los receptores de superficie celular frente al transporte intracelular.
- Para determinar si una proteína de fusión de aFGF y DT podría eludir los requisitos de receptores de superficie celular para la señalización.
- Para aclarar la contribución de la translocación nuclear a la síntesis de ADN mediada por el FGF.
Principales métodos:
- Construcción y aplicación de una proteína de fusión de toxina de difteria aFGF.
- Utilizando líneas celulares resistentes a toxinas y deficientes en el receptor aFGF (NIH 3T3).
- Evaluación de la síntesis de ADN y la fosforilación de tirosina en respuesta al aFGF y la proteína de fusión.
Principales resultados:
- La proteína de fusión aFGF-DT estimuló la síntesis de ADN en células que carecían de receptores aFGF funcionales pero que poseían receptores DT.
- En las células 3T3 de NIH (que carecen de receptores DT pero tienen receptores aFGF), tanto aFGF como la proteína de fusión indujeron la fosforilación de tirosina.
- Solo el aFGF nativo, no la proteína de fusión, se translocó al núcleo y estimuló la síntesis de ADN en las células NIH 3T3.
Conclusiones:
- La señalización celular por aFGF involucra tanto las vías mediadas por el receptor de la superficie celular como el transporte intracelular.
- La entrada nuclear de aFGF es esencial para estimular la síntesis de ADN.
- El estudio pone de relieve los complejos mecanismos que rigen la señalización del factor de crecimiento y la respuesta celular.
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