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p73 está regulado por la tirosina quinasa c-Abl en la respuesta apoptótica al daño del ADN

Z M Yuan¹, H Shioya, T Ishiko

¹Department of Cancer Cell Biology, Harvard School of Public Health, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA.

|July 3, 1999

Resumen

La tirosina quinasa c-Abl se une y fosforila la proteína p73, estimulando su papel en la apoptosis. Esta interacción es crucial para la muerte celular inducida por daño al ADN, destacando una nueva vía reguladora para p73.

Área de la Ciencia:

Biología Molecular Biología Molecular
Biología celular Biología celular.
Oncología Oncología.

Sus antecedentes:

p73 es un homólogo del supresor tumoral p53, pero no es inducido por daño al ADN.
La tirosina quinasa c-Abl se activa por el daño del ADN y promueve la apoptosis a través de vías p53-dependientes e independientes.

Objetivo del estudio:

Investigar la interacción entre c-Abl y p73.
Para determinar si c-Abl regula la actividad de p73 en respuesta al daño del ADN.

Principales métodos:

Co-inmunoprecipitación para detectar la unión c-Abl/p73 en las células.
Ensayos de fosforilación in vitro y en células utilizando radiación ionizante.
Ases para medir la transactivación mediada por p73 y la apoptosis.

Principales resultados:

c-Abl se une a p73 a través de su dominio SH3 y el dominio carboxiterminal de p73.
c-Abl fosforila p73 en la tirosina 99 en respuesta a la radiación ionizante.
c-Abl mejora la transactivación mediada por p73 y la apoptosis.
La interrupción de la interacción c-Abl-p73 perjudica la apoptosis inducida por la radiación ionizante.

Conclusiones:

p73 está regulado por un mecanismo dependiente de c-Abl.
p73 juega un papel en la respuesta apoptótica al daño del ADN.
La interacción c-Abl-p73 es crítica para la apoptosis inducida por daño al ADN.

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