Identificación de los mecanismos moleculares que median la función de la proteína Gas1 a través del receptor tirosina quinasa Ret
Author
Cabrera Heredia, Jorge RubénAdvisor
Melstöm, BrittEntity
UAM. Departamento de Biología MolecularDate
2006-06-15Subjects
Proteínas G - Tesis doctorales; Biología y Biomedicina / BiologíaNote
Tesis Doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Ciencias, Departamento de Biología Molecular. Fecha de Lectura : 15-06-2006Abstract
The growth arrest-specific gene 1 (Gasi) protein has been proposed to function during
development as an inhibitor of growth and a mediator of cell death, and is also re-expressed in adult
neurons during excitotoxic insult.
Here we demonstrate that the Gasi protein shows high structural similarity to the GDNF (Glial
celi-derived neurotrophic factor) family receptors <x, which mediate GDNF responses through the
receptor tyrosine kinase Ret. We found that Gasi binds Ret in a ligand-independent manner and
sequesters Ret in lipid rafts.
Signaling downstream of Ret is thus modified through a mechanism that involves the adaptar
protein Shc as well as Erk2, eventually blocking Akt activation. Consequently, when Gasi is induced,
Ret-mediated GDNF-dependent survival effects are compromised.
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Google Scholar:Cabrera Heredia, Jorge Rubén
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