Galphaq-dependent activation of mitogen-activated protein kinase kinase 4/c-Jun N-terminal kinase cascade.
Biochem Biophys Res Commun
; 288(5): 1087-94, 2001 Nov 16.
Article
em En
| MEDLINE
| ID: mdl-11700022
G-protein-coupled receptors (GPCRs) typically activate c-Jun N-terminal kinase (JNK) through the G protein betagamma subunit (Gbetagamma), in a manner dependent on Rho family small GTPases, in mammalian cells. Here we show that JNK activation by the prototypic Gq-coupled alpha1B-adrenergic receptor is mediated by the alpha subunit of Gq (Galphaq), not by Gbetagamma, using a transient transfection system in human embryonic kidney cells. JNK activation by the alpha1B-adrenergic receptor/Galphaq was selectively mediated by mitogen-activated protein kinase kinase 4 (MKK4), but not MKK7. Also, MKK4 activation by the alpha1B-adrenergic receptor/Galphaq required c-Src and Rho family small GTPases. Furthermore, activation of the alpha1B-adrenergic receptor stimulated JNK activity through Src family tyrosine kinases and Rho family small GTPases in hamster smooth muscle cells that natively express the alpha1B-adrenergic receptor. Together, these results suggest that the alpha1B-adrenergic receptor/Galphaq may up-regulate JNK activity through a MKK4 pathway dependent on c-Src and Rho family small GTPases in mammalian cells.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteínas Heterotriméricas de Ligação ao GTP
/
Quinases de Proteína Quinase Ativadas por Mitógeno
/
Proteínas Quinases Ativadas por Mitógeno
/
Sistema de Sinalização das MAP Quinases
/
Subunidades beta da Proteína de Ligação ao GTP
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Subunidades gama da Proteína de Ligação ao GTP
/
MAP Quinase Quinase 4
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Biochem Biophys Res Commun
Ano de publicação:
2001
Tipo de documento:
Article
País de afiliação:
Japão
País de publicação:
Estados Unidos