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Over-expression of EphrinA2 in the Anterior Region of the Developing Mouse Midbrain and Diencephalon / 대한해부학회지
Korean Journal of Anatomy ; : 177-186, 2006.
Artigo em Coreano | WPRIM | ID: wpr-647862
ABSTRACT
The Eph family is thought to exert its function through the complementary expression of receptors and ligands. The dorsal mesencephalon appears to be segmented into two broad regions demarcated by the mutually exclusive expression of EphA receptors and ephrinA ligands. In this study, we analyzed transgenic embryos expressing ephrinA2 in the anterior region of the developing midbrain where the EphA8 receptor is expressed. First, 1% of transgenic embryos showed cephalic neural tube closure defects. Second, it was confirmed that mis-expression of ephrin-A2 in the anterior mesencephalon induced an increase in the EphA8 tyrosine kinase activity. Accordingly, an increased MAPK activity was also detected in the anterior mesencephalon of E14.5 transgenic embryo. Third, cell adhesion assay revealed that mis-expression of ephrinA2 promoted cell attachment to fibronectin. Taken together, these findings suggest that co-expression of EphA receptors and ephrinA ligands significantly alter cell behaviors including cell adhesion.
Assuntos

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Proteínas Tirosina Quinases / Mesencéfalo / Camundongos Transgênicos / Adesão Celular / Fibronectinas / Receptores da Família Eph / Receptor EphA8 / Efrina-A2 / Diencéfalo / Estruturas Embrionárias Limite: Animais / Humanos Idioma: Coreano Revista: Korean Journal of Anatomy Ano de publicação: 2006 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Proteínas Tirosina Quinases / Mesencéfalo / Camundongos Transgênicos / Adesão Celular / Fibronectinas / Receptores da Família Eph / Receptor EphA8 / Efrina-A2 / Diencéfalo / Estruturas Embrionárias Limite: Animais / Humanos Idioma: Coreano Revista: Korean Journal of Anatomy Ano de publicação: 2006 Tipo de documento: Artigo