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EphA5 and EphA6: regulation of neuronal and spine morphology.
Das, Gitanjali; Yu, Qili; Hui, Ryan; Reuhl, Kenneth; Gale, Nicholas W; Zhou, Renping.
Afiliación
  • Das G; Susan L. Cullman Laboratory for Cancer Research, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854 USA.
  • Yu Q; Susan L. Cullman Laboratory for Cancer Research, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854 USA.
  • Hui R; Susan L. Cullman Laboratory for Cancer Research, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854 USA.
  • Reuhl K; Department of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854 USA.
  • Gale NW; Regeneron Pharmaceuticals, Inc., Tarrytown, NY 10591 USA.
  • Zhou R; Susan L. Cullman Laboratory for Cancer Research, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854 USA.
Cell Biosci ; 6: 48, 2016.
Article en En | MEDLINE | ID: mdl-27489614
ABSTRACT

BACKGROUND:

The Eph family of receptor tyrosine kinases plays important roles in neural development. Previous studies have implicated Eph receptors and their ligands, the ephrins, in neuronal migration, axon bundling and guidance to specific targets, dendritic spine formation and neural plasticity. However, specific contributions of EphA5 and EphA6 receptors to the regulation of neuronal cell morphology have not been well studied.

RESULTS:

Here we show that deletion of EphA5 and EphA6 results in abnormal Golgi staining patterns of cells in the brain, and abnormal spine morphology.

CONCLUSION:

These observations suggest novel functions of these Eph receptors in the regulation of neuronal and spine structure in brain development and function.
Palabras clave

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Cell Biosci Año: 2016 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Cell Biosci Año: 2016 Tipo del documento: Article
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