Por favor, use este identificador para citar o enlazar este ítem: DOI: 10.14670/HH-11-820

Título: Dock3-NMDA receptor interaction as a target for glaucoma therapy
Fecha de publicación: 2017
Editorial: Universidad de Murcia. Departamento de Biología Celular e Histología
Cita bibliográfica: Histology and Histopathology, Vol.32, nº3, (2017)
ISSN: 1699-5848
0213-3911
Materias relacionadas: CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología
Palabras clave: Dock3
GluN2B
Glutamate neurotoxicity
Neuroprotection
Glaucoma
Resumen: y. Glaucoma is a neurodegenerative disease of the eye and it is one of the major causes of blindness. Glaucoma is usually associated with elevated intraocular pressure (IOP) and the current therapy focuses on reduction of IOP. However, neuroprotective strategies could also be beneficial for treatment of glaucoma because the pathology of the disease involves retinal ganglion cell (RGC) death and damage to the optic nerve. Dedicator of cytokinesis 3 (Dock3) is an atypical guanine exchange factor (GEF) that belongs to a family of Dock proteins, Dock1-11. Dock3 exerts neuroprotective effects on the retina and optic nerve, and studies revealed that some of the Dock3-mediated effects are GEF-independent. One of these mechanisms is that Dock3 directly binds to the GluN2B subunit of the Nmethyl-D-aspartate (NMDA) receptor. Upon stimulation by NMDA or optic nerve crush, overexpression of Dock3 promotes internalization and degradation of the NMDA receptor in the retina in vivo. It is suggested that this process is mediated by inhibition of Fyn, a Src family tyrosine kinase. Reduction in NMDA receptor expression results in decreased excitotoxic damage and oxidative stress, thereby promoting RGC survival. In this review, we discuss the therapeutic potential of neuroprotection for glaucoma and the effects of Dock3 on NMDA receptors. We also discuss apoptosis signalregulating kinase 1 (ASK1), a member of mitogenactivated protein kinase kinase kinase that is a key regulator of cellular responses to oxidative stress, as an innovative therapeutic target for glaucoma.
Autor/es principal/es: Kimura, Atsuko
Namekata, Kazuhiko
Guo, Xiaoli
Harada, Chikako
Harada, Takayuki
URI: http://hdl.handle.net/10201/117025
DOI: DOI: 10.14670/HH-11-820
Tipo de documento: info:eu-repo/semantics/article
Número páginas / Extensión: 7
Derechos: info:eu-repo/semantics/openAccess
Attribution-NonCommercial-NoDerivatives 4.0 Internacional
Aparece en las colecciones:Vol.32, nº3 (2017)

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