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Post-translational Regulation of GLT-1 in Neurological Diseases and Its Potential as an Effective Therapeutic Target

Glutamate transporter-1 (GLT-1) is a Na(+)-dependent transporter that plays a key role in glutamate homeostasis by removing excess glutamate in the central nervous system (CNS). GLT-1 dysregulation occurs in various neurological diseases including Huntington’s disease (HD), Alzheimer’s disease (AD),...

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Detalles Bibliográficos
Autores principales: Peterson, Allison R., Binder, Devin K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6629900/
https://www.ncbi.nlm.nih.gov/pubmed/31338020
http://dx.doi.org/10.3389/fnmol.2019.00164
Descripción
Sumario:Glutamate transporter-1 (GLT-1) is a Na(+)-dependent transporter that plays a key role in glutamate homeostasis by removing excess glutamate in the central nervous system (CNS). GLT-1 dysregulation occurs in various neurological diseases including Huntington’s disease (HD), Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and epilepsy. Downregulation or dysfunction of GLT-1 has been a common finding across these diseases but how this occurs is still under investigation. This review aims to highlight post-translational regulation of GLT-1 which leads to its downregulation including sumoylation, palmitoylation, nitrosylation, ubiquitination, and subcellular localization. Various therapeutic interventions to restore GLT-1, their proposed mechanism of action and functional effects will be examined as potential treatments to attenuate the neurological symptoms associated with loss or downregulation of GLT-1.