NDLI: Combining valosin-containing protein (VCP) inhibition and suberanilohydroxamic acid (SAHA) treatment additively enhances the folding, trafficking, and function of epilepsy-associated Î³-aminobutyric acid, type A (GABAA) receptors.

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Combining valosin-containing protein (VCP) inhibition and suberanilohydroxamic acid (SAHA) treatment additively enhances the folding, trafficking, and function of epilepsy-associated Î³-aminobutyric acid, type A (GABAA) receptors.

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Combining valosin-containing protein (VCP) inhibition and suberanilohydroxamic acid (SAHA) treatment additively enhances the folding, trafficking, and function of epilepsy-associated Î³-aminobutyric acid, type A (GABAA) receptors.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Fu, Yan-lin Mu, Ting-wei Han, Dong-yun Di, Xiao-jing
Description	Author Affiliation: Han DY ( From the Department of Physiology and Biophysics, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106.); Di XJ ( From the Department of Physiology and Biophysics, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106.); Fu YL ( From the Department of Physiology and Biophysics, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106.); Mu TW ( From the Department of Physiology and Biophysics, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106 tingwei.mu@case.edu.)
Abstract	GABAA receptors are the primary inhibitory ion channels in the mammalian central nervous system. The A322D mutation in the 1 subunit results in its excessive endoplasmic reticulum-associated degradation at the expense of plasma membrane trafficking, leading to autosomal dominant juvenile myoclonic epilepsy. Presumably, valosin-containing protein (VCP)/p97 extracts misfolded subunits from the endoplasmic reticulum membrane to the cytosolic proteasome for degradation. Here we showed that inhibiting VCP using Eeyarestatin I reduces the endoplasmic reticulum-associated degradation of the 1(A322D) subunit without an apparent effect on its dynamin-1 dependent endocytosis and that this treatment enhances its trafficking. Furthermore, coapplication of Eeyarestatin I and suberanilohydroxamic acid, a known small molecule that promotes chaperone-assisted folding, yields an additive restoration of surface expression of 1(A322D) subunits in HEK293 cells and neuronal SH-SY5Y cells. Consequently, this combination significantly increases GABA-induced chloride currents in whole-cell patch clamping experiments than either chemical compound alone in HEK293 cells. Our findings suggest that VCP inhibition without stress induction, together with folding enhancement, represents a new strategy to restore proteostasis of misfolding-prone GABAA receptors and, therefore, a potential remedy for idiopathic epilepsy.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	1
Volume Number	290
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2015-01-02
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Adenosine Triphosphatases Genetics Cell Cycle Proteins Endoplasmic Reticulum-Associated Degradation Drug Effects Hydrazones Pharmacology Hydroxamic Acids Hydroxyurea Analogs & Derivatives Receptors, GABA-A Chemistry Action Potentials Physiology Antagonists & Inhibitors Metabolism Adolescent Cell Line, Tumor Chlorides Drug Synergism Dynamin I Endocytosis Endoplasmic Reticulum HEK293 Cells Myoclonic Epilepsy, Juvenile Pathology Neurons Patch-Clamp Techniques Proteasome Endopeptidase Complex Protein Folding Protein Stability Signal Transduction Gamma-Aminobutyric Acid Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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