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Chorein deficiency leads to upregulation of gephyrin and GABA(A) receptor.

Abstract：

:Chorea-acanthocytosis (ChAc) is a hereditary neurodegenerative disorder caused by loss of function mutations in the VPS13A gene encoding chorein. Recently, using a gene-targeting technique to delete exons 60-61, we produced a ChAc-model mouse that corresponds to a human disease mutation. In this study, a comparative microarray analysis of gene expression in the striatum revealed an increased level of gephyrin gene expression in the ChAc-model mice compared with wild type mice. Since gephyrin is known as a GABA(A) receptor-anchoring protein, we compared the protein-level expression and localization of gephyrin and the GABA(A) receptor alpha1 (GABRA1) and gamma2 (GABRG2) subunits. Gephyrin and GABRG2 immunoreactivities in the striatum and hippocampus of the ChAc-model mice were significantly higher than those in the wild types. Our results suggest that chorein functional loss may lead to a compensatory upregulation of gephyrin and GABRG2 in the pathologic condition in ChAc.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Kurano Y,Nakamura M,Ichiba M,Matsuda M,Mizuno E,Kato M,Izumo S,Sano A

doi

10.1016/j.bbrc.2006.10.070

subject

Has Abstract

pub_date

2006-12-15 00:00:00

pages

438-42

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(06)02295-9

journal_volume

351

pub_type

杂志文章

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