PQBP-1 increases vulnerability to low potassium stress and represses transcription in primary cerebellar neurons

被引：12

作者：

Enokido, Y

Maruoka, H

Hatanaka, H

Kanazawa, I

Okazawa, H ^{[1
]}

机构：

[1] Univ Tokyo, Grad Sch Med, Dept Neurol, Tokyo, Japan

[2] Osaka Univ, Inst Prot Res, Div Prot Biosynthesis, Suita, Osaka 565, Japan

[3] Natl Ctr Neurol & Psychiat, Natl Inst Neurosci, Dept Mol Genet, Kodaira, Tokyo, Japan

[4] Tokyo Metropolitan Inst Neurosci, Dept Mol Theraeut, Fuchu, Tokyo 1838528, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2002年 / 294卷 / 02期

关键词：

D O I：

10.1016/S0006-291X(02)00477-1

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

PQBP-1 is a polyglutamine tract binding protein implicated in transcription. We previously reported that PQBP-1 and mutant ataxin-1, product of the spinocerebellar atrophy type 1 (SCA1) causative gene, cooperatively induce cell death in culture cells. Simultaneously, we showed that mutant ataxin-1 promoted interaction between PQBP-1 and RNA polymerase II and enhanced repression of the basal transcription by PQBP-1. In this study, we have examined the effects of overexpression of PQBP-1 to the primary-cultured cerebellar neurons. Our results indicate that overexpression of PQBP-1 inhibits the basal transcription in cerebellar neurons and increases their vulnerability to low potassium conditions. (C) 2002 Elsevier Science (USA). All rights reserved.

引用

页码：268 / 271

页数：4

共 22 条

[1] Fourteen and counting: unraveling trinucleotide repeat diseases [J].