HAP1-huntingtin interactions do not contribute to the molecular pathology in Huntington's disease transgenic mice

被引：32

作者：

Bertaux, F

Sharp, AH

Ross, CA

Lehrach, H

Bates, GP

Wanker, E

机构：

[1] United Med & Dent Sch Guys & St Thomas Hosp, Guys Hosp, Div Med & Mol Genet, London SE1 9RT, England

[2] Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21205 USA

[3] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA

[4] Max Planck Inst Mol Genet, D-14195 Berlin, Germany

来源：

FEBS LETTERS | 1998年 / 426卷 / 02期

基金：

英国惠康基金;

关键词：

Huntington's disease; triplet repeat; polyglutamine; HAP1;

D O I：

10.1016/S0014-5793(98)00352-4

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：

HAP1 (huntingtin associated protein) has previously been found to interact with huntingtin (htt) in a glutamine length dependent manner and has been proposed to play a role in the cell specific neurodegeneration observed in Huntington's disease (HD), We have isolated mouse HAP1 (hap1) and have shown that expression is not enriched in areas specifically affected in HD, We hale used the yeast two hybrid system to demonstrate that htt amino acids 171-230 are necessary for the hap1-htt binding and that hap1 does not interact with the transgene exon 1 protein in a transgenic model of HD. (C) 1998 Federation of European Biochemical Societies.

引用

页码：229 / 232

页数：4

共 24 条

[1]

[Anonymous], [No title captured]

[2]

[Anonymous], NEUROBIOL DIS

[3] Fast transport and retrograde movement of huntingtin and HAP 1 in axons [J].