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

FEBS Letters

Ross, Christopher A³  Sharp, Alan H³  Bertaux, Fabien¹  Lehrach, Hans²  Wanker, Erich²  Bates, Gillian P¹ 

[1] Division of Medical and Molecular Genetics, UMDS, 8th Floor Guy's Tower, Guy's Hospital, London SE1 9RT, UK;Max Planck Institute for Molecular Genetics, Dahlem, D14195 Berlin, Germany;Departments of Psychiatry and Neuroscience, The Johns Hopkins School of Medicine, Baltimore, MD 21205-2196, USA

关键词: Huntington's disease;    Triplet repeat;    Polyglutamine;    HAP1;    HD;    Huntington's disease;    HAP;    huntingtin associated protein;    HIP1;    huntingtin interacting protein;    htt;    huntingtin;    gln;    glutamine;   

DOI  :  10.1016/S0014-5793(98)00352-4

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 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 have 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.

【 授权许可】

Unknown