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

FEBS Lett. 1998 Apr 17;426(2):229-32. doi: 10.1016/s0014-5793(98)00352-4.

F Bertaux ¹, A H Sharp, C A Ross, H Lehrach, G P Bates, E Wanker

Affiliations

Affiliation

1 Division of Medical and Molecular Genetics, UMDS, Guy's Hospital, London, UK.

PMID: 9599014 DOI: 10.1016/s0014-5793(98)00352-4

Abstract

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 hapl does not interact with the transgene exon 1 protein in a transgenic model of HD.

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