HAP1-huntingtin interactions do not contribute to the molecular pathology in Huntington's disease transgenic mice.
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.
Bertaux
F
F
Division of Medical and Molecular Genetics, UMDS, Guy's Hospital, London, UK.
Sharp
A H
AH
Ross
C A
CA
Lehrach
H
H
Bates
G P
GP
Wanker
E
E
D000595:Amino Acid Sequence; D000818:Animals; D001665:Binding Sites; D003001:Cloning, Molecular; D015870:Gene Expression; D006801:Humans; D000071058:Huntingtin Protein; D006816:Huntington Disease / Q000503:physiopathology*; D051379:Mice; D008822:Mice, Transgenic; D008969:Molecular Sequence Data; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism*; D009687:Nuclear Proteins / Q000378:metabolism*; D011485:Protein Binding; D051381:Rats; D013329:Structure-Activity Relationship
C096896:HAP1 protein, human; C086055:HTT protein, human; C490758:Hap1 protein, mouse; C490757:Hap1 protein, rat; C506812:Htt protein, mouse; C499524:Htt protein, rat; D000071058:Huntingtin Protein; D009419:Nerve Tissue Proteins; D009687:Nuclear Proteins