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

First Author  Bertaux F Year  1998
Journal  FEBS Lett Volume  426
Issue  2 Pages  229-32
PubMed ID  9599014 Mgi Jnum  J:47245
Mgi Id  MGI:1206607 Doi  10.1016/s0014-5793(98)00352-4
Citation  Bertaux F, et al. (1998) HAP1-huntingtin interactions do not contribute to the molecular pathology in Huntington's disease transgenic mice. FEBS Lett 426(2):229-32
abstractText  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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