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Papers In Press, published online ahead of print October 16, 2000
J. Biol. Chem, 10.1074/jbc.M008099200
Submitted on September 5, 2000
Revised on October 12, 2000
Accepted on October 16, 2000
Department of Psychiatry, Johns Hopkins University, Baltimore, MD 21205
Corresponding Author: mfpeters{at}jhmi.edu
Huntington?s disease (HD) is caused by an expanded CAG trinucleotide repeat coding for a polyglutamine stretch within the huntingtin protein. Currently, the function of normal huntingtin and the mechanism by which expanded huntingtin causes selective neurotoxicity remain unknown. Clues may come from identification of huntingtin-associated proteins. Here, we show that huntingtin co-purifies with a single novel 40 kDa protein, termed HAP40. HAP40 is encoded by the open reading frame F8A located within intron 22 of the factor VIII gene. In transfected cell extracts, HAP40 co-immunoprecipitates with full-length huntingtin but not an N-terminal huntingtin fragment. Recombinant HAP40 is cytoplasmic in the presence of huntingtin but is actively targeted to the nucleus in the absence of huntingtin. These data indicate HAP40 is likely to contribute to the function of normal huntingtin and is a candidate for involvement in the aberrant nuclear localization of mutant huntingtin found in degenerating neurons in HD.
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