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Mutant huntingtin protein (Htt<jats:sup>exp<\/jats:sup>) specifically binds to and activates type 1 inositol 1,4,5-trisphosphate receptor (InsP<jats:sub>3<\/jats:sub>R1), an intracellular Ca<jats:sup>2+<\/jats:sup>release channel. Htt<jats:sup>exp<\/jats:sup>\u2013InsP<jats:sub>3<\/jats:sub>R1 association is mediated by a cytosolic C-terminal tail of InsP<jats:sub>3<\/jats:sub>R1 (a 122-aa-long IC10 fragment). To evaluate an importance of Htt<jats:sup>exp<\/jats:sup>association with InsP<jats:sub>3<\/jats:sub>R1 for HD pathology, we generated lentiviral and adeno-associated viruses expressing GFP-IC10 fusion protein and performed a series of experiments with YAC128 HD transgenic mouse. Infection with Lenti-GFP-IC10 virus stabilized Ca<jats:sup>2+<\/jats:sup>signaling in cultured YAC128 MSNs and protected YAC128 MSNs from glutamate-induced apoptosis. Intrastriatal injections of AAV1-GFP-IC10 significantly alleviated motor deficits and reduced MSN loss and shrinkage in YAC128 mice. Our results demonstrate an importance of InsP<jats:sub>3<\/jats:sub>R1\u2013Htt<jats:sup>exp<\/jats:sup>association for HD pathogenesis and suggested that InsP<jats:sub>3<\/jats:sub>R1 is a potential therapeutic target for HD. Our data also support potential use of IC10 peptide as a novel HD therapeutic agent.<\/jats:p>","DOI":"10.1523\/jneurosci.4411-08.2009","type":"journal-article","created":{"date-parts":[[2009,2,4]],"date-time":"2009-02-04T18:33:35Z","timestamp":1233772415000},"page":"1257-1266","source":"Crossref","is-referenced-by-count":84,"title":["Neuroprotective Effects of Inositol 1,4,5-Trisphosphate Receptor C-Terminal Fragment in a Huntington's Disease Mouse 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