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• W1982910974 abstract "Huntington disease (HD) is an autosomal-dominant neurodegenerative disorder that primarily affects medium spiny striatal neurons (MSN). HD is caused by polyglutamine (polyQ) expansion (exp) in the amino-terminal region of a protein huntingtin (Htt). The connection between polyQ expansion in Httexp and MSN neurodegeneration remains elusive. Here we discuss recent data that link polyQ expansion in Httexp and deranged Ca2+ signaling in MSN neurons. Experimental evidence indicates that (1) Ca2+ homeostasis is abnormal in mitochondria isolated from lymphoblasts of HD patients and from brains of the YAC72 HD mouse model; (2) Httexp leads to potentiation of NR1/NR2B NMDA receptor activity in heterologous expression systems and in MSN from YAC72 HD mouse model; and (3) Httexp binds to the type 1 inositol 1,4,5-trisphosphate receptor (InsP3R1) carboxy-terminus and causes sensitization of InsP3R1 to activation by InsP3 in planar lipid bilayers and in MSN. Based on these results we propose that Httexp-induced cytosolic and mitochondrial Ca2+ overload of MSN plays an important role in the pathogenesis of HD and that Ca2+ signaling blockers may play a beneficial role in treatment of HD." @default.
• W1982910974 created "2016-06-24" @default.
• W1982910974 creator A5047722409 @default.
• W1982910974 creator A5074668880 @default.
• W1982910974 date "2004-10-01" @default.
• W1982910974 modified "2023-09-23" @default.
• W1982910974 title "Deranged neuronal calcium signaling and Huntington disease" @default.
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• W1982910974 doi "https://doi.org/10.1016/j.bbrc.2004.08.035" @default.
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• W1982910974 hasPublicationYear "2004" @default.
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