Targeting Gpr52 lowers mutant HTT levels and rescues Huntington's disease-associated phenotypes - Song, Haikun; Li, Hexuan; Guo, Shimeng; Pan, Yuyin; Fu, Yuhua; Zhou, Zijian; Li, Zhaoyang; Wen, Xue; Sun, Xiaoli; He, Bingqing; Gu, Haifeng; Zhao, Quan; et al. (Brain (London, England : 1878), 2018)
Keywords: Age Factors; Animals; Benzamides - therapeutic use; Corpus Striatum - metabolism; Cyclic AMP - metabolism; Disease Models, Animal; Drosophila; Drosophila Proteins - genetics; Drosophila Proteins - metabolism; Exploratory Behavior - physiology; Gait - physiology; HEK293 Cells; Humans; Huntingtin Protein - genetics; Huntington Disease - drug therapy; Huntington Disease - genetics; Huntington Disease - metabolism; Huntington Disease - physiopathology; Induced Pluripotent Stem Cells - drug effects; Induced Pluripotent Stem Cells - metabolism; Mice; Mice, Transgenic; Mutation - genetics; Neurons - pathology; Original; Phenotype; Quinoxalines - therapeutic use; Receptors, G-Protein-Coupled - antagonists & inhibitors; Receptors, G-Protein-Coupled - deficiency; Receptors, G-Protein-Coupled - genetics; Thiophenes - therapeutic use; Walking - physiology; antagonists; neurodegeneration; GPCR; polyQ; target validation