A striatal-enriched intronic GPCR modulates huntingtin levels and toxicity - Yao, Yuwei; Cui, Xiaotian; Al-Ramahi, Ismael; Sun, Xiaoli; Li, Bo; Hou, Jiapeng; Difiglia, Marian; Palacino, James; Wu, Zhi-Ying; Ma, Lixiang; Botas, Juan; Lu, Boxun (eLife, 2015)
Keywords: Animals; Animals, Genetically Modified; Blotting, Western; Brain research; Cells, Cultured; Collaboration; Corpus Striatum - cytology; Corpus Striatum - metabolism; cyclic AMP; Cytotoxicity; Disease Models, Animal; Drosophila melanogaster - genetics; Drosophila melanogaster - physiology; Endoplasmic reticulum; Epistasis; Female; G protein-coupled receptors; GPCR; Human Biology and Medicine; Humans; Huntingtin; Huntington Disease - genetics; Huntington Disease - metabolism; Huntington's disease; Huntingtons disease; Infections; intron; Introns; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Microscopy, Confocal; Motor Activity - genetics; Motor Activity - physiology; Mutation; Neostriatum; Neurodegeneration; Neurodegenerative diseases; Neuroscience; Polyglutamine; polyQ; Protein kinase A; Proteins; Psychomotor Performance - physiology; Receptors, G-Protein-Coupled - genetics; Receptors, G-Protein-Coupled - metabolism; Reverse Transcriptase Polymerase Chain Reaction; RNA Interference; Rodents; Serotonin Plasma Membrane Transport Proteins - genetics; Serotonin Plasma Membrane Transport Proteins - metabolism; Therapeutic applications; Toxicity; human biology; mouse; intron; neuroscience; huntington's disease; neurodegeneration; GPCR; cyclic AMP; medicine; polyQ; D. melanogaster; human