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A striatal-enriched intronic GPCR modulates huntingtin levels and toxicity.

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第一作者： Yuwei,Yao

第一单位： State Key Laboratory of Genetic Engineering, Department of Biophysics, School of Life Sciences, Fudan University, Shanghai, China.

作者： Yuwei,Yao ^[1] ; Xiaotian,Cui ^[1] ; Ismael,Al-Ramahi ^[2] ; Xiaoli,Sun ^[1] ; Bo,Li ^[1] ; Jiapeng,Hou ^[1] ; Marian,Difiglia ^[3] ; James,Palacino ^[4] ; Zhi-Ying,Wu ^[5] ; Lixiang,Ma ^[6] ; Juan,Botas ^[2] ; Boxun,Lu ^[1]

作者单位： State Key Laboratory of Genetic Engineering, Department of Biophysics, School of Life Sciences, Fudan University, Shanghai, China. ^[1] Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, United States. ^[2] MassGeneral Institute for Neurodegenerative Diseases, Massachusetts General Hospital, Boston, United States. ^[3] Developmental Molecular Pathways, Novartis Institutes for Biomedical Research, Cambridge, United States. ^[4] Department of Neurology and Research Center of Neurology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China. ^[5] Department of Anatomy, Histology and Embryology, Shanghai Medical College, Fudan University, Shanghai, China. ^[6]

关键词 D. melanogaster GPCR cyclic AMP human human biology huntington's disease intron medicine mouse neurodegeneration neuroscience polyQ