李学义 长聘教轨副教授

邮箱：xueyili@sjtu.edu.cn



个人简历 研究方向 发表论文 科研成果
2003 德国海德堡大学生物化学中心，分子细胞生物学专业，博士学位
2003－2004 耶鲁大学医学院细胞生物学系，博士后
2004－2011 哈佛大学医学院附属麻省总院神经病学系，博士后、讲师
2011－ 哈佛大学医学院附属麻省总院神经病学系，助理教授
2014－ 上海交通大学药学院，药理学，特别研究员
2003 Ph.D., Heidelberg University Biochemistry Center
2003-2004 Postdoc, Department of Cell Biology, Yale University School of Medicine
2004-2011 Postdoc & Instructor, Department of Neurology, Massachusetts General Hospital & Harvard Medical School
2011-Present Assistant Professor of Neurology, Massachusetts General Hospital & Harvard Medical School
2014-Present Principal Investigator, School of Pharmacy, SJTU

内体囊泡运输（侧重于胞吞后再循环）的分子机制
胞吞后再循环在神经发育及神经退行性疾病发病过程中的作用
干预胞吞后再循环的新药研发
Mechanism of endocytic recycling
Role of endocytic recycling in neurodevelopmental & neurodegenerative diseases
Discovery & development of drugs targeting endocytic recycling

1. McCory H, Williams D, Sapp E, Gatune LW, Wang P, DiFiglia M, Li X*. Glucose transporter 3 is a rab11-dependent trafficking cargo and its transport to the cell surface is reduced in neurons of CAG140 Huntington’s disease mice. Acta Neuropathol Commun, 2014, 2:178.
2. Li X*, Valencia A#, Sapp E, Masso N, Alexander J, Patrick R, Kegel KB, Aronin N, DiFiglia M. Aberrant Rab11-dependent trafficking of the neuronal glutamate transporter EAAC1 causes oxidative stress and cell death in Huntington’s disease. J Neurosci, 2010, 30: 4552-4561.
3. Li X*, Sapp E, Chase K, Comer-Tierney LA, Masso N, Alexander J, Patrick R, Kegel KB, Valencia A, Esteves M, Aronin N, DiFiglia M. Disruption of Rab11 activity in a knock-in mouse model of Huntington’s disease. Neurobiol Dis, 2009, 36: 374-383.
4. Li X, Standley C, Sapp E, Valencia A, Qin ZH, Kegel KB, Yoder J, Comer-Tierney LA, Esteves M, Chase K, Alexander J, Masso N, Sobin L, Zeitlin S, Bellve K, Tuft R, Lifshitz L, Fogarty K, Aronin N, DiFiglia M. Mutant huntingtin impairs vesicle formation from recycling endosomes by interfering with rab11 activity. Mol Cell Biol, 2009, 29: 6106-6116.
5. Li X, Kaloyanova D, van Eijk M, Eerland R, van der Goot G, Oorschot V, Klumperman J, Lottspeich F, Starkuviene V, Wieland FT & Helms JB. Involvement of a GPI-anchored protein in maintenance of the Golgi structure. Mol Biol Cell, 2007, 18:1261-1271.

主要从事遗传性神经退行性疾病亨廷顿氏病的发病机制研究，揭示了亨廷顿氏病致病突变通过干预单体三磷酸鸟苷酸酶Rab11的激活而影响膜受体及运载蛋白内吞后再循环到细胞表面再利用，并阐释内吞后再循环障碍是引起神经元氧化应激失调及葡萄糖摄取降低的重要原因。