名校名师讲坛:世界知名神经生物学家、国家“千人计划”获得者李晓江教授学术讲座

来源:生命科学学院发稿时间:2017-09-08 浏览次数:126

一、学术报告题目和地点

报告人:李晓江 教授

报告题目:基因修饰大动物疾病模型

报告时间:2017年9月13日10:30-12:00

报告地点:会2-102(大学中区第一阶梯教室102室)

二、个人简介


李晓江,男,博士生导师,美国Emory大学人类遗传系杰出教授、世界知名神经生物学家,在神经退行性疾病领域的研究成果蜚声国内外,现任暨南大学粤港澳中枢神经再生研究院教授。2010年入选中组部“千人计划”并回国在中国科学院遗传与发育生物学研究所建立实验室,先后承担国家科技部“973”项目、中科院战略性先导专项项目(B类)、国家自然科学基金重点项目等多项重大研究课题。研究成果发表于《Nature》、《Nature Genetics》等国际核心刊物逾百篇,累计引用率达到12000余次。李晓江教授同时也是教育部长江讲座教授、华中科技大学客座教授、中南大学客座教授、苏州大学客座教授;曾任Molecular Brain杂志主编; Molecular Neurodegeneration 副主编;Journal of Genetics and Genomics副主编; J Biol Chem、Plos One等杂志的编委。担任 Nature、NatMed、Nat Genet、Neuron, PNAS, J Neurosci等40多种杂志的审稿人;美国NIH基金二审评委;中国国家自然科学基金重点项目及面上项目二审评委;The Willcome Trust Foundation、Medical Res Council、PhilipMorris、National Ataxia Foundation等基金评委。

李晓江教授近年来在大动物疾病模型方面的研究屡有建树,2008年在世界上首次利用转基因的方法建立了非人灵长类的亨廷顿疾病模型,随后利用体细胞克隆的方法建立了猪的亨廷顿疾病 、肌萎缩侧索硬化症(“渐冻人”)模型。此外,回国后李晓江教授潜心于非人灵长类基因修饰模型的攻关研究,2015年制备出了世界首例帕金森病的转基因猴模型 。同时,利用最新的CRISPR/Cas9技术在世界上制备出了首例实现功能性基因敲除的杜氏肌营养不良症猴模型。此外,利用这些创新性的模型,通过分子生物学分析研究,李晓江研究团队更深层的揭示了疾病的发病机理,使我国在大动物模型制备与疾病研究领域跻身世界先列。

邮箱:xli2@emory.edu

埃默里大学个人简介:http://genetics.emory.edu/faculty/primary/li-xiao-jiang.html

暨南大学个人简介:http://ghmicr.jnu.edu.cn/sunshine.asp?a_id=1074&b_id=1582&c_id=0&id=2348&forum=show

三、近年来发表论文

1. Havel LS, Wang CE, Huang B, Wade B, Li SH, Li X-J. Preferential localization of N-terminal mutant huntingtin in striatal neurons cause neurological symptoms and is regulated by phosphorylation. Hum Mol Genet. 20:1424-37, 2011

2. Huang SS, Ling JJ, Yang S. *Li X-J, *Li SH.?Neuronal expression of TATA box binding protein containing expanded polylgutamine in knock-in mice reduces chaperone protein response by impairing the function of NF-Y transcription factor.

3. Weng L, Lin YF, Li AL, Wang CE, Yan S, Sun M, Gaertig MA, Mitha N, Kosaka J, Wakabayashi T, Xu X, Tang B, Li S, Li XJ. Loss of Ahi1 affects early development by impairing BM88/Cend1-mediated neuronal differentiation. J Neurosci. 33:8172-84. 2013.

4. Xu Q.Q., Huang S.S., Song M.K., Wang C.E. Yan S., Liu X.D., Gaertig M.A., Yu. S.P., Li H., Li S.H., Li X-J. Synaptic Mutant Huntingtin Inhibits Synapsin-1 Phosphorylation and Causes Neurological Symptoms. J. Cell Biol. 202:1123-1138, 2013.

5. Xiang JX, Yang H, Zhao T, Sun M, Xu XS, Zhou X.F., Li SH, Li X-J. Huntingtin-Associated Protein 1 is essential for postnatal growth by regulating neurogenesis. J Clin Invest. 124(1):85-98. 2014

6. Yang HQ, Wang GH, Sun HT, Shu RZ, Liu T, Wang CE, Liu ZM, Zhao Y, Zhen QY, Yang DS, Huang J, Zhou YL, Li SH, Jiang XD, Xiao ZC, Li X-J*, Lai LX. Species-dependent neuropathology in transgenic SOD1 pigs. Cell Res 24(4):464-81. 2014. (*Corresponding author)

7. Yan S, Wang CE, Wei W, Gaertig MA, Lai L, Li S, Li X-J. TDP-43 causes differential pathology in neuronal versus glial cells in the mouse brain. Hum Mol Genet. 23(10):2678-93. 2014.

8. Yang S, Huang SS, Wang GH, Gaertig MA, Li X-J*, Li SH*. Age-dependent decrease in chaperone activity impairs MANF expression leading to Purkinje cell degeneration in inducible SCA17 mice. Neuron, 81, 349–365 2014 (*Corresponding author)

9. Bhat KP, Yan S, Wang CE, Li SH, Li X-J. Differential ubiquitination and degradation of huntingtin fragments modulated by E3 ligase Ube3a. Proc Natl Acad Sci U S A. 111(15):5706-11. 2014

10. Wade B, Wang CE, Yan S, Bhat K, Huang B, Li SH, Li X-J. Ubiquitin-activating enzyme activity contributes to differential accumulation of mutant huntingtin in brain and peripheral tissues. J Neurosci. 34(25):8411-22, 2014

11. Huang, B, Wei, WJ, Wang,GH, Geartig, MA, Feng, Y, Wang, W, Li, X-J and Li, SH. Mutant huntingtin down-regulates Myelin Regulatory Factor-mediated myelin gene expression and affects mature oligodendrocytes. Neuron, 85(6):1212-26 ,2015 (* corresponding author).

12. Yin P, Tu Z, Yin A, Zhao T, Yan S, Chang R, Zhang L, Hong Y, Huang X, Zhou J, Wang Y, Li SH, Li X-J. Aged Monkey Brains Reveal the Role of Ubiquitin-Conjugated Enzyme UBE2N in Synaptosomal Accumulation of Mutant Huntingtin. Hum Mol Genet. 24(5):1350-62. 2015

13. Xiang JX, Yan S, Li SH, Li X-J. Postnatal Loss of Hap1 Reduces Hippocampal Neurogenesis and Causes Adult Depressive-Like Behavior in Mice. Plos Genet. Apr 15;11(4):e1005175., 2015.

14. Chen YC, Zheng YH, Kang Y, Yang WL, Niu YY, ?Guo XY, Tu ZC, Si C, Wang H, Xing RX, Yang SH, Li SH, Ji WZ, Li X-J. Functional disruption of the dystrophin gene in Rhesus Monkey Using CRISPR/Cas9. Hum Mol Genet. 24(13):3764-74. 2015

15. Yang WL, Wang GH, Wang CE, Guo XY, Yin P, Gao JQ, Tu ZC, Wang ZB, Wu J, Hu XT, Li SH, Li X-J. Mutant Alpha-Synuclein Causes Age-Dependent Neuropathology in Monkey Brain. J Neurosci. 35(21):8345– 8358, 2015

16. Huang SS, Yang S, Guo JF, Yan S, Geartig, MA, Li SH, Li X-J. Large Polyglutamine Repeats Cause Muscle Degeneration in SCA17 Mice. ?Cell Reports 13, 196–208. 2015.

17. Wang GH, Liu XD, Geartig, MA, Li SH, Li X-J. Ablation of huntingtin in adult neurons is non-deleterious but its depletion in young mice causes acute pancreatitis. Proc. Natl. Acad . Sci. USA . Mar 22;113(12):3359-64. 2016

18. Liu XD, Wang CE, Hong Y, Zhao T, Wang GH, Gaertig MA, SunM, Li SH, Li X-J. N-terminal Huntingtin Knock-in Mice: Implications of Removing the N-terminal Region of Huntingtin for Therapy. Plos Genetic, May 20;12(5):e1006083. 2016

19. Zhao T, Hong Y, Li SH, Li X-J. Compartment-Dependent Degradation of Mutant Huntingtin Accounts for Its Preferential Accumulation in Neuronal Processes. J. Neurosci. 36(32):8317– 8328, 2016.