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分子神经生物学研究团队

作者:佚名    来源:实验中心    发布时间:2018/1/8 15:16:35    点击量:    【打印文章】

团队人员

1.   研究组长:陈捷光博士,1995年博士毕业于美国印第安纳大学,随后在耶鲁大学进行博士后的研究工作(1995-1999)。出站后成为美国爱因斯坦医学院的研究人员(1999-2003),后续在耶鲁大学以副研究员的身份工作(2003-2008)。2008年回国在温州医科大学组建了自己的实验室。

2.   工作人员:李雪、肖剑、涂晓萌、黄宝珊

研究方向

体内投射神经元发育及病变的分子机理研究: 我们采用基因表达分析和胚胎内基因转染技术,研究中枢神经系统,包括大脑皮质和神经视网膜中,孤独症相关的投射神经元发育异常及其分子机制。神经元的发育包括 神经前体细胞的增值和分化,新生神经元的迁移,以及轴树突的生长成熟。这一过程中的任何异常将导致神经或精神疾病的产生。

孤独症谱系障碍是一类发病于儿童早期的广泛性神经发育障碍性疾病。其临床特征为交往障碍、语言障碍、重复刻板等行为, 并时常表现出视觉功能异常。已知多个转录因子,包括皮质神经元发育的关键基因Tbr1, Foxp1, 以及Otx1可能和孤独症发生有关。但这些基因是如何影响孤独症目前尚不清楚。在自然科学基金的支持下,我们将分析转录因子及其突变体对投射神经元发育的影响,以加深对孤独症分子和神经基础的认识。更多信息可参阅我们最近发表的文章 (JBC 10.1074/jbc.RA117.001249, 2017; JBC 291: 7661-7668, 2016; PLoS One 10:1-19, 2015; Neuroscience 285:139-54, 2015) 。

 

Laboratory of Molecular Neurobiology

 

Team Members

1.       Principle Investigator: Jie-Guang Chen, PhD

Jie-Guang Chen received his PhD degree at Indiana University, USA in 1995. He did his post-doc at Yale Univeristy. Then, he joined at Albert Einstein College of Medicine as Instructor (1999-2003). Later, he became the Associate Research Scientist at Yale University (2003-2008). After that, he returned to china in 2008 and established his own lab at Wenzhou Medical University.

2.       Team Staff: Xue Li, Jian Xiao, Tu Xiaomeng, Baoshan Huang

Scope of Research Proposal

In Vivo Molecular Studies of Development and Disorders of Projection Neurons: By using gene expression analysis and in utero gene electroporation, our current research aims to reveal the molecular mechanisms underlying the autism-related development disorders of projection neurons in the central nervous systemincluding the cerebral cortex and neural retina. The development of projection neurons involves the proliferation and differentiation of neural progenitors, migration of nascent neurons, and the growth and maturation of axon and dendrites.  Any disruption of these processes will lead to neurological and or psychiatric diseases.

Autism spectrum disorders are a group of conditions that onset early in childhood. The clinical features of autism include dyslexia, speech impairment, repeated stereotype behaviors, and often show abnormal visual function. Multiple transcription factors, including Tbr1, Foxp1, and Otx1, the key genes regulating the development of cerebral cortex, are involved in the incidence of autism. But how these genes affect autism is as yet unclear. With the support from the Natural Science Foundation, we are currently studying the functions of these transcription factors and their autism-related mutants in the neural development.  Our studies will provide new understandings on the molecular and neurological bases of autism. For more information, please refer to our recent publications (J Biol Chem. doi: 10.1074/jbc.RA117.001249, 2017; J Biol Chem. 291: 7661-7668, 2016; PLoS One 10:1-19, 2015; Neuroscience 285:139-54, 2015).