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贾怡昌
 
电子邮件: yichangjia@mail.tsinghua.edu.cn
实验室网站: www.jialabtsinghua.com
 
科研方向

  神经系统疾病,包括神经退行性疾病和神经发育性疾病,的疾病机制是神经科学领域的重大科学问题。这类疾病影响着全球数数以百万计病人的生命健康,但迄今为止仍缺乏针对这类疾病的有效治疗手段和方案,部分原因是我们对疾病机制理解非常有限。由于小鼠与人类基因相似度超过90%,因此研究携带神经退行性和神经发育性表型的化学诱导突变小鼠,大大增进我们对疾病机制的理解,并加速治疗手段和方案的诞生。此外,我们的疾病致病基因的研究也很大程度上加深我们对这些基因生理功能的认识。

  贾怡昌实验室的长期目标是将分子生物学和小鼠遗传学相结合,以更好地了解神经退行性和神经发育性疾病的机制,并将基础研究成果向临床转化。目前,贾怡昌实验室的研究重点主要包括以下三个方面:(1)RNA代谢异常和内质网稳态失调引起的神经退行性和神经发育障碍的疾病机制;(2)哺乳动物语音的分子机制及其在神经发育疾病中的作用;(3)建立新的神经系统疾病细胞和动物模型。

 
代表性科研论文

1. Disruption of ER ion homeostasis maintained by an ER anion channel leads to ALS-like pathology. Liang Guo, Qionglei Mao, Ji He, Xiaoling Liu, Xuejiao Piao, Li Luo, Xiaoxu Hao, Bailong Xiao, Dongsheng Fan, Zhaobing Gao, and Yichang Jia. Cell Research. 2023 May 04. doi:10.1038/s41422-023-00798-z. PMID: 37142673. 

2. A molecular brake that modulates spliceosome pausing at detained introns contributes to neurodegeneration. Dawei Meng, Qian Zheng, Xue Zhang, Li Luo, and Yichang Jia. Protein & Cell. 2023 May 08;14(5):318-336. PMID: 37027487. 

3. TCF7L2 acts as a molecular switch in midbrain to control mammal vocalization through its DNA binding domain but not transcription activation domain. Huihui Qi, Li Luo, Caijing Lu, Runze Chen, Xiaohui Zhang, and Yichang Jia. Molecular Psychiatry. 2023 Feb 13. doi: 10.1038/s41380-023-01993-5. PMID: 36782064. 

4. Dual-gRNA approach with limited off-target effect corrects C9ORF72 repeat expansion in vivo. Xuejiao Piao, Dawei Meng, Xue Zhang, Qiang Song, Hailong Lv, and Yichang Jia. Sci Rep. 2022 Apr 5;12(1):5672. doi: 10.1038/s41598-022-07746-8. PMID: 35383205. 

5. In vivo stress granule misprocessing evidenced in a FUS knock-in ALS mouse model. Zhang X, Wang F, Hu Y, Chen R, Meng D, Guo L, Lv H, Guan J, Jia Y. Brain. 2020 May 1. doi: 10.1093/brain/awaa076. PMID: 32358598. 

6.  An ENU-induced mutation in Twist1 transactivation domain causes hindlimb polydactyly with complete penetrance and dominant-negatively impairs E2A-dependent transcription. Chen RZ, Cheng X, Tan Y, Chang TC, Lv H, Jia Y. Sci Rep. 2020 Feb 12;10(1):2501. doi: 10.1038/s41598-020-59455-9. PMID: 32051525. 

7. Loss of Clcc1 results in ER stress, misfolded protein accumulation, and neurodegeneration. Jia Y, Jucius TJ, Cook SA, Ackerman SL. J Neurosci. 2015 Feb 18;35(7):3001-9. doi: 10.1523/JNEUROSCI.3678-14.2015. PMID: 25698737. 

8. Mutation of a U2 snRNA gene causes global disruption of alternative splicing and neurodegeneration. Jia Y, Mu JC, Ackerman SL. Cell. 2012 Jan 20;148(1-2):296-308. doi: 10.1016/j.cell.2011.11.057. PMID: 22265417. 

9. TRPC channels promote cerebellar granule neuron survival. Jia Y, Zhou J, Tai Y, Wang Y. Nat Neurosci. 2007 May;10(5):559-67. PMID: 17396124. 

10. Critical role of TRPC6 channels in the formation of excitatory synapses. Zhou J, Du W, Zhou K, Tai Y, Yao H, Jia Y, Ding Y, Wang Y. Nat Neurosci. 2008 Jul;11(7):741-3. doi: 10.1038/nn.2127. PMID:18516035. 

11. Essential role of TRPC channels in the guidance of nerve growth cones by brain-derived neurotrophic factor. Li Y, Jia YC, Cui K, Li N, Zheng ZY, Wang YZ, Yuan XB. Nature. 2005 Apr 14;434(7035):894-8. PMID: 15758952. 

 

 

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