Principal Investigator, Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences.

Postdoctoral Fellow, The Salk Institute for biological studies, 2006-2007

                                  Massachusetts Institute of Technology, 2008-2013

Ph.D., Chinese Academy of Science, 1999-2005

B.S., Gansu University of Tranditional Chinese Medicine, 1994-1999

The research focuses of Professor Wenyuan Wang’s laboratory are on utilizing induced Pluripotent Stem Cells (iPSCs)-derived cells for disease modeling, Drug development, and Cell therapy. The fibroblast cells harboring disease-causal mutations from patients are reprogrammed to iPSCs and then differentiated into neurons, glia cells, and 3D organoids for disease mechanism studies. Combined with CRISPR/Cas9 genome editing tools, his laboratory is systematically studying the mechanism that mediates the pathogenesis of ALS/FTD and discovering potential therapeutic targets.

While traditionally considered as two separate disease identities, FTLD and ALS are now believed to form one clinical continuum, in which overlapping syndromes link distinct forms of diseases. Currently, very little is known about the underlying mechanism of this concurrence. Conversely, how the same disease gene gives rise to three diagnostically different diseases, i.e., ALS, FTLD, and FTLD-ALS, are equally unknown. The answers to these questions will significantly advance our understanding of the pathogenesis of the diseases and provide a novel rational basis for developing therapeutic strategies. Because available rodent models for most neurodegenerative disorders have not proven predictive of clinical outcomes, Professor Wang’s laboratory uses human iPSCs and their derivatives, 3D organoids, and microphysiological systems to study these critical scientific questions. Professor wang’s papers have been published in some top-tier journals, including Nature, Nature Neuroscience, Neuron, Nature Communications, et al.    

Currently, Professer Wang’s group is working on: (1) Uncovering the molecular networks underlying the convergence of pathogenic mechanisms of ALS and FTD; (2) Investigating the contribution of the non-coding RNAs in neuronal DNA damage response and neurological diseases; (3) Developing iPSCs-based cell therapy strategies.

Selected publications

1.    Wang JY, Ma GM, Tang XQ, Shi QL, Yu MH, Lou MM, He KW, Wang WY*. Brain region-specific synaptic function of FUS underlies the FTLD-linked behavioral disinhibition. Brain, 2022 

2.    Zhang KJ, Wang AL, Zhong KK, Qi SY, Wei C, Shu XQ, Tu WY, Xu WT, Xiao YT, Chen AZ, Bai L, Zhang JM, Jing NH, Wang WY*, Shen CY*. UBQLN2-HSP70 axis reduces poly-Gly-Ala aggregates and alleviates behavioral defects in the C9orf72 disease model. Neuron, 2021

3.    Lou MM, Tang XQ, Wang GM, He J, Luo F, Guan MF, Wang F, Zou H, Wang JY, Zhang Q, Xu MJ, Shi QL, Shen LB, Ma GM, Wu Y, Zhang YY, Liang AB, Wang TH, Xiong LL, Wang J, Xu J, Wang WY*. Long noncoding RNA BS-DRL1 modulates DNA damage response and genome stability in central nervous system by interacting with HMGB1. Nature communication, 2021

4.    Wang WY*, Pan L, Qiu HY, Lee S, Su S, Quinn E, Sasaki M, Jimenez J, Brown R Jr, Hayward LJ, Huang EJ, Tsai LH. Interaction of FUS and HDAC1 regulations DNA damage response and repair in neurons. Nature Neuroscience, 2013

5.    Gao J*, Wang WY*, Mao YW, Gräff J, Guan JS, Pan L, Mak G, Kim D, Su SC, Tsai LH. A novel pathway regulates memory and plasticity via SIRT1 and miR-134. Nature. 2010, 466:1105-1109. (* Equal Contribution. Highlighted by Nature Neuroscience Review; Selected as EDITORS’ Choice of Science; recommended by F1000.)

6.    Wang WY*, Takimoto JK, Louie DV, Baiga TJ, Noel JP, Lee KF, Slesinger PA, Wang L. Genetically encoding unnatural amino acids for cellular and neuronal studies. Nature Neuroscience. 2007, 10: 1063-1072. (Reported by Economist as a Science &Technology breakthrough)