The metabolic decline is one of the most common features of aging, and it is closely involved in developing multiple neurodegenerative diseases (NDDs), including ALS and FTD. Genetic mutation-associated or aging-associated metabolic decline can be a powerful mechanism to trigger defective signal transductions, intracellular stress build-up, and protein homeostasis collapse, ultimately leading to neuronal cell death in ALS/FTD. We will leverage multiple model systems to identify how the metabolic decline is induced in the process of ALS/FTD and through which pathways the metabolic decline triggers the molecular cascades of neuronal death.
Our recent research interests include：
1. Uncovering the underlying mechanisms and critical regulators for mitochondrial dysregulation and metabolic disturbance in ALS/FTD.
2. Elucidating the interplay between metabolic disturbance and pathological alternations during the development of NDDs.
Email:15659706031@163.com
Research Direction:Cellular stress response and neurodegenerative diseases
Email:ntguling@163.com
Research Direction:Metabolic regulation in mitochondria
Email:22111520040@m.fudan.edu.cn
Research Direction:Cellular stress response and neurodegenerative diseases
Email:22211520009@m.fudan.edu.cn
Research Direction:The dynamic regulatory mechanism of protein homeostasis
Email:23111530005@m.fudan.edu.cn
Research Direction:Regulation and homeostasis of protein synthesis
Email:wuyou_9602@163.com
Research Direction:Regulation and homeostasis of protein synthesis
Email:24111530020@fudan.edu.cn
Research Direction:Regulation of neuronal metabolism in neurodegeneration
Wang, T. #*, Tian, X#., Kim, H. B., Jang, Y., Huang, Z., Na, C. H. and Wang, J*. Intracellular energy controls dynamics of stress-induced ribonucleoprotein granules. Nature communications 2022, 13, 5584. (Co-first and co-corresponding author)
Wang T, Liu H, Itoh K, Oh S, Zhao L, Murata D, Sesaki H, Hartung T, Na C, Wang J. C9orf72 Regulates Energy Homeostasis by Stabilizing Mitochondrial Complex I Assembly. Cell Metabolism 2021, 33(3): 531-546 e539.
Xu W, Bao P, Jiang X, Wang H, Qin M, Wang R, Wang T, Yang Y, Lorenzini I, Liao L, Sattler R, Xu J. Reactivation of nonsense-mediated mRNA decay protects against C9orf72 dipeptide-repeat neurotoxicity. Brain 2019, 142(5): 1349-1364.
Liu Y, Wang T, Ji YJ, Johnson K, Liu H, Bailey S, Suk Y, Lu YN, Liu M, Wang J. A C9orf72-CARM1 axis regulates lipid metabolism under glucose starvation-induced nutrient stress. Genes & development 2018, 32(21-22): 1380-1397.
Jiang X, Zhang T, Wang H, Wang T, Qin M, Bao P, Wang R, Liu Y, Chang HC, Yan J, Xu J. Neurodegeneration-associated FUS is a novel regulator of circadian gene expression. Translational neurodegeneration 2018, 7: 24
Wang T, Xu W, Qin M, Yang Y, Bao P, Shen F, Zhang Z, Xu J. Pathogenic Mutations in the Valosin-containing Protein/p97(VCP) N-domain Inhibit the SUMOylation of VCP and Lead to Impaired Stress Response. The Journal of biological chemistry 2016, 291(27): 14373-14384.
Wang T#, Jiang X#, Chen G, Xu J. Interaction of amyotrophic lateral sclerosis/frontotemporal lobar degeneration-associated fused-in-sarcoma with proteins involved in metabolic and protein degradation pathways. Neurobiology of aging 2015, 36(1): 527-535.
Address: Building B, Medical Research Building, 131 Dong
Postcode: 200032
Email: wang_tao@fudan.edu.cn
Address:No.138, medical college road 
Postcode:200032 
Tel/Fax:021-54237056
Emial:itbr@fudan.edu.cn220 Handan Rd., Shanghai(200433) Operator：+86-21-65642222 © 2019 FUDAN UNIVERSITY.
