Interdisciplinary Research Center of Biology and Chemistry

Shanghai Institute of Organic Chemistry

Chinese Academy of Sciences 

Education

2002/09 ~ 2007/12: University of Pennsylvania School of Medicine, USA, Ph.D., Neuroscience 
1997/09 ~ 2002/07: Peking University Health Science Center, China, Bachelor of Medicine

Employment History

2013/09 ~ Present: SIOC, IRCBC, Chinese Academy of Sciences, Investigator
2008/06 ~ 2013/08: Howard Hughes Medical Institute (HHMI), USA, Research Associate
2008/01 ~ 2008/05: University of Pennsylvania, USA, Postdoctoral Fellow

Welcome to the Fang Lab Homepage! 
Our lab is generally interested in neurobiology of human disease. Specifically, our research focuses on the fundamental mechanisms underlying the maintenance of the nervous system and the molecular and cellular processes that lead to axon degeneration in neural injury as well as age-related neurodegenerative diseases, such as ALS, AD, PD, etc. 

Here, we apply molecular genetics, cell biology, pharmacology, in vivo fluorescent imaging, and evolving high-throughput RNA-seq and mass spec-based proteomic and metabolomic approaches to define genes and pathways that regulate neurodegeneration. In doing so, we hope to uncover evolutionarily conserved core programs that control neural integrity, which will provide the foundation for identifying and developing novel therapeutic strategies to delay, mitigate, prevent or even reverse neurodegeneration in injury and disease.

General Research and Teaching Interests
Neural Injury and Axon De/Re-generation 
Neurobiology of Human Disease
Aging and Neurodegeneration
Cellular and Molecular Neuroscience 
Molecular Genetics

1. Li S, Qian B, Qiu F, Duan Y, Hu R, Cui J, Li W^# and FANG Y^#. (2026) “CDC5L functions as a transcriptional repressor to safeguard against overactive stress response and promote survival.” Genome Biology. (in press)

2. Long W, Li S, Wang Q, Yue W, Fu Y, Wang H, Jiang M, Hu X, Li Y, Cui J, Li A, Zhang Y, Zhang Z and FANG Y. (2025) “SCF^FBXO21-mediated ubiquitination and degradation of NMNAT2 regulates axon survival in nerve injury.” Journal of Cell Biology, 224(11):e202501072.

3. Wang Z, Li Z, Luan T, Cui G, Shu S, Liang Y, Zhang K, Xiao J, Yu W, Cui J, Li A^#, Peng G^# and FANG Y^#. (2024) “A spatiotemporal molecular atlas of mouse spinal cord injury identifies a distinct astrocyte subpopulation and therapeutic potential of IGFBP2.” Developmental Cell, 59(20):2787-2803.e8.

4. Shu S, Jiang M, Deng X, Yue W, Cao X, Zhang K, Wang Z, He H, Cui J, Wang Q, Qu K and FANG Y. (2023) “Heterochromatic silencing of immune-related genes in glia is required for BBB integrity and normal lifespan in Drosophila.” Aging Cell, 22:e13947.

5. Deng X, Sun X, Yue W, Duan Y, Hu R, Zhang K, Ni J, Cui J, Wang Q, Chen Y, Li A^# and FANG Y^#. (2022) “CHMP2B regulates TDP-43 phosphorylation and cytotoxicity independent of autophagy via CK1.” Journal of Cell Biology, 221(1): e202103033.

6. Zhang K, Jiang M and FANG Y. (2021) “The drama of Wallerian degeneration: the cast, crew and script.” Annual Review of Genetics, 55:93-113.

7. Gu J, Wang C, Hu R, Li Y, Zhang S, Sun Y, Wang Q, Li D, FANG Y^# and Liu C^#. (2021) “Hsp70 chaperones TDP-43 in dynamic, liquid-like phase and prevents it from amyloid aggregation.” Cell Research, 31(9):1024-1027.

8. Wang C, Duan Y, Duan G, Wang Q, Zhang K, Deng X, Qian B, Gu J, Ma Z, Zhang S, Guo L, Liu C^# and FANG Y^#. (2020) “Stress induces dynamic, cytotoxicity-antagonizing TDP-43 nuclear bodies via paraspeckle lncRNA NEAT1-mediated liquid-liquid phase separation.” Molecular Cell, 79(3):443-458.e7. (Highlighted with commentary by Malik and Barmada in Molecular Cell).

9. Duan Y, Du A, Gu J, Duan G, Wang C, Gui X, Ma Z, Qian B, Deng X, Zhang K, Sun L, Tian K, Zhang Y, Jiang H, Liu C^# and FANG Y^#. (2019) “PARylation regulates stress granule dynamics, phase separation, and neurotoxicity of disease-related RNA-binding proteins.” Cell Research, 29(3):233-247.

10. Wang H, Wang X, Zhang K, Wang Q, Cao X, Wang Z, Zhang S, Li A^# Liu K^# and FANG Y^#. (2019) “Rapid depletion of ESCRT protein Vps4 underlies injury-induced autophagic impediment and Wallerian degeneration.” Science Advances, 5(2):eaav4971.