· 2004.9 - 2008.6

Martin-Luther University, Halle-Wittenberg,Germany   -  Biochemistry   - 博士

· 1995.9 - 1998.6

Shenyang Pharmaceutical University, China   - Microbial Pharmacy   - 硕士

· 1991.9 - 1995.9

Shenyang Pharmaceutical University, China   - Pharmaceutics   - 学士

· 2016.9 - 2019.12

 Tianjin University → Associate Professor 

· 2009.9 - 2016.6

 St. Jude Children's Research Hospital, USA → Postdoctoral Fellow 

· 2008.9 - 2009.6

 Martin-Luther University, Halle-Wittenberg, Germany → Postdoctoral Fellow 

· 2002.9 - 2003.6

 Osaka University & Kyoto University, Japan → UNESCO Course Participant 

· 1998.9 - 2002.6

 East China University of Science and Technology → Lecture 

· Our lab uses genetically-manipulated mouse model combined with an array of methodologies of biochemistry, cell biology, and structural biology to reveal the genetic pathway and molecular insights that underlie the disorders caused by imbalanced polyglutamylation homeostasis.  

· Interestingly, a growing body of evidence shows that not only deficits of the catabolic process but also the anabolic process of polyglutamylation can cause varieties of neurodegenerative disorders, as well as other anormlies such as male infertility and defective hemostasis.

· The prototype of CCP family, Nna1 (a.k.a CCP1) was discovered in an axon regeneration model and its dysfunction was later found underlying the phenotypes of Purkinje cell degeneration (pcd) mutant mice, in which certain types of neurons undergo progressive degeneration.

·  Polyglutamylation is a dynamic process in which glutamate residues are added to the γ-carboxyl of a glutamate in the primary amino acid chain of substrate proteins by tubulin tyrosine ligase-like enzymes (TTLLs) and removed by the Cytosolic Carboxypeptidase (CCP) family.

· Our primary interests focus on the novel mechanisms common in neuronal degeneration and regeneration contributed by a unique protein post-translational modification, polyglutamylation.

· The research interest of Wu's Lab is to elucidate novel molecular mechanisms that underlie pathological neuronal death and neuronal regeneration and to provide the new therapeutic strategy to treat neurodegenerative disorders.