Bingwei Lu
Key Documents
Contact Information
- Academic Offices
Personal Information Email
Professional Overview
Honors and Awards
- Brain Disorders Award, The McKnight Endowment Fund for Neurosciences (2008)
- McKnight Scholar Award, The McKnight Endowment Fund for Neurosciences (2002)
- Career Scientist Award, Monique Weill-Caulier Trust (2002)
- Speaker's Fund for Biomedical Research Award, New York Academy of Sciences (2002)
- Young Investigator Award, The Arnold and mabel Beckman Foundation (2002)
Professional Education
| Ph.D.: | Cornell University, Genetics and Development (1995) |
| B.S.: | Fudan University, Genetics (1987) |
Graduate & Fellowship Program Affiliations
Scientific Focus
Current Research Interests
Our laboratory is interested in understanding how the diverse neuronal cell types are generated and maintained in the nervous system. We are taking a combined molecular, cellular, genetic, and genomic approach in the model organisms Drosophila and mouse. To study how neuronal diversity is generated, we focus on investigating the mechanisms of asymmetric division of neural stem cell that balances the self-renewal and differentiation potentials of neural stem cells. Of particular interest to us is the mechanism by which aberrant regulation of neural stem cell asymmetric division leads to brain tumor-like phenotypes. To study how neurons are properly maintained after they are integrated into neural networks, we are creating neurodegenerative phenotypes in Drosophila similar to that observed in Alzheimers and Parkinsons diseases in humans. We are employing the power of fly genetics to identify genetic modifiers that can suppress or enhance these disease phenotypes. Given the unanticipated high level conservation of signaling pathways, regulatory mechanisms, and physiological processes between flies and mammals, our research promises to provide insights into fundamental mechanisms that control the generation and maintenance of neuronal diversity in humans.
Publications
- PAR-1 kinase phosphorylates Dlg and regulates its postsynaptic targeting at the Drosophila neuromuscular junction. Neuron. 2007; (2): 201-15
- Polo inhibits progenitor self-renewal and regulates Numb asymmetry by phosphorylating Pon. Nature. 2007; (7158): 96-100
- Mitochondrial pathology and muscle and dopaminergic neuron degeneration caused by inactivation of Drosophila Pink1 is rescued by Parkin. Proc Natl Acad Sci U S A. 2006; (28): 10793-8
- PAR-1 kinase plays an initiator role in a temporally ordered phosphorylation process that confers tau toxicity in Drosophila. Cell. 2004; (5): 671-82
- Parkin suppresses dopaminergic neuron-selective neurotoxicity induced by Pael-R in Drosophila. Neuron. 2003; (6): 911-24

