- Title Instructor, Harris laboratory
- Education PhD: Institute of Neuroscience, Chinese Academy of Sciences
Postdoctoral training: Brigham and Women’s Hospital
- Office K2
- Email email@example.com
- Phone 617-638-4117
- Area of Interest neurobiology, electrophysiology, neurodegenerative diseases, Alzheimer’s disease, prion disease
Prion diseases, or transmissible spongiform encephalopathies, comprise a group of rapidly progressive and invariably fatal neurodegenerative disorders for which there are no effective treatments or cures. Much is known about prion infection and propagation, which is mediated by the conversion of the cellular prion protein (PrPC) to an aggregated isoform (PrPSc) through a self-templating mechanism. However, the pathways underlying prion-mediated neurotoxicity are poorly understood, and progress has been hampered by the lack of robust cellular assays. Deletion of conserved residues in the central region of PrP has been shown to produce a highly toxic molecule (ΔCR PrP) that causes death within a week of birth in mice lacking wild-type PrP. Deletion of conserved residues in the central region of PrP has been shown to produce a highly toxic molecule (ΔCR PrP) that causes death within a week of birth in mice lacking wild-type PrP. ΔCR PrP induces large, spontaneous inward currents.
My research work is focused on: 1) to understand the mechanism of PrP-induced abnormal ionic activities using electrophysiological method 2) to investigate how the mutated forms of PrP or anti-prion antibodies, which induce spontaneous currents, induce neuronal toxicity 3) to investigate whether PrP-induced currents are the pathogenic mechanism underlying prion toxicity.
- Wu B, McDonald AJ, Markham K, Rich CB, McHugh KP, Tatzelt J, Colby DW, Millhauser GL, Harris DA. The N-terminus of the prion protein is a toxic effector regulated by the C-terminus. Elife. 2017 May 20; 6. PMID: 28527237.
- Zhang Z, Almeida S, Lu Y, Nishimura AL, Peng L, Sun D, Wu B, Karydas AM, Tartaglia MC, Fong JC, Miller BL, Farese RV, Moore MJ, Shaw CE, Gao FB. Downregulation of microRNA-9 in iPSC-derived neurons of FTD/ALS patients with TDP-43 mutations. PLoS One. 2013; 8(10):e76055. PMID: 24143176. View in: PubMed
Wu B, Yamaguchi H, Lai FA, Shen J. Presenilins regulate calcium homeostasis and presynaptic function via ryanodine receptors in hippocampal neurons. Proc Natl Acad Sci U S A. 2013 Sep 10; 110(37):15091-6. PMID: 23918386.
Kaufmann MR, Barth S, Konietzko U, Wu B, Egger S, Kunze R, Marti HH, Hick M, Müller U, Camenisch G, Wenger RH. Dysregulation of hypoxia-inducible factor by presenilin/?-secretase loss-of-function mutations. J Neurosci. 2013 Jan 30; 33(5):1915-26. PMID: 23365231.
Cheng J, Dong J, Cui Y, Wang L, Wu B, Zhang C. Interacting partners of AMPA-type glutamate receptors. J Mol Neurosci. 2012 Oct; 48(2):441-7. PMID: 22361832.
Yang Y, Kim AH, Yamada T, Wu B, Bilimoria PM, Ikeuchi Y, de la Iglesia N, Shen J, Bonni A. A Cdc20-APC ubiquitin signaling pathway regulates presynaptic differentiation. Science. 2009 Oct 23; 326(5952):575-8. PMID: 19900895.
Zhang C, Wu B, Beglopoulos V, Wines-Samuelson M, Zhang D, Dragatsis I, Südhof TC, Shen J. Presenilins are essential for regulating neurotransmitter release. Nature. 2009 Jul 30; 460(7255):632-6. PMID: 19641596.
Kitada T, Pisani A, Karouani M, Haburcak M, Martella G, Tscherter A, Platania P, Wu B, Pothos EN, Shen J. Impaired dopamine release and synaptic plasticity in the striatum of parkin-/- mice. J Neurochem. 2009 Jul; 110(2):613-21. PMID: 19457102.
Liao CY, Li XY, Wu B, Duan S, Jiang GB. Acute enhancement of synaptic transmission and chronic inhibition of synaptogenesis induced by perfluorooctane sulfonate through mediation of voltage-dependent calcium channel. Environ Sci Technol. 2008 Jul 15; 42(14):5335-41. PMID: 18754390.
Shen W, Wu B, Zhang Z, Dou Y, Rao ZR, Chen YR, Duan S. Activity-induced rapid synaptic maturation mediated by presynaptic cdc42 signaling. Neuron. 2006 May 4; 50(3):401-14. PMID: 16675395.
Complete list can be found at BU Profiles