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Deng, Wenbin

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Wenbin Deng
Title:
Assistant Professor
Office Address: 2425 Stockton Blvd, Room 631A
Sacramento, CA 95817
Office Phone:
(916) 453-2287
E-Mail Address: wbdeng (at) ucdavis.edu
Education: Postdoctoral Fellowship, Harvard Medical School
Ph.D., Rutgers University
Research Papers: Click Here for Research Paper Links

Research Interests:

Nervous system development and disease; Receptor biology and signal transduction; Basic and translational research in neural injury and repair.

Current Research:

Our lab is interested in studying molecular mechanisms controlling nervous system development and disease. A central theme of our research program has been on pursuing links between genes, gene products, and physiological/pathological processes. Specifically, we use combined biochemical/molecular/cellular and integrative approaches applied to both in vitro and in vivo models to study the role of neurotransmitter receptors and their signaling pathways in the regulation of neural cell proliferation, survival, and differentiation in a cell-specific manner. This research has helped to define at the molecular level the plasticity of brain cells and their potential for enhancing repair of damage caused by brain injury and disease.

Glutamate is a major excitatory neurotransmitter in the brain, but can also cause excitotoxic injury to the nervous system under many pathological circumstances. Previous research has been focused largely, if not exclusively, on neuronal excitotoxicity. However, emerging evidence indicates that the precursors of oligodendrocytes, the myelin-forming glial cells in the central nervous system, share with neurons a high vulnerability to glutamate excitotoxicity that may underlie many nervous system disorders. These precursor cells emerge early in development and remain persistent throughout the adult life. We have been determining the role of glutamate receptors expressed on these cells in nervous system development and injury.

This work has important implications in nervous system diseases from cerebral palsy to multiple sclerosis, in which oligodendroglial injury plays an important role. This research has also opened up exciting new directions in uncovering novel mechanisms of glial excitotoxicity in other neurological and psychiatric disorders.


Noteworthy Publications:

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AUTHOR(s)
YEAR
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PARP-1 deficiency increases the severity of disease in a mouse model of multiple sclerosis. (2009) J Biol Chem, July 2009, doi:10.1074/jbc.M109.013474. Vimal Selvaraj, Mangala Soundarapandian, Olga Chechneva, Ambrose J. Williams, Maxim K. Sidorov, Athena Soulika, David E. Pleasure and Deng W. 2009
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Progress in periventricular leukomalacia. Arch Neurol 65, 1291-1295. 2008 Deng W, Pleasure J, Pleasure D. 2008
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Alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor subunit composition and cAMP-response element-binding protein regulate oligodendrocyte excitotoxicity. J Biol Chem. 281(47):36004-11 Deng W, Neve RL, Rosenberg PA, Volpe JJ, Jensen FE. 2006
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AMPA receptor composition and CREB regulate oligodendrocyte excitotoxicity. Deng W, Neve RL, Rosenberg PA, Volpe JJ, Jensen FE. 2006

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Oligodendrocyte excitotoxicity determined by local glutamate accumulation and mitochondrial function. J. Neurochem. 98, 213-222. Deng W, Yue Q, Rosenberg PA, Volpe JJ, Jensen FE. 2006
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Role of metabotropic glutamate receptors in oligodendrocyte excitotoxicity and oxidative stress. Proc. Natl. Acad. Sci. USA 101, 7751-7756. Deng W, Wang H, Rosenberg PA, Volpe JJ, Jensen FE. 2004
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Glutamate receptor-mediated oligodendrocyte toxicity in periventricular leukomalacia: a protective role for topiramate. J. Neurosci. 24, 4412-4420. Follett PL, Deng W, Dai W, Talos DM, Massillon L, Rosenberg PA, Volpe JJ, Jensen FE. 2004
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Calcium-permeable AMPA/kainate receptors mediate toxicity and preconditioning by oxygen-glucose deprivation in oligodendrocyte precursors. Proc. Natl. Acad. Sci. USA 100, 6801-6806. Deng W, Rosenberg PA, Volpe JJ, Jensen FE. 2003
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Oligodendroglia in developmental neurotoxicity. Neurotoxicology 24, 161-178 178 (featured with cover illustration). Deng W, Poretz RD. 2003
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Protein kinase C activation is required for the lead-induced inhibition of proliferation and differentiation of cultured oligodendroglial progenitor cells. Brain Res. 929, 87-95. Deng W, Poretz RD. 2002
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Chronic dietary lead exposure affects galactolipid metabolic enzymes in the developing rat brain. Toxicol. Appl. Pharmacol. 172, 98-107. Deng W, Poretz RD. 2001
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2425 Stockton Blvd.
Sacramento, CA 95817
(916) 453-2290
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