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Thomas MaynardAssociate Research Professor of Pharmacology and Physiology
Office Phone: 202-994-8597
Department: Pharmacology and Physiology
- BA, University of California, Santa Barbara, 1993
- PhD, University of Oregon, 1999
My laboratory’s work focuses on the role of cell signaling during neural development, and how signaling is disrupted by genetic disorders that alter chromosomal dosage. The major focus of this work examines mouse models of 22q11 deletion syndrome, a neurodevelopmental disorder associated with psychiatric diseases. We have found that 22q11 deletion alters the development and function of cortical circuitry; our ongoing work is analyzing how 22q11 deletion alters the cell signaling events that instruct embryonic development, and the role of individual 22q11 genes in neural development. I am also the Director of the GWU Neuroscience Institute’s Biomarkers Discovery Core, a core facility that provides support for molecular and cell biological analysis of gene function in the developing and adult nervous system.
Centers and Institutes
GW Institute for Neuroscience
View publications by this faculty member from January 1, 2013 - present
Lehtinen, M.K., Zappaterra, M.W., Chen, X., Yang, Y.J., Hill, A.D., Lun, M., Maynard, T.M., Gonzalez, D., Kim, S., Ye, P., D'Ercole, A.J., Wong, E.T., Lamantia ,A.S., Walsh, C.A. (2011). The cerebrospinal fluid provides a proliferative niche for neural progenitor cells. Neuron 69:893-905. PMID: 21382550
Tucker, E.S. Lehtinen, M.K., Maynard, T.M., Zirlinger, M., Dulac, C., Rawson, N., Pevny, L., and LaMantia, A.S. (2010). Proliferative and transcriptional identity of distinct classes of neural precursors in the mammalian olfactory epithelium, Development, 137:2471-81. PMID: 20573694
Meechan, D.W. Tucker, E.S., Maynard, T.M. and LaMantia, A.-S. (2009). Diminished dosage of 22q11 genes disrupts neurogenesis and cortical development in a mouse model of 22q11 deletion/DiGeorge syndrome. Proc Nat Acad Sci USA, 106:16434-16439. PMC2752572
Maynard T.M., Meechan D.W., Dudevoir M.L., Gopalakrishna D., Peters A.Z., Heindel C.C., Sugimoto T.J., Wu Y., Lieberman J.A., Lamantia A-.S. (2008). Mitochondrial localization and function of a subset of 22q11 deletion syndrome candidate genes. Mol Cell Neurosci 39:439-51. PMC2729512.
Meechan, D.W., Maynard, T.M., Wu, Y., Gopalakrishna, D., Lieberman, J.A. and LaMantia, A.-S. (2006). Gene dosage in the developing and adult brain in a mouse model of 22q11 deletion syndrome. Mol Cell Neurosci 33:412-28.
6. Maynard, T. M., Haskell, G. T., Peters, A. Z., Sikich, L., Lieberman, J. A., and LaMantia, A.S. (2003). A Comprehensive Analysis of 22q11 Gene Expression in the Developing and Adult Brain. Proc Nat Acad Sci USA 100:14433-8. PMC283609
Maynard T.M., Haskell G.T., Lieberman J.A., LaMantia A.-S. (2002). 22q11 DS: genomic mechanisms and gene function in DiGeorge/velocardiofacial syndrome. International Journal of Developmental Neuroscience 20, 407-419.
Maynard, T. M., Sikich, L, Lieberman, J. A., and LaMantia, A.-S. (2001). Neural development, cell-cell signaling, and the “Two-Hit” Hypothesis of Schizophrenia. Schizophrenia Bulletin 27, 457-76.
Wakamatsu, Y., Maynard, T. M., Jones, S. U., and Weston, J. A. (1999). NUMB localizes in the basal cortex of mitotic avian neuroepithelial cells and modulates neuronal differentiation by binding to NOTCH-1. Neuron 23, 71-81.
Additional publications published before January 1, 2013 may be available within Himmelfarb Library's database.
Industry Relationships and Collaborations
This faculty member (or a member of their immediate family) has reported a financial interest with the healthcare related companies listed below. These relations have been reported to the University and, when appropriate, management plans are in place to address potential conflicts.