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MARTIN LABORATORY
Dr. Martin's research is focused on the role of glycoyslation in synapse formation and muscular dystrophy. Dr. Martin discovered the expression of novel cell surface carbohydrate structures at the neuromuscular synapse, and has shown that overexpression of such structures in skeletal muscle can functionally compensate for the loss of proteins in the mouse model of Duchenne muscular dystrophy. The laboratory is currently designing therapeutic strategies, including gene therapy, to alter glycosylation in patients with various forms of muscular dystrophy. Additional work involves defining the function of proteins in forms of congenital muscular dystrophy involving defects in protein glycosylation. Other studies involve understanding the role of particular carbohydrate structures in the development of the brain, and the development of diagnostic and therapeutic reagents for Alzheimer's disease.
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| Education |
| 1996 |
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Postdoctoral |
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Neurobiology |
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Washington University Medical School, St. Louis, MO |
| 1992 |
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PhD |
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Biochemistry |
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University of California, Berkeley, Berkeley, CA |
| 1987 |
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B.A. |
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Chemistry |
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Oberlin College, Oberlin, OH |
| Professional Experience |
| 2005- PRES |
Associate Professor of Pediatrics, Departmet of Pediatrics, The Research Institute at Nationwide Children's Hospital, and The Ohio State University |
| 2004- PRES |
Principal Investigator, Center for Gene Therapy The Research Institute at Nationwide Children's Hospital |
| 2004- 2004 |
Associate Professor, Department of Neuroscience, University of California, San Diego California |
| 1996- 2004 |
Assistant Professor, Department of Neurosciences, University of California, San Diego |
MARTIN LABORATORY STAFF
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Principal Investigator:
Paul Taylor Martin, PhD
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| Selected Publications |
Xu, R, Camboni, M., Martin, P.T., Postnatal overexpression of the CT GalNAc transferase inhibits muscular dystrophy in mdx mice without altering muscle growth or neuromuscular development: Evidence for a utrophin-independent mechanism. Neuromuscul Disord. 2007 Feb. 12; [Epub ahead of print] PubMed ID: 17300937 |
| Mendell, J.R., Boue, D., and Martin, P.T. The congenital muscular dystrophies: recent advances and insights. Pediatr Dev Pathol, 2006 Nov-Dec; 9 (6): 427-43 PubMed ID: 17163796 |
| Martin, P.T. Congenital muscular dystrophy – Glycosylation takes center stage. Nature Clinical Practice Neurology. 2006 Apr; 2 (4) 222-230. PubMed ID: 16932553 |
| Martin, P.T., The dystroglycanopathies: the new disorders of O-linked glycosylation. Semin. Pediatr. Neurol., 2005 Sep; 12:152-8. PubMed ID: 16584074 |
| Hoyte K, Jayasinha V, Xia B and Martin P.T. Transgenic Overexpression of dystroglycan does not inhibit muscular dystrophy in mdx mice. Am J Pathol. 2004 Feb; 164 (2): 711-8 PubMed ID: 14742274 |
| Martin P.T. Freeze H., Glycobiology of neuromuscular disorders. Glycobiology 2003 Aug; 13 (8): 67R-75R PubMed ID: 12736200 |
| Martin, P.T. Dystroglycan glycosylation and its role in matrix binding in skeletal muscle. Glycobiology 2003 Aug;13 (8): 55R-66R. PubMed ID: 12736199 |
| Martin PT., Role of transcription factors in skeletal muscle and the potential for pharmacological manipulation. Curr Opin Pharmacol. 2003 Jun;3 (3): 300-8 PubMed ID: 12810197 |
| Jayasinha, V., Hoyte, K., Xia, B., and Martin, P.T. Overexpression of the CT GalNAc transferase inhibits muscular dystrophy in a cleavage-resistant dystroglycan mutant mouse. Biochem. Biophys. Res. Commun. 2003 Mar 21; 302 (4): 831-6 PubMed ID: 12646245 |
| Jayasinha, V., Nguyen, H.H., Xia, B., Kammesheidt, A., Hoyte, K., Martin, P.T., Inhibition of dystroglycan cleavage causes muscular dystrophy in transgenic mice. 2003 Jun; 13 (5): 365-75 PubMed ID: 12798792 |
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