Paul T. Martin, PhD :: Nationwide Children's Hospital, Columbus, Ohio

Paul T. Martin, PhD

Paul T. Martin, PhD

Center for Gene Therapy
Principal Investigator

Neurology Residency
Faculty

Neuromuscular Disorders
Principal Investigator

Contact Information

The Research Institute at Nationwide Children's Hospital
700 Childrens Drive
Columbus, OH 43205 [ map ]
PH: (614) 722-2678
FX: (614) 722-3273
E-mail Me

Biography

Paul T. Martin, PhD, is a Principal Investigator in the Center for Gene Therapy at The Research Institute at Nationwide Children’s Hospital. He is Professor of Pediatrics and Professor of Physiology and Cell Biology at The Ohio State University College of Medicine. He is Director of Training and Education for the Paul D. Wellstone Muscular Dystrophy Cooperative Research Center at Nationwide Children’s Hospital. Dr. Martin’s NIH-funded research program focuses on defining functional roles for cell surface carbohydrates in neuromuscular development and disease. Dr. Martin’s lab has identified particular carbohydrates that, when overexpressed in muscle cells, can prevent muscular dystrophy from occurring in a number of forms of the disease. Current work is focused on translating these findings into therapies that can be used by patients with these disorders.

View CV »

Gender:

  • Male

Languages Spoken:

  • English

Research Interests

Research Center:

Areas of Interest:

  • 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.

Education and Training

Undergraduate School

  • Oberlin College
    Date Completed: 06/30/1987

Post Doctoral

  • University of California, Berkeley
    Date Completed: 06/30/1992

Post Doctoral

  • Washington University Medical School
    Date Completed: 06/30/1996

Professional Experience

2009–present

  • Professor of Pediatrics, Department of Pediatrics, The Research Institute at Nationwide Children's Hospital, and The Ohio State University, Columbus, OH

2005–present

  • Associate Professor of Pediatrics, Departmet of Pediatrics, The Research Institute at Nationwide Children's Hospital, and The Ohio State University

2004–present

  • Principal Investigator, Center for Gene Therapy The Research Institute at Nationwide Children's Hospital, Columbus, OH 

2004–present

  • Principal Investigator, Center for Gene Therapy The Research Institute at Nationwide Children's Hospital

2005–2009

  • Associate Professor of Pediatrics, Department of Pediatrics, The Research Institute at Nationwide Children's Hospital, and The Ohio State University, Columbus, OH

2004–2004

  • Associate Professor, Department of Neuroscience, University of California, San Diego, California

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

Publications

  • Camboni, M., Wang, C-M. Xu, R., Miranda, C., Yoon, J.H., Zygmunt, D., Kaspar, B. and Martin, P.T. 2014. Active and passive immunization strategies based on the SDPM1 peptide demonstrate pre-clinical efficacy in the APPSwePSEN1delE9 mouse model for Alzheimer’s disease.  Neurobiol. Dis. Vol. 62, no. February: 31-43.
  • Martin, P.T., Golden, B., Okerblom, J., Camboni, M., Chandraskeharan, K., Xu, R., Varki, A. Flanigan, K.M. and Kornegay, J.N. 2014. Martin, P.T., Golden, B., Okerblom, J., Camboni, M., Chandraskeharan, K., Xu, R., Varki, A. Flanigan, K.M. and Kornegay, J.N.  PLOS ONE. Vol. N/A, no. February: eN/A.
  • Chicoine, L.G., Montgomery, C.L., Bremer, W.G., Shontz, K., Griffin, D.A., Heller, K.N., Lewis, S., Malik, V. Grose, W.E., Shilling, C.J., Campbell, K.J., Preston, T.J., Coley, B.D., Martin, P.T Walker, C.M., Clark, K.R., Sahenk, Z., Mendell, J.R. and Rodino-Klapac, L.R. 2014. Plasmapheresis eliminates the negative impact of AAV antibodies on micro-dystrophin gene expression following vascular delivery.  Mol. Therapy. Vol. 2, no. February: 338-347.
  • Chicoine, L.G., Rodino-Klapac, L.R., Shao, G., Xu, R., Bremer, W.G., Camboni, M., Golden, B., Montgomery, C.L., Shontz, K., Heller, K.N., Griffin, D.A., Lewis, S., Coley, B.D., Walker, C.M., Clark, K.R., Sahenk, Z., Mendell, J.R. and Martin, P.T. 2013. Vascular delivery of rAAVrh74.MCK.GALGT2 to the gastrocnemius muscle of the rhesus macaque stimulates expression of dystrophin and laminin a2 surrogates.  Mol. Therapy. Vol. 10, no. October: e244.
  • Johnson, E., Li, B, Yoon, J.H., Flanigan, K.M., Martin, P.T., Ervasti, J. and Montanaro, F. 2013. Identification of new dystroglycan complexes in skeletal muscle.  PLOS ONE. Vol. 8, no. August: eN/A.
  • Martin, P.T., Camboni, M., Xu, R., Golden, B., Chandrasekharan, K., Wang, C.-M., Varki, A. and Janssen. 2013. N-glycolylneuraminic acid deficiency worsens cardiac and skeletal muscle pathophysiology in alpha sarcoglycan-deficient mice.  Glycobiology. Vol. 23, no. March: 833-43.
  • Yoon, J.H., Xu, R. and Martin, P.T. 2013. A method to produce and purify recombinant full-length alpha dystroglycan:Analysis of N- and O-linked monosaccharide composition in CHO cells with or without LARGE overexpression.  PLOS Currents-Muscular Dystrophy. Vol. N/A, no. January: eN/A.
  • Singhal,Neha; Xu,Rui; Martin,Paul,T. 2012. Distinct contributions of Galgt1 and Galgt2 to carbohydrate expression and function at the mouse neuromuscular junction.  MOLECULAR AND CELLULAR NEUROSCIENCE. Vol. 51, no. 3-4. (November): 112-126.
  • Singhal, N., Xu, R., and Martin, P.T. 2012. Distinct contributions of Galg1 and Galgt2 to synaptic carbohydrate expression and function at the mouse neuromuscular junction.  Mol.Cell. Neuroscience. Vol. 51, no. November: 112-126.
  • Marshall, J.L., Holmberg, J., Chou,E., Ocampo,A.C,J.,Lee, J., Peter, A.K., Martin, P.T. and Crosbie-Watson, R.H. 2012. Sarcospan-dependent Akt activation is required for utrophin expression and muscle regeneration.  J. Cell Biol.. Vol. 197, no. August: 1009-1027.
  • Yoon,J.H., Johnson, E., Xu,R., Martin, L.t., Martin,P.T. and Montanaro, F. 2012. Comparative proteomic profiling of dystroglycan-associated proteins in wild type, mdx and Galgt2 transgenic mouse skeletal muscle.  J.Proteome Res.. Vol. 11, no. January: 4413-4424.
  • McCarty, D.M., Dirosario, J., Gulaid, K., Oosterof, A., Van Kuppevelt, T.H., Martin, P.T. and Fu, H. 2011. Differential distribution of heparan sulfate glycoforms and elevated expression of heparan sulfate biosynthetic enzymes in the brain of mucopolysaccharidosis IIIB mice.  Metabolic and Brain Disease.
  • Fernandez, K., Serinagaoglu, Y., Hammond, S., Martin, L.T., and Martin, P.T. 2010. Mice lacking dystrophin or alpha sarcoglycan develop embryonal rhabdomyosarcoma with cancer-associated p53 mutations and alternatively spliced or mutant Mdm2 transcripts.  American Journal of Pathology.
  • Chandraskharan,K., Yoon, J.H., Xu, Y., deVries, S., Camboni, M., Janssen, P.J., Varki, A.,and Martin, P.T. 2010. A human-specific deletion in mouse Cmah increases disease severity in the mdx model of Duchenne muscular dystrophy.  Science Translational Medicine.
  • Chandrasekharan, K. and Martin, P.T. 2010. Genetic Defects in muscular dystrophy.  Methods in Enzymology.
  • F. Montanaro and Martin, P.T. 2010. Defective glycosylation of dystroglycan in muscular dystrophy and cancer.  Protein Reviews.
  • Wang, C-M., Camboni, M., Glass, M., and Martin, P.T. 2010. Immunization with the SDPM1 peptide lowers amyloid plaque burden and improves cognitive function inteh APPswePSEN1(A246E) transgenic mouse model of Alzheimer's disease.  Neurobiology of Disease.
  • Chandraskeharan K, Martin PT. 2009. Embryonic overexpression of Galgt2 inhibits skeletal muscle growth via activation of myostatin signaling.  Muscle Nerve. Vol. 39, no. 1. (January): 25-41.
  • Martin, P.T., Xu, R., Rodino-Kaplac, L.R., Oglesbay, E., Camboni, M., Montgomery, C., Shontz, K., Chicoine, L., Clark, K.R., Sahenk, Z., Mendell, J.R., and Janssen, P.M.L. 2009. Overexpression of Galgt2 in skeletal muscle prevents injury resulting from eccentric contractions in boht mdx and wild type mice.  Am. J. Physiol. Cell. Physiol. Vol. 296, no. January: C476-488.
  • Xu, R., DeVries, S., Camboni, M., and Martin, P.T. 2009. Overexpression of Galgt2 inhibits the development of muscular dystrophy in the skeletal muscles of alpha sarcoglycan deficient mice.  Am. J. Pathol. Vol. 175, no. January: 235-247.
  • Yoon, J.H., Chandrasekharan, K., Xu, R., Glass, M., Singhal, N., and Martin, P.T. 2009. The synaptic CT carbohydrate modulates binding and expression of extracellular matrix proteins in skeletal muscle: partial dependence on utrophin.  Mol. Cell. Neurosci. Vol. 41, no. January: 448-463.
  • Montanaro, F., and Martin, P.T. 2009. Defective glycosylation of dystroglycan in muscular dystrophy and cancer. In Protein Reviews: Post-translational modifications in health and disease. Edited by C.J. Vidal. New York, NY: Kluwer Academic Press.
  • Martin PT, Shelton GD, Dickinson PJ, Sturges BK, Xu R, Lecouteur RA, Guo LT, Grahn RA, Lo HP, North KN, Malik R, Engvall E, Lyons LA. 2008. Muscular dystrophy associated with alpha-dystroglycan deficiency in Sphynx and Devon Rex cats.  . Neuromuscul Disord.. Vol. 18, no. 12. (December): 942-952.
  • Haidet AM, Rizo L, Handy C, Umapathi P, Eagle A, Shilling C, Boue D, Martin PT, Sahenk Z, Mendell JR, Kaspar BK. 2008. Long-term enhancement of skeletal muscle mass and strength by single gene administration of myostatin inhibitors.  Proc Natl Acad Sci U S A.. Vol. 105, no. 11. (March): 4318-4322.
  • Martin PT, Xu R, Rodino LR, Oglesbay E, Camboni M, Montgomery C, Shontz K, Chicoine L, Clark KR, Sahenk Z, Mendell JR, Janssen PM. 2008. Overexpression of Galgt2 in skeletal muscle prevents injury resulting from eccentric contractions in both mdx and wild type mice.  Am. J. Physiol. Cell Physiol..
  • Kim, ML, Chandrasekharan K, Glass M, Shi S, Stahl M, Kaspar B, Stanley P, Martin PT. 2008. O-fucosylation of muscle agrin determines its ability to cluster acetylcholine receptors.  Mol. Cell. Neurosci.. Vol. 39, no. January: 452-464.
  • Martin, P.T. 2007. Defective glycosylation and muscular dystrophies. In Protein Reviews: Protein misfolding, aggregation, and conformational diseases. Edited by Vladimir N. Uveresky. New York, N.Y.: Kluwer Academic Press.
  • Martin LT, Glass M, Dosunmu E, Martin PT. 2007. Altered expression of natively glycosylated alpha dystroglycan in pediatric solid tumors.  Human Pathology. Vol. 38, no. 11. (January): 1657-1668.
  • Xu R, Chandrasekharan K, Yoon JH, Camboni M, Martin PT. 2007. Overexpression of the cytotoxic T cell (CT) carbohydrate inhibits muscular dystrophy in the dyW mouse model of congenital muscular dystrophy 1A.  American Journal of Pathology. Vol. 171, no. 1. (January): 181-199.
  • Martin PT. 2007. Congenital muscular dystrophies involving the O-mannose pathway.  Current Molecular Medicine. Vol. 7, no. 4. (January): 417-425.
  • Xu R, Camboni M, Martin PT. 2007. 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.  Neuromuscular Disorders. Vol. 17, no. 3. (January): 209-220.
  • Martin, P.T. 2006. Congenitial muscular dystrophies - Glycosylation takes center stage.  Nature Clin. Pract. Neurol. Vol. 2, no. January: 222-230.
  • Mendell, J.R., Boue, D., and Martin, P.T. 2006. The congenital muscular dystrophies: recent advances and insights.  Pediatric and Developmental pathology. Vol. 9, no. January: 427-443.
  • Martin, P.T. 2006. Disorders of O-linked glycosylation.  Sem. Ped. Neurol. Vol. 12, no. January: 152-158.
  • Hoyte, K., Jayasinha, V., Xia, B., and Martin, P.T. 2004. Overexpression of dystroglycan in skeletal muscles of mdx mice does not inhibit muscular dystrophy.  Am. J. Pathol. Vol. 164, no. January: 711-718.
  • Jones, B.R., Brennan, S., Mooney, C.T., Callanan, J.J., McAllister, H., Guo, L.T., Martin, P.T. Engvall, E., and Shelton, G.D. 2004. Muscular dystrophy with truncated dystrophin in a family of Japanese Spitz dogs.  J. Neurol. Sci. Vol. 217, no. January: 143-149.
  • Martin, P.T. and Freeze, H. 2003. Glycobiology of neuromuscular disorders.  Glycobiology. Vol. 13, no. January: 67R-75R.
  • Jayasinha, V., Hoyte, K., Xia, B., and Martin, P.T. 2003. Overexpression of the CT CalNAc transferase inhibits muscular dystrophy in a cleavage-resistant dystroglycan mutant mouse.  Biochem. Biophys. Res. Commun. Vol. 302, no. January: 831-836.
  • Kang, C., Jayasinha, V., and Martin, P.T. 2003. Identification of peptides that specifically bind the amyloid form of AB1-40 in vitro and amyloid plaques in Alzheimer's disease brain using phage display.  Neurobiology of Disease. Vol. 14, no. January: 146-156.
  • Martin, P.T. 2003. Glycobiology of the neuromuscular junction.  J. Neurocytol. Vol. 32, no. January: 915-929.
  • Jayasinha, V., Nguyen, H.H., Xia, B., Kammesheidt, K., Hoyte, K., and Martin, P.T. 2003. Inhibition of dystroglycan cleavage causes muscular dystrophy in transgenic mice.  Neuromuscular Disorders. Vol. 13, no. January: 365-375.
  • Martin, P.T. 2003. Dystroglycan glycosylation and its role in matrix binding in skeletal muscle.  Glycobiology. Vol. 13, no. January: 55R-66R.
  • Martin, P.T. 2003. Role of transcription factors in skeletal muscle and the potential for pharmacological manipulation.  Curr. Opin. Pharmacol. Vol. 3, no. January: 300-308.
  • Nguyen, H.H., Jayasinha, V., Xia, B., Hoyte, K., and Martin, P.T. 2002. Overexpression of the cytotoxic T cell GalNAc transferase in skeletal muscle inhibits muscular dystrophy in mdx mice.  Proc. Natl. Acad. Sci. USA. Vol. 99, no. January: 5616-5621.
  • Martin, P.T. 2002. Glycobiology of the synapse.  Glycobiology. Vol. 12, no. January: 1R-7R.
  • Xia, B. and Martin, P.T. 2002. Modulation of agrin binding and activity by the CT and related carbohydrate antigens.  Mol. Cell. Neurosci. Vol. 19, no. January: 539-551.
  • Xia, B., Hoyte, K., Kammesheidt, A., Deerinck, T., Ellisman, E., and Martin, P.T. 2002. Overexpression of the CT GalNAc transferase in skeletal muscle alters myofiber growth, neuromuscular structure, and laminin expression.  Dev. Biol.. Vol. 242, no. January: 58-73.
  • Hoyte, K., Kang, C., and Martin, P.T. 2002. Definition of pre- and postsynaptic forms of the CT carbohydrate antigen at the neuromuscular junction: ubiquitous expression of the CT.  Brain Res. Mol. Brain Res.. Vol. 109, no. January: 146-160.
  • Parkhomovskiy, N. and Martin, P.T. 2000. α-galactosidase stimulates acetylcholine receptor aggregation in skeletal muscle cells via PNA-binding carbohydrates.  Biochem. Biophys. Res. Commun. Vol. 270, no. January: 899-902.
  • Parkhomovskiy, N., Kammesheidt, A., and Martin, P.T. 2000. N-acetyllactosamine and the CT carbohydrate antigen mediate agrin-dependent activation of MuSK and acetylcholine receptor clustering in skeletal muscle.  Mol. Cell. Neurosci. Vol. 15, no. January: 380-397.
  • Martin, P.T., Scott, L.J.C., Porter, B.E., and Sanes, J.R. 1999. Distinct structures and functions of related pre- and postsynaptic carbohydrates at the mammalian neuromuscular junction.  Mol. Cell. Neuroscience. Vol. 13, no. January: 105-118.
  • Patton, B.L., Connolly, A.M., Martin, P.T., Cunningham, J.M., Mehta, S., Pestronk, A., Miner, J.H., and Sanes, J.R. 1999. Distribution of ten laminin chains in dystrophic and regenerating muscles.  Neuromuscular Disorders. Vol. 9, no. January: 423-433.
  • Sanes, J.R., Apel, E.D., Gautam, M., Glass, D., Grady, R.M., Martin, P.T., and Yancopoulos, G.D. 1998. Agrin receptors at the skeletal neuromusclar junction.  Annals N. Y. Acad. Sci.. Vol. 841, no. January: 1-13.
  • Martin, P.T. and Sanes, J.R. 1997. Integrins mediate adhesion to agrin and modulate agrin signaling.  Development. Vol. 124, no. January: 3909-3917.
  • Ackermann, M.N., Fairbrother, W.G., Amin, N.S., Deodene, C.J., Lamborg, C.M. and Martin, P.T. 1996. Tetracarbonylmolybdenum complexes of 2-(phenylazo)pyridine ligands - correlations of molybdenum-95 chemical shifts with electronic, infrared, and electrochemical properties.  Organometallic Chem. Vol. 523, no. January: 145-151.
  • Martin, P.T., Kaufman, S.J., Kramer, R.H., and Sanes, J.R. 1996. Synaptic integrins in developing, adult, and mutant muscle: Selective association of the α1, α7A, and α7B subunits with the neuromuscular junction.  Dev. Biol.. Vol. 174, no. January: 125-139.
  • Martin, P.T., Ettinger, A.J., and Sanes, J.R. 1995. A synaptic localization domain in the synaptic cleft protein laminin β2 (s-laminin).  Science. Vol. 269, no. January: 413-416.
  • Martin, P.T. and Koshland, D.E. Jr. 1995. Neurosecretory habituation in PC12 cells: Modulation during parallel habituation.  Proc. Natl. Acad. Sci. USA. Vol. 92, no. January: 5052-5056.
  • Martin, P.T. and Sanes, J.R. 1995. Role for a synapse-specific carbohydrate in agrin-induced clustering of acetycholine receptors.  Neuron. Vol. 14, no. January: 743-754.
  • Martin, P.T., Chung, B.T.P., and Koshland, D.E. Jr. 1993. Regulation of neurosecretory habituation by cAMP in PC12 cells: Role of adaptation of cAMP signals.  Eur. J. Biochem.. Vol. 217, no. January: 259-265.
  • Martin, P.T. and Koshland, D.E. Jr. 1992. Regulation of neurosecretory habituation by cAMP: Parallel pathways used by cAMP and calcium.  Proc. Natl. Acad. Sci USA. Vol. 89, no. January: 10257-10261.
  • Martin, P.T. and Koshland, D.E. Jr. 1991. The biochemistry of the neuron: neurosecretory habituation to repetitive depolarizations in PC12 cells.  J. Biol. Chem. Vol. 266, no. January: 7388-7392.
  • Martin, P.T., Golden, B., Okerblom, J., Camboni, M., Chandraskeharan, K., Xu, R., Varki, A. Flanigan, K.M. and Kornegay, J.N. A comparative study of N-glycolylneuraminic acid (Neu5Gc) and Cytotoxic T cell (CT) carbohydrate expression in normal and dystrophin-deficient dog and human skeletal muscle.  PLOS ONE.
  • Martin, P.T., Camboni, M., Xu, R., Golden, B., Chandrasekharan, K., Wang, C.-M., Varki, A. and Janssen, P.M.L. N-glycolylneuraminic acid deficiency worsens cardiac and skeletal muscle pathophysiology in alpha sarcoglycan-deficient mice.  Glycobiology,.
  • Yoon, J.H., Xu, R. and Martin, P.T. A method to produce and purify recombinant full-length alpha dystroglycan:Analysis of N- and O-linked monosaccharide composition in CHO cells with or without LARGE overexpression.  PLOS Currents-Muscular Dystrophy.
  • Singhal,Neha; Martin,Paul,T. Role of extracellular matrix proteins and their receptors in the development of the verterate neuromuscular junction.  Dev.Neurobiol.
  • Yoon, J.H., Xu, R. and Martin, P.T. A method to produce and purify recombinant full-length alpha dystroglycan:Analysis of N- and O-linked monosaccharide composition in CHO cells with or without LARGE overexpression.  PLOS Currents-Muscular Dystrophy 2013.
  • Singhal, N. and Martin, P.T. 0. Role of extracellular matrix proteins and their receptors in the development of thevertebrate neuromuscular junction.  Dev. Neurobiol..
  • Chicoine, L.G., Rodino-Klapac, L.R., Shao, G., Xu, R., Bremer, W.G., Camboni, M., Golden, B., Montgomery, C.L., Shontz, K., Heller, K.N., Griffin, D.A., Lewis, S., Coley, B.D., Walker, C.M., Clark, K.R., Sahenk, Z., Mendell, J.R. and Martin, P.T. Vascular delivery of rAAVrh74.MCK.GALGT2 to the gastrocnemius muscle of the rhesus macaque stimulates expression of dystrophin and laminin a2 surrogates.  Mol. Therapy 2013.
  • Camboni,Marybeth; Hammond,Sue; Martin,Laura,T; Martin,Paul,T. Induction of a regenerative microenvironment in skeletal muscle is sufficient to induce embryonal rhabdomyosarcoma in p53-deficient mice.  J. Pathol..
  • Martin, P.T., Camboni, M., Golden, B., Chandraskeharan, K., Xu, R., Varki, A. and Kornegay, J.N. A comparative study of N-glycolylneuraminic acid (Neu5Gc) and Cytotoxic T cell (CT) carbohydrate expression in normal and dystrophin-deficient dog and human skeletal muscle.  Neuromuscular Disorders,.
  • Lineburg, K.E., Amaya, D., Ekberg, J.A., Cherehasa, F., Mackay-Sim, A., Martin, P.T., Key, B. and St John, J.A. 0. The carbohydrate CT1 is expressed in topographically fixed glomeruli in the mouse olfactory bulb.  Mol. Cell. Neurosci..
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