Paul T. Martin, Ph.D.

Center for Gene Therapy,
The Research Institute at Nationwide Children’s Hospital,
700 Children’s Drive,
Columbus, OH 43205

Phone: (614) 722-4072
Fax: (614) 722-5893


Paul T. Martin, Ph.D.

Education & Training:
University of California, Berkeley, Ph.D. in Biochemistry with Daniel E. Koshland, Jr. Washington University Medical School, postdoctoral fellow in Neurobiology with Joshua Sanes
Neurosciences at the University of California, San Diego, Assistant and Associate Professor
Center for Gene Therapy, and The Ohio State University Medical School, Associate Professor of Pediatrics and of Physiology and Cell Biology

Research Interest:
Dr. Martin’s laboratory studies functional roles for glycosylation in the mammalian development and in neuromuscular disorders. Current work involves understanding therapeutic roles for glycosyltransferases in skeletal muscle and heart and assessing their impact on neuromuscular disease progression.  Other work relates to the study of genes that stimulate skeletal muscle growth. In addition, the laboratory works on projects involving the development of therapeutics for Alzheimer’s disease, the glycobiology of adult neural stem cells, and pediatric cancer.

Selected Publications:

  • Cramer ML, Shao G, Rodino-Klapac LR, Chicoine LG, Martin PT. Induction of T-Cell Infiltration and Programmed Death Ligand 2 Expression by Adeno-Associated Virus in Rhesus Macaque Skeletal Muscle and Modulation by Prednisone. Hum Gene Ther. 2017 Jun;28(6):493-509.
  • Zygmunt, D., Singhal, N., Kim, M.-L., Cramer, M.L., Crowe, K.E., Xu, R., Jia, Y., Adair, J., Pena, I. M., Akaaboune, M., Janssen, P.M.J. and Martin, P.T. (2017) Deletion of Pofut1 in skeletal myofibers accelerates muscle aging-related phenotypes in cis and in trans. Mol Cell Biol. 2017 May 2;37(10).
  • Singhal, N. and Martin, P.T. (2015) A role for Galgt1 in skeletal muscle regeneration. Skeletal Muscle 5:3.
  • Xu, R., Singhal, N., Serinagaoglu, Y., Chandrasekharan, K., Joshi, M., Bauer, J., Janssen, P.M.L. and Martin, P. T. (2015) Deletion of Galgt2 (b4Galnt2) reduces muscle growth in response to acute injury and increases muscle inflammation and pathology in dystrophin-deficient mice. Am. J. Pathol., 185:2668-2684
  • 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. (2014) Vascular delivery of rAAVrh74.MCK.GALGT2 to the gastrocnemius muscle of the rhesus macaque stimulates expression of dystrophin and laminin 2 surrogates. Mol. Therapy 22:713-724.
  • 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 22:338-347
  • 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. 62C:31-43.
  • Camboni, M., Hammond, S., Martin, L.T. and Martin, P.T. (2012) Induction of a regenerative microenvironment in skeletal muscle is sufficient to induce embryonal rhabdomyosarcoma in p53- deficient mice. J. Pathol. 226, 40-49
  • 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. 11:4413-4424.
  • Marshall, J.L., Holmberg, J., Chou, E., Ocampo, A. C., Oh, 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. 197;1009-1027.
  • Singhal, N., Xu, R., and Martin, P.T. (2012) Distinct contributions of Galgt1 and Galgt2 to synaptic carbohydrate expression and function at the mouse neuromuscular junction. Mol. Cell. Neurosci. 51:112-126.
  • Chandrasekharan, 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, Transl. Med. 2:42-54.

My NCBI link: