Makoto Senoo, PhD
Assistant Professor of Developmental Biology, Department of Biomedical Sciences, Institute for Regenerative Medicine
University of Pennsylvania School of Veterinary Medicine
Contact information
Department of Biomedical Sciences
153E Old Vet Quad
University of Pennsylvania School of Veterinary Medicine
Philadelphia, PA 19104
153E Old Vet Quad
University of Pennsylvania School of Veterinary Medicine
Philadelphia, PA 19104
Office: 215-746-2062
Email:
msenoo@vet.upenn.edu
msenoo@vet.upenn.edu
Education:
BS (Applied Chemistry)
Keio University, 1992.
MS (Biomedical Engineering)
Keio University Graduate School, 1994.
PhD (Medicine)
Tokai University School of Medicine, 2002.
BS (Applied Chemistry)
Keio University, 1992.
MS (Biomedical Engineering)
Keio University Graduate School, 1994.
PhD (Medicine)
Tokai University School of Medicine, 2002.
Post-Graduate Training
Post-doctoral Research Fellow, Harvard Medical School, 2002-2007.
Permanent linkPost-doctoral Research Fellow, Harvard Medical School, 2002-2007.
Description of Research Expertise
KEY WORDS:Stem Cells; Tissue Regeneration; Animal Models
RESEARCH INTERESTS:
Stem Cell Biology; Regenerative Medicine
RESEARCH FIELDS:
Molecular Biology; Cell Biology; Oncology, Mouse Genetics
Selected Publications
Suzuki, D. and Senoo, M.: Increased p63 phosphorylation marks early transition of epidermal stem cells to progenitors. Journal of Investigative Dermatology 132(doi: 10.1038/jid.2012.165): 2461-2464, 2012.Carter, R.A. Engiles, J.B. Megee, S.O. Senoo, M.* and Galantino-Homer, H.L.* (*co-corresponding authors): Decreased expression of p63, a regulator of epidermal stem cells, in the chronic laminitic equine hoof. Equine Veterinary Journal 43: 543-551, 2011.
Senoo, M., Pinto, F., Crum, C. P. and McKeon, F. : p63 is essential for the proliferative potential of stem cells in stratified epithelia. Cell 129: 523-536, 2007.
Ueki, Y., Lin, C.Y., Senoo, M., Ebihara, T., Agata, N., Onji, M., Saheki, Y., Kawai, T., Mukherjee, P. M., Reichenberger, E. and Olsen, B. R: Increased myeloid cell responses to M-CSF and RANKL cause bone loss and inflammation in SH3BP2 "cherubism" mice. Cell 128: 71-83, 2007.
