Shaowei Li

M.D., Ph.D.

Department of Primary Appointment:
School of Medicine
Dermatology
Title
Research Assistant Professor
Location: Uniformed Services University of the Health Sciences, Bethesda, MD
Research Interests:
Cancer Research
Regenerative medicine
Office Phone

Education

Ph. D., Norman Bethune University of Medical science, Changchun, China 1984
M.S., Norman Bethune University of Medical science, Changchun, China 1987
M.D., Norman Bethune University of Medical science, Changchun, China 1992

Biography

Dr. Shaowei Li earned a Doctor of Medicine, Master of Science, and Doctor of Philosophy from Norman Bethune University of Medical Science in China. After completing a postdoctoral fellowship in the Division of Biochemistry and Cellular Biology at the National Institute of Neuroscience in Japan, he moved to the United States as a visiting fellow in the Laboratory of Cellular Oncology at the National Cancer Institute in Maryland. While there, Dr. Li discovered TSC1 (hamartin) and TSC2 (tuberin) form a complex that promotes protein stability and function. At USU, Dr. Li is studying TSC skin hamartomas focused on the molecular and cellular mechanisms of hamartoma formation and potential therapies. He has received funding as principal investigator by the Tuberous Sclerosis Alliance and has been a recipient of travel awards from the TS Alliance in the US and the Tuberous Sclerosis Association in the United Kingdom. Dr. Li developed and characterized a novel xenograft mouse model of TSC skin hamartomas that shows de novo hair follicle neogenesis. This discovery opened up a new research field of skin regeneration in the department. In 2014, Dr. Li started his work partially on a new area of malignant melanomas by focusing on tumor microenvironment and genetic studies.

Representative publications, projects, and/or deployments

2005-present: Research Assistant Professor, Department of Dermatology, Uniformed Services University, Bethesda, MD, USA

2003-2005: Staff Scientist, Department of Dermatology, Uniformed Services University, Bethesda, MD, USA

2002-2003: Research Instructor, Institute of Genetic Medicine, Johns Hopkins University School of Medicine, USA

1997-2002: Visiting Fellow, Laboratory of Cellular Oncology, National Cancer Institute, NIH Maryland, USA

1993-1997: Postdoctoral Fellow, Division of Biochemistry and Cellular Biology, National Institute of Neuroscience, Tokyo, Japan

1992-1993: STA Fellowship, Division of Molecular Genetics, National Institute of Neuroscience, NCNP, Tokyo, Japan

2008: Travel Award, TSC international research conference, in Brighton, UK issued by Tuberous Sclerosis Association, UK

2005: Travel Award, TSC/LAM International Research Symposium in Cincinnati, Ohio issued by Tuberous Sclerosis Alliance, USA

1992: Award for the STA Fellowship issued by Japan International Science and Technology Exchange Center, Japan

Bibliography

Li S, Thangapazham RL, Wang J-A, Rajesh S, Kao T-C, Sperling L, Moss J, Darling TN. Human TSC2-Null Fibroblast-Like Cells Induce Hair Follicle Neogenesis and Hamartoma Morphogenesis. Nature Communications. 2011. March; 2:235, 2011

Li S, Takeuchi F., Wang J, Fan Q, Komurasaki T, Billings E, Pacheco-Rodriguez G, Moss J and Darling TN. Mesenchymal-epithelial Interactions involving epiregulin in tuberous sclerosis complex hamartomas. Proceedings of the National Academy of Sciences 105(9): 3539-44, 2008

Li S, Takeuchi F, Wang J, Fuller C, Pacheco-Rodriguez G, Moss J, and Darling TN. MCP-1 overexpressed in tuberous sclerosis lesions acts as a paracrine factor for tumor development. J Exp Med. 202:617-24, 2005.

Li, S., Braverman., R. Li, H., Vass, W.C., Lowy D and DeClue., J.: Regulation of cell morphology and adhesion by the tuberous sclerosis complex (TSC1/2) gene products in human kidney epithelial cells through increased E-cadherin/beta-catenin activity. Mol Carcinog. 37:98-109, 2003.

Benvenuto, G., Li, S.(co-first author), Brown, S., Braverman., R., Sampson., J., Halley., D., Wienecke, R., and DeClue., J., : The tuberous sclerosis-1 (TSC1) gene product hamartin suppresses cell growth and augments the expression of the TSC2 product tuberin by inhibiting its ubiquitination. Oncogene, 19: 6306-16, 2000.

Li, S., Nakamura, S. and Hattori, S.: Activation of R-Ras GTPase by GTPase-activating proteins for Ras, Gap1m and p120GAP. J Biol Chem, 272: 19328-19332, 1997.

Li, S., Satoh, H.,Watanabe, T., Nakamura, S. and Hattori, S.: cDNA cloning and chromosomal mapping of a novel human GAP (GAP1M) a GTPase-activating protein of Ras. Genomics, 35: 625-627, 1996.

Maekawa M, Li, S, Iwamats A, Morishita T, Yokota K, Imai Y, Kohsaka S, Nakamura S and Hattori S: A novel mammalian Ras GTPase-activating protein which has phospholipid-binding and Btk homology regions. Molecular and Cellular Biology. 10: 6879-6885, 1994

Nabeshima Y, Hanaoka K, Hayasaka M, Esumi E, Li S, Nonaka I and Nabeshima Y: Myogenin gene disruption results in perinatal lethality because of severe muscle defect. Nature. 364: 532-535, 1993