Neurocell CultureNeurocell Transplantation |
Stem Cell BiologyNeurobiologyStem Cells & CancerNeuro-regeneration |
Dr. Robert Yu-Lin Tsai
Biography
Education:
1981-1987 National Taiwan University School of Medicine (M.D.)
1987-1988 National Taiwan University Hospital (Internship)
1991-1996: The Johns Hopkins University School of Medicine (Ph.D. in Neuroscience Program)
Thesis title: Cloning and Functional Analysis of Roaz: a Zn Finger Protein that Regulates Olfactory Gene Expression (Dr. Randall R. Reed)
Professional Experience:
1988-1991 Medical Resident in Neurology; National Taiwan University Hospital
1996-1997 Howard Hughes Associate, The Johns Hopkins University School of Medicine
1997-2003 Research Fellow; National Institute of Neurological Disorders and Stroke, National Institutes of Health
2003-2007 Assistant Professor; Center for Cancer and Stem Cell Biology, Institute of Biosciences and Technology, The Texas A&M Health Science Center
2008-present Associate Professor; Center for Cancer and Stem Cell Biology, Institute of Biosciences and Technology, The Texas A&M Health Science Center
Research
The research interest of my laboratory is focused on the molecular mechanism that drives the self-renewing proliferation of stem cells, with the hope that we can use this knowledge to enhance the endogenous regenerative process to repair damaged tissues caused by diseases or injuries, particularly in the central nervous system, and, on the flip side, to reduce the uncontrolled proliferation seen in metastatic and high-grade tumors. The biological systems we use are ES, primary neural stem cell culture, and cancer cell lines, as well as mouse genetic models. The molecular target of our present studies is a family of nucleolar GTPases, one of which, nucleostemin (NS), confers a unique nucleolar state in the stem cells. NS was previously identified as enriched in the stem cell population, and shown to play important roles in keeping the neural stem cells and cancer cells in the cell cycle. The activity of NS is regulated by a small molecule in the cells (GTP) that serves as a molecular switch controlling the on and off states. Our work suggests a model in which continuously dividing cells use NS as a sensor to control their rate of division in response to changes that take place in their microenvironment. The mechanism by which NS and NS-related genes control tissue homeostasis in adult animals is being addressed in the following directions: 1) defining the unique nucleolar state in stem cells; 2) determining the signaling pathway that regulates the expression and activity of nucleostemin (NS) in stem cells and during adult tissue regeneration; and 3) establishing the role of NS-expressing cells in the tumorigenic process, with an emphasis on the brain, breast, and prostate tumors.
Five Most Significant Publications Prior to 2007
Tsai, R.Y.L. and McKay, R.D.G (2000) Cell Contact Regulates Fate Choice by Cortical Stem Cells. J. Neurosci. 20:3725-3735.
Tsai, R.Y.L. and McKay, R.D.G (2002) A Nucleolar Mechanism Controlling Cell Proliferation in Stem Cells and Cancer Cells. Genes Dev.: 16:2991-3003.
Tsai, R.YL. and McKay R.DG (2005) A Multistep, GTP-driven Mechanism Controlling the Dynamic Cycling of Nucleostemin. J. Cell Biol. 168:179-184.
Zhu, Q., Yasumoto, H., and Tsai, R. YL. (2006) Nucleostemin Delays Cellular Senescence and Negatively Regulates TRF1 Protein Stability. Mol Cell Biol. Vol. 24. No. 26. p9279-9290.
Meng, L., Yasumoto, H., and Tsai, R.YL. (2006) Multiple Controls Regulate Nucleostemin Partitioning between Nucleolus and Nucleoplasm. J Cell Sci. Vol. 119. No. 24. p5124-5136.
Publications 2007
Yasumoto, H., Meng, L., Lin, T., Zhu, Q., and Tsai, R.YL. (2007) GNL3L Inhibits Activity of Estrogen-Related Receptor g by Competing for Coactivator Binding. J Cell Sci. Vol. 120: 2532-2543.
Lin, T., Yasumoto, H., and Tsai, R.YL. (2007) BAC Transgenic Expression Efficiency: Bicistronic vs. ATG-Fusion Strategies. Genesis. 45:647-652.
Meng, L, Zhu, Q, and Tsai, RYL. (2007) Nucleolar Trafficking of Nucleostemin Family Proteins: Common versus Protein-Specific Mechanisms. Mol Cell Biol. 27:8670-82. [EPub 2007 Oct. 8]
Publications 2008
Meng, L., Lin, T., and Tsai, R.YL. (2008) Nucleoplasmic Mobilization of Nucleostemin Stabilizes MDM2 and Promotes G2-M Progression and Cell Survival. J Cell Sci. Vol. 121. No. 24. p4037-4046 [EPub 2008 Nov. 25].
Publications 2009
Lin, Y., Chen, L., Lin, C., Luo, Y., Tsai, R.YL., and Wang, F. (2009) Neuron-derived FGF9 Is Essential for Scaffold Formation of Bergmann Radial Fibers and Migration of Granule Neurons in The Cerebellum. Dev Biol. 329: 44-54 [EPub 2009 Feb 20].
Pederson, T. and Tsai, R.YL. (2009) In Search of Non-Ribosomal Nucleolar Protein Function and Regulation. J Cell Biol. 184:771-776 [EPub 2009 Mar 16].
Zhu, Q., Meng, L., Hsu, J.K., Lin, T., Teishima, J., and Tsai, R.YL. (2009) GNL3L Stabilizes the TRF1 Complex and Promotes Mitotic Transition. J Cell Biol. 185:827-839.
Tsai, R.YL. and Meng, L. (2009) Nucleostemin: A Latecomer with New Tricks. Int J Biochem Cell Biol. 41: 2122-2124 [EPub 2009 Jun 6].
Tsai, R.YL. (2009) Nucleolar Modulation of TRF1: A Dynamic Way to Regulate Telomere and Cell Cycle by Nucleostemin and GNL3L. Cell Cycle. 8:2912-2916 [EPub 2009 Sep 16].


