Faculty Profile, National Health Research Institutes, Taiwan

Faculty Profiles

Liang-Tung Yang, Ph.D.

Assistant Investigator
Institute of Cellular and Systems Medicine


  • Ph.D., Basic Biomedical Science, New York University, USA, 1999
  • M.S., Pharmacology, New York University, USA, 1996
  • B.S., Agricultural Chemistry, National Taiwan University, Taiwan, 1990


  • Assistant Investigator, Stem Cell Research Center, National Health Research Institutes, Taiwan (2007-present)
  • Research Associate, Department of Pathology, Childrens Hospital Los Angeles, University of Southern California, USA (2004-2007)
  • Postdoctoral fellow, Department of Biological Chemistry, School of Medicine, University of California Los Angeles (UCLA), USA (1999-2004)


    The research interests of Dr. Yang are Notch and TGF- signaling pathways, and how these signaling pathways regulate developmental processes and tissue homeostasis. He is currently studying the role of TGF- and Notch signaling in maintaining the stem cell property of hair follicle bulge cells, and the role of TGF- signaling in vascular stability during germinal matrix development. Dr. Yang will apply molecular biology, cell biology, and mouse conditional knockout studies to accomplish his research interests.


    During Dr. Yangs postdoctoral period, he studied the mechanism of how mammalian fringe homolog modifies Notch1 signaling. He found functional diversities among different fringe homolog and demonstrated that fringe homologs modify Delta1-induced and Jagged1-induced Notch1 signaling via distinct mechanism. He then studied the role of TGF-  3 in palatogenesis and made two knock-in mouse lines: Tgfb3::Tgfb1 and Tgfb3-Cre.  From the study of Tgfb3::Tgfb1 homozygote mice, he demonstrated an isoform-specific role for TGF-  3 during palatogenesis. He used Tgfb3-Cre mouse driver line to delete TGF-   type I receptor Alk5 specifically in TGF-  3 expressing cells, and the mutant mice display cleft palate as well as hydrocephalus and severe intracranial bleeding due to germinal matrix hemorrhage.  These data demonstrated that Tgfb3-Cre allele can induce efficient recombination in the palatal epithelium, and that TGF-   signaling is important for the vascular stability during germinal matrix development. Moreover, he crossed Tgfb3-Cre mice with floxed o-fucosyltransferase 1 mice and the resulting mutant displayed a postnatal hair loss phenotype with a conversion of hair follicles into epidermal cysts. These data suggested that specific abrogation of all the Notch signaling in the TGF-   3 expressing domain resulted in a loss of stem cell pool in the hair follicle.


  • Postdoctoral fellowship, California Institute of Regenerative Medicine, USA, 2006
  • Predoctoral fellowship for overseas study, Ministry of Education, Taiwan, 1992


    1. Yang LT and Kaartinen V. Tgfb1 expressed in the Tgfb3 locus partially rescues the cleft palate phenotype of Tgfb3 null mutants. Developmental Biology, 312(1):384-95, 2007.
    2. Dudas M, Li WY, Kim J, Yang LTA and Kaartinen V. Palatal fusion - Where do the midline cells go? A review on cleft palate, a major human birth defect. Acta Histochem, 109(1):1-14, 2007.
    3. Ladi E, Nichols JT, Ge W, Miyamoto A, Yao C, Yang LT, Boulter J, Sun YE, Kintner C and Weinmaster G. The divergent DSL ligand Dll3 does not activate Notch signaling but cell autonomously attenuates signaling induced by other DSL ligands. Journal of Cell Biology, 170(6):983-92, 2005.
    4. Yang LT, Nichols JT, Yao C, Manilay JO, Robey EA and Weinmaster G. Fringe glycosyltransferases differentially modulate Notch1 proteolysis induced by Delta1 and Jagged1. Molecular Biology of the Cell, 16(2):927-942, 2005.
    5. Yang LT, Alexandropoulos K and Jan Sap J. c-SRC mediates neurite outgrowth through recruitment of Crk to the scaffolding protein Sin/Efs without altering the kinetics of ERK activation. Journal of Biological Chemistry, 277(20):17406-17414, 2002.