Expertise at Chang Gung System

Hung-Yao Ho , Ph.D.
Institution: Chang Gung University
Position: Associate Professor
Department: Department of Medical Biotechnology and Laboratory Science
Tel: +886-3-211-8800 ext.3318
E-mail: hoh01@mail.cgu.edu.tw

Focus of Interest:
  • Metabolomics
  • Redox Biology
  • Virology

Research Summary
Redox environment can be the host factor affecting pathogenesis of degenerative and infection diseases. Oxidative stress enhances viral replication and cytopathic effects in virus-infected cells; the infection itself leads to increased oxidative stress. Additionally, the mechanism accounting for virus-induced oxidative stress is not completely clear. The main theme of my laboratory is to study how oxidative stress/damage is related to pathogenesis of degenerative diseases and viral infection, and how cellular metabolism changes during pathogenesis.

Employment Records:
2003 - 2009 Assistant Professor, Department of Medical Biotechnology and Laboratory Science, Chang Gung University, Kweishan, Taiwan

Education:
1994 – 2000 PhD, Institute of Life Science,National Defense Medical Center
2001 – 2002 Postdoc, Department of Dermatology, New York University Medical Center, New York, USA

Honor and Awards:

1999 Young Investigator Award of Society of Free Radical Biology and Medicine


Selected Publications:
1. Lin, C. J., Ho, H. Y.*, Cheng, M. L., Yu, J. S., Chiu, D. T. Y. (2010). Impaired dephosphorylation renders G6PD-knockdown HepG2 cells more susceptible to H2O2-induced apoptosis. Free Radic. Biol. Med. 49, 361-373 (*Co-first author).
2.  Cheng, M. L., Shiao, M. S., Chiu, D. T. Y., Weng, S. F., Tang, H. Y., Ho, H. Y. (2011). Biochemical disorders associated with antiproliferative effect of dehydroepiandrosterone in hepatoma cells as revealed by LC-based metabolomics. Biochem. Pharmacol. 82, 1549-1561 (Corresponding author).
3. Ho, H. Y., Cheng, M. L., Shiao, M. S., Chiu, D. T. Y. (2013) Characterization of global metabolic responses of glucose-6-phosphate dehydrogenase-deficient hepatoma cells to diamide-induced oxidative stress. Free Radi. Biol. Med. 54, 71-84.

Source:
Mouse strains: none
Cell lines: HepG2, SK-Hep1
Special technology: none