Ping H. Wang
Medicine, School of Medicine
Biological Chemistry, School of Medicine
Phone: (949) 824-6981
Email: phwang@uci.edu
http://www.faculty.uci.edu/profile.cfm?faculty_id=2371
Ping Wang
Insulin-like growth factor I (IGF-1) plays a key role in the regulation of cell growth and apoptosis; ample literature indicates that IGF-1 is involved in the growth and apoptosis of cancer cells. Dr. Wang’s research is focused on molecular steps of IGF-1receptor signaling in cells and in animals. His research helped elucidate how IGF-1 receptor signaling, through PI 3 kinase and Erk pathways, modulates mitochondria function and apoptosis. His laboratory has identified two heat shock proteins, Hsp60 and Hsp10, that can modulate IGF-1 receptor abundance and signaling through inhibition of IGF-1 receptor ubiquitination, and identified Hsp60 as a new intracellular element that regulates IGF-1 receptor signaling. His lab also developed a novel and valid strategy to define IGF-1 transcriptional regulatory actions on global gene expression. This is based on his hypothesis that genes similarly regulated by IGF-1 should have the same regulatory motifs in their promoter regions and IGF-1 should regulate these motifs. His computational strategy identified an Sp1 binding site as a potential target of IGF-1 receptor signaling in cardiac muscle cells. Subsequent studies confirmed that IGF-1 increased Sp1 and Sp3 binding to the Sp1 motif and activation of Sp1 motif was necessary for the transcriptional regulatory effect of IGF-1. The computational strategy his team has developed may be further developed to identify specific promoter motifs in response to hormonal stimulation during mammalian cell growth, repair, and remodeling.
Selected Publications:
Shan, Y. X., Yang, T. L., Mestril, R., and Wang, P. H. (2003). Hsp10 and Hsp60 suppress ubiquitination of insulin-like growth factor-1 receptor and augment insulin-like growth factor-1 receptor signaling in cardiac muscle: implications on decreased myocardial protection in diabetic cardiomyopathy. J Biol Chem 278(46), 45492-8.
Li, T., Chen, Y. H., Liu, T. J., Jia, J., Hampson, S., Shan, Y. X., Kibler, D., and Wang, P. H. (2003). Using DNA microarray to identify Sp1 as a transcriptional regulatory element of insulin-like growth factor 1 in cardiac muscle cells. Circ Res 93(12), 1202-9.
Chen, H. S., Shan, Y. X., Yang, T. L., Lin, H. D., Chen, J. W., Lin, S. J., and Wang, P. H. (2005). Insulin deficiency downregulated heat shock protein 60 and IGF-1 receptor signaling in diabetic myocardium. Diabetes 54(1), 175-81.
Lai, H. C., Liu, T. J., Ting, C. T., Yang, J. Y., Huang, L., Wallace, D., Kaiser, P., and Wang, P. H. (2007). Regulation of IGF-I receptor signaling in diabetic cardiac muscle: dysregulation of cytosolic and mitochondria HSP60. Am J Physiol Endocrinol Metab 292(1), E292-7.
Liu, T. J., Lai, H. C., Ting, C. T., and Wang, P. H. (2007). Bidirectional regulation of upstream IGF-I/insulin receptor signaling and downstream FOXO1 in cardiomyocytes. J Endocrinol 192(1), 149-58. |
