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UC Davis Health System

Su Hao Lo, Ph.D.

Clinical/Research Interests

Su Hao Lo conducts research intended to increase understanding of the molecular mechanisms that underlie the structure and function of focal adhesions. Focal adhesions are integrin-mediated junctions that attach a variety of different cell types to their underlying substratum. They are signal transduction organelles and play a major role in diverse biological processes, including cell growth, attachment, migration, death, polarization and differentiation. As such, focal adhesion dysfunction is known to have profound repercussions in embryogenesis, tissue development and repair, as well as in many pathological conditions, including various forms of cancer. Lo's recent research projects focus on determining the roles of tensins in skeletal development, cell migration, signal transductions and prostate cancer using molecular, biochemical and cell biological approaches, as well as transgenic and knockout mice techniques.

Title:

 Assistant Professor

Specialty:

 Cell Biology and Human Anatomy

Center/Program Affiliation:

 UC Davis Cancer Center

Other Languages:

 Chinese, Taiwanese

Education:

 Harvard Medical School
Boston, Massachusetts
Ph.D. 1993

National Taiwan University
Taipei, Taiwan
Republic of China
B.S. 1986

Fellowships:

 University of Chicago
Chicago, Illinois
1994-97
MGCB

Professional Memberships:

 American Association for the Advancement of Science
American Society of Cell Biology

Select Recent Publications:

Lo, S. H. Molecules in focus: Tensin. Int J Biochem Cell Biol. 2004, 36:31-34.

Chen, H. and Lo, S. H. Regulation of tensin-promoted cell migration by its focal adhesion-binding and Src Homology 2 domains. Biochem J. 2003, 370:1039-1045.

Vinall, R. L., Lo, S. H. and Reddi, A. H. Bone morphogenetic protein 7 and cellular context regulate chondrocyte cytoskeleton and influence phenotype. Exp. Cell Res. 2002, 272: 32-44.

Chen, H. Duncan, I. C. Bozorgchami, H. and Lo, S. H. Tensin1 and a previously undocumented family member, tensin2, positively regulate cell migration. Proc. Natl. Acad. Sci. USA 2002, 99:733-738.

Lo, S. H. and Lo, T. B. CTEN, a C-terminal tensin-like protein with prostate restricted expression, is down regulated in prostate cancer. Cancer Res. 2002, 62:4217-4221.

Ishii, A., and Lo, S. H. A role of tensin in skeletal muscle regeneration. Biochem J. 2001, 356:737-745.

Guo, L., Burke, P., Lo, S. H., Gandour-Edward, R., Lau, D. Quantitative analysis of angiogenesis using confocal laser scanning microscopy. Angiogenesis. 2001, 4:187-91.

Chen, H., Ishii, A., Wong, W., Chen, L. B., and Lo, S. H. Molecular characterization of human tensin. Biochem J. 2000, 351:403-411.

Lo, S. S., Lo, S. H., Wang, S. C., Hung, M. C. Focal contact formation is inhibited in cell transformed by p185neu. Mol Carcinog 1999, 25(2):150-4

Tikoo, A., Cutler, H., Lo, S. H., Chen, L. B., Maruta, H. Treatment of RAS-induced cancers by F-actin cappers, tensin and chaetoglobosin K, in combination with the caspase-1 inhibitor N1445. Cancer J Sci Am. 1999, 5:293-300.