Ph.D., Biozentrum, University of Basel, Switzerland • Postdoctoral, University of Wisconsin-Madison
• Associate Professor, Department of Biology, School of Science and Technology, Nazarbayev University, Astama, Kazakhstan; 2014 – Present
• Assistant Professor, Department of Molecular Physiology and Biophysics at Baylor College of Medicine in Houston, Texas; 2001 – Present
Elucidating the role of PI4,5P2 signaling networks in cell migration and cancer metastasis We are interested in how signaling networks control normal cell migration and cancer cell metastasis. Cell migration is an essential part of many normal biological processes, including wound healing, the immune response, and embryonic development. Cell migration is also what drives the spread of cancer and a better understanding of this process is essential for improving the treatment of cancer patients and patient survival. Intricate molecular communication networks have evolved to control these processes. Our work is focusing on how cells receive, read and relay such signals, and how disruptions in these processes lead to tumor formation and cancer metastasis. We are approaching these questions by focusing on the signaling processes regulated by the lipid phosphatidylinositol-4,5-bisphosphate (PIP2). Our research focuses on PIP2, because PIP2 is central to the control of multiple signaling networks critical for cell migration. We are interested in a number of research areas and have projects focusing on different aspects of cell migration and phosphoinositide signaling. One major interest of our current research is to decipher how actin polymerization and focal adhesion assembly and disassembly are regulated and coordinated, as these processes are key drivers of cell migration. A second area of research is focused on the emerging role that the trafficking of cell surface receptors plays in cell migration. In particular the endo-exocytic trafficking of integrins back and forth from the plasma membrane represents an important, yet poorly understood, mechanism that regulates the polarity and migration of normal cells and drives tissue invasion and metastasis of tumor cells. We anticipate that a better understanding of these processes and how they drive cell migration will enable the development of new therapeutic anti-cancer approaches.
1. Kunz, J., Wilson, M. P., Kisseleva, M., Hurley, J. H., Majerus, P. W., and Anderson, R. A. (2000). The activation loop of phosphatidylinositolphosphate kinases determines signaling specificity. Mol Cell 5, 1-11;
2. Chao, W.T., Daquinag, A., Ashcroft, F., and Kunz, J. (2010). Type I phosphatidylinositol phosphate kinase I alpha regulates directed cell migration by modulating Rac1 membrane targeting and activation. J. Cell Biol. 190(2):247-62;
3. Chao, W.T., Ashcroft, F., Daquinag, A., Vadakkan, T. Wei, Z., Zhang. P, Dickinson, M.E., and Kunz, J. (2010). Type I phosphatidylinositol phosphate kinase I beta regulates focal adhesion disassembly by promoting beta1 integrin endocytosis. Mol. Cell Biol. 30(18):4463-79.