The University of Texas Health Science Center at Houston
McGovern Medical School
Department of Integrative Biology and Pharmacology
Ras proteins are small GTPases, molecular switches that toggle between active and inactive states, and play key roles in cell growth, survival and proliferation. RAS genes are among the most mutated in human cancer. Approximately 20% of all human tumors contain oncogenic mutations in RAS genes. Three isoforms of Ras (H-, N- and K-Ras) play different roles in tumor development, with K-Ras as the most prevalent isoform. Specifically, 90% of pancreatic, 45% of colorectal and 30% of lung tumors contain oncogenic mutants of K-Ras. Thus, better understanding how Ras functions in cells becomes a critical step in efforts to treat and cure cancer. My research focuses on elucidating potential molecular mechanisms for Ras proteins to function in mammalian cells.
Ras signaling is highly compartmentalized in mammalian cells and occurs mostly on the plasma membrane although Ras proteins distribute among various intracellular membrane compartments. How Ras proteins traffic between cell plasma membrane and endomembranes is still very poorly understood. My focus is to utilize quantitative imaging, such as electron microscopy and fluorescence lifetime imaging in in vitro liposomes, cultured cells and ex vivo human tissues, to explore detailed molecular mechanism underlying Ras intracellular trafficking. As diverting Ras proteins from the cell surface is one of the most efficient ways to inhibit Ras signaling and Ras-dependent tumor development, our efforts may contribute to devising new cancer treatment strategies.
Education & Training
Ph.D. - Rice University - 2007