Dr. David W. Litchfield
Professor; Vice Dean, Research & Innovation at Schulich
B.Sc. McMaster University
Ph.D. University of Western Ontario
Postdoctoral Fellow, Howard Hughes Medical Institute & University of Washington
Office: CSB 2712 and MSB 350
Phone: 519.661.2111, ext 80250 and 84186
Signal transduction events controlling cell proliferation and survival.
Research in our laboratory is directed towards elucidation of the molecular mechanisms that control the growth and survival of mammalian cells since defects in these mechanisms underlie many human diseases including cancer, atherosclerosis, neurological disorders and immune dysfunction. For our research, we employ a variety of complementary strategies involving molecular and cellular biology, structural biology, functional proteomics and bioinformatics. In particular, we are interested in understanding why cancer cells continue to divide in the absence of the appropriate cues and how they can acquire enhanced survival as compared to normal cells. Our studies have been primarily focused on components of regulatory signal transduction pathways, protein kinase CK2 and two of its novel partners (namely CKIP-1 and Pin1), that are frequently expressed at inappropriate levels in cancer cells and that promote leukemia and/or tumor formation when expressed at abnormal levels in mice. In addition to improving our understanding of the molecular basis of tumorigenesis, we hope that our studies will help fulfill the promise of protein kinases such as CK2 as potential targets for molecular targeted therapies.
Our laboratory has established a number of collaborations locally and internationally to advance our studies. Furthermore, we have been involved in the establishment of a Functional Proteomics Facility to foster research within our research community in conjunction with other facilities comprising the London Regional Proteomics Centre.
Keywords: protein kinase, protein phosphorylation, cancer research, cell cycle, apoptosis, functional proteomics, signal transduction, protein kinase CK2, CKIP-1, Pin1