Dr. Roger J. Davis is an Investigator of the Howard Hughes Medical Institute and is the H. Arthur Smith Professor and Chair, Program in Molecular Medicine at the University of Massachusetts Medical School. He received his initial training as a student at Cambridge University. He also trained as a Damon Runyon Cancer Research Foundation fellow with Michael P. Czech at the University of Massachusetts Medical School. He subsequently joined the faculty of the University of Massachusetts Medical School and was a founding member of the Program in Molecular Medicine.
Dr. Davis’ studies of signal transduction mechanisms led to the molecular cloning of the first human stress-activated MAP kinase, the cJun NH2-terminal kinase (JNK). Subsequent studies defined the molecular structure of the JNK pathway, including the identification of upstream and down-stream pathway components and scaffold proteins. This signaling pathway is activated in response to many pathological / physiological stimuli and is implicated in inflammatory diseases (e.g. arthritis), cancer, stroke, heart disease, and diabetes. The overall goal of Dr. Davis’ research is to understand the molecular basis for these diseases and to design novel therapeutic strategies.
Dr. Davis has served as a Howard Hughes Medical Institute Investigator for 30 years. He was identified as the most highly cited scientist world-wide in 1995-1996 by the Citation Index (Thompson Reuters) and is the author of more than 400 scientific papers. He was elected to the National Academy of Sciences, The Royal Society, American Academy of Microbiology, American Association for the Advancement of Sciences, National Academy of Inventors, and the European Molecular Biology Organization. He was also the recipient of the Steven C. Beering Award from Indiana University. Dr. Davis was the Editor-in-Chief of the journal Molecular and Cellular Biology, and he currently serves on the Editorial Boards of eLife, Genes & Development, and Molecular Cell. He also served as the Chair of the Cellular Aspects of Diabetes & Obesity Study Section (National Institutes of Health).
Mechanisms by which growth factors regulate cellular proliferation
The goal of this laboratory is to understand the molecular mechanism by which growth factors and cytokines regulate cellular proliferation and survival. A specific focus of our studies is to understand how MAP kinase signaling pathways, which are initiated at the cell surface, regulate the expression of genes in the nucleus.
These MAP kinase pathways include the extracellular signal-regulated kinases (ERKs), the c-Jun amino-terminal kinases (JNKs), and the p38 MAP kinases. The methods that we are using include recombinant DNA technology, protein chemistry, somatic cell genetics, and general biochemical techniques.
The significance of this research is that there are many disease states, such as cancer, that are characterized by abnormal cellular proliferation. A detailed understanding of the molecular processes involved in the control of cell growth is required for the design of rational treatments for these diseases.
Schematic representation of the human MAP kinase signal transduction pathway network.
Laboratory rotations are available to study signal mammalian transduction mechanisms. Several projects are available, including studies of protein kinase cascades, gene expression, the cell cycle, and apoptosis. Targeted gene disruption approaches in mice combined with biochemical and molecular biology studies will be examined.