Roger J. Davis is a molecular biologist recognized for his studies of mechanisms that mediate stress responses that contribute to inflammation, cancer, and metabolic dysfunction. A focus of his work has been to understand the role of stress-activated signaling pathways in disease processes. Davis was born in the United Kingdom. He attended Cambridge University and graduated with a B.A. degree in Natural Sciences (1979) and a Ph.D. degree in Biochemistry (1983). He was subsequently a Research Fellow of Queens’ College at Cambridge University and then a Damon Runyon Cancer Research Foundation Fellow at the University of Massachusetts Medical School. Davis joined the faculty of the University of Massachusetts Medical School in 1985 and was appointed as an Investigator of the Howard Hughes Medical Institute in 1990. He is a fellow of the Royal Society and a member of the National Academy of Sciences.

Research Interests

Roger J. Davis is interested in signal transduction mechanisms that mediate the physiological response to stress. Biochemical studies of protein phosphorylation by the Davis laboratory 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 as a three-tiered kinase cascade that is activated by cytokines, growth factors, and environmental changes. JNK activation mediates, in part, the cellular response to these stimuli; for example, a program of gene expression controlled by AP1 transcription factors. JNK function is implicated in many disease processes, including inflammation, tissue degeneration, and aberrant tissue growth. This is exemplified by the contribution of JNK to metabolic stress responses that promote metabolic syndrome and the development of diabetes.

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Primary Section

Section 42: Medical Physiology and Metabolism

Secondary Section

Section 41: Medical Genetics, Hematology, and Oncology