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| Name |
Davis, Roger J. |
| Location
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University of Massachusetts Chan Medical School |
| Primary Field
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Medical Physiology and Metabolism |
| Secondary Field
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Medical Genetics, Hematology and Oncology |
 Election Citation
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Davis is a preeminent research leader on mechanisms that mediate cellular stress responses. His seminal discoveries on the c-Jun NH2-terminal kinase (JNK) signaling pathway provide a foundation for understanding the molecular basis of metabolis stress responses in the development of obesity, metabolic syndrome, and type 2 diabetes. |
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Research Interests
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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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