Welcome to the Davis Lab

 

Stress-activated MAP Kinase Signaling

A major focus of our work is to understand the role of the cJun NH2-terminal kinase (JNK) family of stress-activated MAP kinases. Our goal is to define molecular mechanisms and the physiological significance of JNK signaling. This information will provide a conceptual foundation for the design of new therapies that target JNK signaling for the treatment of disease.  

The JNK signaling pathway is activated in response to many cytokines and growth factors and when cells are exposed to physical/chemical stress. We have found that metabolic stress represents a major form of JNK regulation in vivo. This is relevant to the etiology of cancer, cognitive disorders, ischemic disease, metabolic syndrome, diabetes, and non-alcoholic steatohepatitis (NASH). A common theme that links these disease processes is the development of inflammation.  

We use mouse models with targeted mutations to examine physiological significance and molecular mechanism. Our findings are confirmed and extended using genome-engineered human models. These studies, using a broad array of experimental approaches, have advanced knowledge of both normal physiology and disease.  

Our research group includes people with very diverse scientific backgrounds. New members – both graduate students and post-doctoral fellows – are always welcome. Contact Roger Davis for further details.