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Academic Background

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 SciencesThe Royal SocietyAmerican Academy of MicrobiologyAmerican Association for the Advancement of SciencesNational 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 eLifeGenes & 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

Photo: Roger DavisThe 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.

Figure

Schematic diagram

Figure Legend

Schematic representation of the human MAP kinase signal transduction pathway network.


One or more keywords matched the following items that are connected to Davis, Roger

Item TypeName
Academic Article The JNK signal transduction pathway.
Academic Article Signal transduction by MAP kinases: regulation by phosphorylation-dependent switches.
Academic Article Murine Lyme arthritis development mediated by p38 mitogen-activated protein kinase activity.
Academic Article Signal transduction. MAP kinase signaling specificity.
Academic Article Interaction of the c-Jun/JNK pathway and cyclin-dependent kinases in death of embryonic cortical neurons evoked by DNA damage.
Academic Article Inhibition of the p38 pathway upregulates macrophage JNK and ERK activities, and the ERK, JNK, and p38 MAP kinase pathways are reprogrammed during differentiation of the murine myeloid M1 cell line.
Academic Article Survival signaling mediated by c-Jun NH(2)-terminal kinase in transformed B lymphoblasts.
Academic Article Deficiency in the c-Jun NH2-terminal kinase signaling pathway confers susceptibility to hyperoxic lung injury in mice.
Academic Article Suppression of inflammatory cytokine production by carbon monoxide involves the JNK pathway and AP-1.
Academic Article The transcriptional repressor HBP1 is a target of the p38 mitogen-activated protein kinase pathway in cell cycle regulation.
Academic Article Role of MLK3 in the regulation of mitogen-activated protein kinase signaling cascades.
Academic Article Signal transduction by the JNK group of MAP kinases.
Academic Article The JNK signal transduction pathway.
Academic Article A genetically encoded fluorescent sensor of ERK activity.
Academic Article A stress signaling pathway in adipose tissue regulates hepatic insulin resistance.
Academic Article c-Jun NH(2)-terminal kinase (JNK)1 and JNK2 signaling pathways have divergent roles in CD8(+) T cell-mediated antiviral immunity.
Academic Article Role of JNK in mammary gland development and breast cancer.
Academic Article JNK and PTEN cooperatively control the development of invasive adenocarcinoma of the prostate.
Academic Article c-Jun NH(2)-terminal kinase is essential for the regulation of AP-1 by tumor necrosis factor.
Academic Article Carbon monoxide modulates Fas/Fas ligand, caspases, and Bcl-2 family proteins via the p38alpha mitogen-activated protein kinase pathway during ischemia-reperfusion lung injury.
Academic Article Diverse mechanisms of myocardial p38 mitogen-activated protein kinase activation: evidence for MKK-independent activation by a TAB1-associated mechanism contributing to injury during myocardial ischemia.
Academic Article Mechanism of p38 MAP kinase activation in vivo.
Academic Article The death domain kinase RIP1 is essential for tumor necrosis factor alpha signaling to p38 mitogen-activated protein kinase.
Academic Article Signalling pathways involved in multisite phosphorylation of the transcription factor ATF-2.
Academic Article The c-Jun NH2-terminal kinase is essential for epidermal growth factor expression during epidermal morphogenesis.
Academic Article Role of the JIP4 scaffold protein in the regulation of mitogen-activated protein kinase signaling pathways.
Academic Article H2AX is a target of the JNK signaling pathway that is required for apoptotic DNA fragmentation.
Academic Article JNK2 is a positive regulator of the cJun transcription factor.
Academic Article Analyzing mitogen-activated protein kinase (MAPK) activities in T cells.
Academic Article AKAP-Lbc enhances cyclic AMP control of the ERK1/2 cascade.
Academic Article JNK expression by macrophages promotes obesity-induced insulin resistance and inflammation.
Concept MAP Kinase Signaling System
Academic Article Diet-induced obesity mediated by the JNK/DIO2 signal transduction pathway.
Academic Article Mnk2 alternative splicing modulates the p38-MAPK pathway and impacts Ras-induced transformation.
Academic Article Impaired JNK signaling cooperates with KrasG12D expression to accelerate pancreatic ductal adenocarcinoma.
Academic Article The PPARa-FGF21 hormone axis contributes to metabolic regulation by the hepatic JNK signaling pathway.
Academic Article Pathological axonal death through a MAPK cascade that triggers a local energy deficit.
Academic Article The cJUN NH2-terminal kinase (JNK) pathway contributes to mouse mammary gland remodeling during involution.
Academic Article The cJUN NH2-terminal kinase (JNK) signaling pathway promotes genome stability and prevents tumor initiation.

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