The overall aim of Dr. Jaeschke's laboratory is to investigate the role of stress-activated protein kinases in metabolic signal transduction. Metabolic syndrome, which is associated with obesity, insulin resistance, type 2 diabetes, and non-alcoholic fatty liver disease (NAFLD), is a major health problem world-wide. The cJun-NH2-stress-activated kinase (JNK) pathway is emerging as important player in the development of obesity-induced insulin resistance and NAFLD. The major goal is to obtain deeper knowledge of the mechanism by which obesity regulates the JNK pathway and how this pathway is involved in the control of metabolic diseases. This information will provide the basis for the design of rational therapeutic strategies for the control of metabolic diseases. The methods that the lab is using include recombinant DNA technology, general biochemical techniques, cell culture and knock-out mice.
Jaeschke, A., Davis, R.J. Metabolic stress signaling mediated by mixed-lineage kinases. (2007) Mol Cell 27 (3),498-508
Jaeschke A., Karasarides M., Ventura JJ., Ehrhardt A., Zhang C., Flavell RA., Shokat KM., Davis RJ (2006) JNK2 is a positive regulator of the cJun transcription factor. Mol Cell 23 (6), 899-911
Jaeschke A., Rincon M., Doran B., Reilly J., Neuberg D., Greiner DL., Shultz LD., Rossini AA., Flavell RA., Davis RJ. (2005) Disruption of the JNK2 (Mapk9) gene reduces insulitis and diabetes in a mouse model of type I diabetes. Proc Natl Acad Sci USA 102(19), 6931-6935
Brancho D., Ventura JJ., Jaeschke A., Doran B., Flavell RA., Davis RJ. (2005) Role of MLK3 in the regulation of mitogen-activated protein kinase signaling cascades. Mol Cell Biol 9, 3670-3681
Jaeschke A., Czech MP., Davis RJ. (2004) An essential role of the JIP1 scaffold protein for JNK activation in adipose tissue. Genes Dev 18, 1976-1980