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  • Anja Jaeschke, PhD
  • Assistant Professor
  •  
  • Metabolic Diseases Institute
  • Phone: (513) 558-3898
  • anja.jaeschke@uc.edu

Specialty/Interest:

  • 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. 

    Research Grants:

    • R01 DK082583 National Institute of Diabetes and Digestive and Kidney Diseases. MLK3 in Metabolic Stress Signaling, PI, 006991-001.

    Peer Reviewed Publications (in chronological order):

    • Lu, J., Borthwick, F., Hassanali, Z., Wang, Y., Mangat, R., Ruth, M., Shi, D., Jaeschke, A., Russell, J. C., Field, C. J., Proctor, S. D., & Vine, D. F. (2011). Chronic dietary n-3 PUFA intervention improves dyslipidaemia and subsequent cardiovascular complications in the JCR:LA- cp rat model of the metabolic syndrome . The British Journal of Nutrition , 1-11.
    • Jaeschke, A., & Davis, R. J. (2007). Metabolic stress signaling mediated by mixed-lineage kinases . Molecular Cell , 27 (3) , 498-508.
    • Hübner, A., Jaeschke, A., & Davis, R. J. (2006). Oncogene addiction: role of signal attenuation . Developmental Cell , 11 (6) , 752-4.
    • Jaeschke, A., Karasarides, M., Ventura, J., Ehrhardt, A., Zhang, C., Flavell, R. A., Shokat, K. M., & Davis, R. J. (2006). JNK2 is a positive regulator of the cJun transcription factor . Molecular Cell , 23 (6) , 899-911.
    • Jaeschke, A., & Davis, R. J. (2006). Chemical genetic analysis of signal transduction pathways . Expert Opinion on Therapeutic Targets , 10 (4) , 485-8.
    • Jaeschke, A., Rincón, M., Doran, B., Reilly, J., Neuberg, D., Greiner, D. L., Shultz, L. D., Rossini, A. A., Flavell, R. A., & Davis, R. J. (2005). Disruption of the Jnk2 (Mapk9) gene reduces destructive insulitis and diabetes in a mouse model of type I diabetes . Proceedings of the National Academy of Sciences of the United States of America , 102 (19) , 6931-5.
    • Brancho, D., Ventura, J., Jaeschke, A., Doran, B., Flavell, R. A., & Davis, R. J. (2005). Role of MLK3 in the regulation of mitogen-activated protein kinase signaling cascades . Molecular and Cellular Biology , 25 (9) , 3670-81.
    • Jaeschke, A., Czech, M. P., & Davis, R. J. (2004). An essential role of the JIP1 scaffold protein for JNK activation in adipose tissue . Genes & Development , 18 (16) , 1976-80.
    • Brancho, D., Tanaka, N., Jaeschke, A., Ventura, J., Kelkar, N., Tanaka, Y., Kyuuma, M., Takeshita, T., Flavell, R. A., & Davis, R. J. (2003). Mechanism of p38 MAP kinase activation in vivo . Genes & Development , 17 (16) , 1969-78.
    • Jaeschke, A., Hartkamp, J., Saitoh, M., Roworth, W., Nobukuni, T., Hodges, A., Sampson, J., Thomas, G., & Lamb, R. (2002). Tuberous sclerosis complex tumor suppressor-mediated S6 kinase inhibition by phosphatidylinositide-3-OH kinase is mTOR independent . The Journal of Cell Biology , 159 (2) , 217-24.