Maureen A. Harrington, Ph.D.



Co-Director of the Medical Scientist Training Program,
Associate Dean of Medical Student Education in Foundational Sciences

Department of Biochemistry and Molecular Biology
Indiana University School of Medicine
John D. Van Nuys Medical Science Building
635 Barnhill Drive, Room 4071F
Indianapolis, Indiana 46202-5126

Phone: (317) 274-7527
Facsimile: (317) 274-4686 



B.S. in Nutrition, 1978, Purdue University, West Lafayette, IN
M.S. in Toxicology, 1980, University of Texas School of Public Health, Houston TX
Ph.D. in Pharmacology, 1985, University of North Carolina, Chapel Hill, NC
Postdoctoral Fellow, 1987, University of Southern California, Los Angeles, CA
Postdoctoral Fellow, 1988, Indiana University School of Medicine, Indianapolis, IN


Area of Study

Regulation and development of innate immune response; TNF signaling; blood cell development.  More details...


Selected Recent Publications

Vig, E., Green, M., Liu, Y., Kang-Yeol, K., Kwon, H-J., Tian, J., Goebl, M. and Harrington, M.A. (2001) SIMPL is a TNF RI-mPLK/IRAK dependent NF-kB activator. J. Biol. Chem. 276(11): 7859-7866.

Yu, Kang-Yeol, Kwon, Hyung-Joo, Norman, D.A.M., Vig, E. and Harrington, M.A. (2002) Mouse Pellino-2 Modulates Interleukin-1 and Lipopolysaccharide Signaling. J. Immunol. Cutting Edge 169: 4075-4078.

Kwon, H-Y, Breese, E.H., Vig-Varga, E., Luo, Y., Lee, Y., Goebl, M.G. and Harrington, M.A. (2004) Tumor Necrosis Factor Alpha Induction of NF-kB requires the Novel Coactivator SIMPL. Mol. Cell. Biol. 24(21): 9317-9326.

Kim, J-a., Yeh, D.C., Ver, M., Li, Y., Carranza, A., Conrads, T.P., Veenstra, T.D., Harrington, M.A., and Quon, M.J. (2005) Phosphorylation of Ser24 in the pleckstrin homology domain of insulin receptor substrate-1 by Mouse Pelle-like kinase/interleukin-1 receptor-associated kinase: cross-talk between inflammatory signaling and insulin signaling that may contribute to insulin resistance. J Biol Chem. 280(24):23173-83.

Haag-Breese, E.., Uversky, V.N., Georgiadis, M.M and Harrington, M.A. (2006) The disordered amino-terminus of SIMPL interacts with members of the 70-kDa Heat-Shock Protein Family. DNA Cell Biol. 25(12):704-14.

Luo, Y., Kwon, H-J., Montano, S., Georgiadis, M., Goebl, M. G., and Harrington, M. A. (2007) Phosphorylation of SIMPL modulates RelA associated NF-κB dependent transcription. Am J Physiol Cell Physiol. 292(3):C1013-23.

Ott, L.W., Resing, K.A., Sizemore, A.W., Heyen, J.W., Cocklin, R.R., Pedrick, N.M., Woods, H.C., Chen, J.Y., Goebl, M.G., Witzmann, F.A. and Harrington, M.A. (2007) Tumor Necrosis Factor-a and interleukin-1 induced cellular response: coupling proteomic and genomic information. J. Proteomic Sciences 6(6):2176-85.

Lockett, Angelia, Goebl, M. and Harrington, M.A. (2008) Transient membrane recruitment of IRAK-1 in response to LPS and IL-1{beta} requires TNF R1. Am J Physiol Cell Physiol. 295(2):C313-23.

Benson, E.A., Goebl, M.G., Yang, F-C., Kapur, R., McClintick, J., Sanghani, S., Clapp, D.W. and Harrington, M.A. (2010) Loss of SIMPL Compromises TNFα Dependent Survival of Hematopoietic Progenitors. Exp. Hematol. 38(2):71-81.

Zhao, W., Breese, E., Bowers, A., Hoggatt, J., Pelus, L.M., Broxmeyer, H.E., Goebl, M.G. and Harrington, M.A. (2013) SIMPL enhancement of tumor necrosis factor-α dependent p65-MED1 complex formation is required for mammalian hematopoietic stem and progenitor cell function PLoS One 8(4):e61123.


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Research Interests

The pathophysiology associated with numerous chronic non-infectious inflammatory diseases, cardiovascular diseases, diabetes and possibly certain cancers is due in part to a dysregulated innate immune response. In vivo, the cytokine, Tumor necrosis factor-alpha (TNFα) is required for innate immune response activation. A key transcriptional regulators of TNFα induced genes is the NF-kappaB/c-rel family of transcription factors. We have determined that the interleukin-1 receptor associated kinase [IRAK-1, also known as the mouse pelle-like kinase (mPLK)] functions in a TNFα dependent pathway that leads to activation of NF-κB dependent gene expression. We have identified an IRAK-1 substrate termed SIMPL (signaler that interacts with mPLK) which is a nuclear protein that synergizes with p65 to promote endogenous NF-κB dependent gene expression. How TNFα regulates IRAK-1 catalytic activity and the functional significance of IRAK-1 induced modulation of SIMPL activity are unknown. We have generated a SIMPL knock-out mouse and are in the process of defining its phenotype in the context of hematopoiesis and non-infectious chronic inflammatory diseases. Proteomic and genomic based approaches are being used to identify controlled cellular events, to determine how IRAK-1 activity is regulated; to determine the role SIMPL plays in the regulation of p65 dependent transcription and to determine how SIMPL activity is regulated. A second research focus in the lab is on the role the inflammatory response plays in the development of ovarian cancer. We are using a syngenic mouse model of ovarian cancer to explore whether the expression of TNFα dependent signaling pathway components alters the development of ovarian epithelial cell cancers. 


635 Barnhill Dr | Indianapolis, IN 46202 | Ph: (317) 274-7151 | Fax: (317) 274-4686