Robert E. Friesel, Ph.D.

Center for Molecular Medicine, (Director)
Maine Medical Center Research Institute
81 Research Drive
Scarborough, ME 04074
(207) 885-8147 Office
(207) 885-8178 Lab
(207) 885-8179 Fax
friesr@mmc.org

Biosketch

Robert E. Friesel, Ph.D., a principal investigator at Maine Medical Center Research Institute (MMCRI) and the Center for Molecular Medicine, received his Ph.D. from George Washington University Medical Center in Washington, D.C. He obtained postdoctoral training in the Laboratory of Molecular Genetics at the National Institute for Child Health and Human Development. Dr. Friesel joined MMCRI in 1998 after 8 years as a principal investigator at the Holland Laboratory for the Biomedical Sciences at the American Red Cross. Dr. Friesel has served as a member of several peer review committees for  a variety of funding agencies.

Research Interests

My laboratory is interested in the role of fibroblast growth factors (FGFs) and their receptors in the regulation of bone growth and homeostasis as well as mesoderm induction and development of the vasculature. FGFs play a significant role in the development of several tissues and organ systems. Recently, we have focused on the functional consequences of mutations in human FGF receptor genes that have been associated with several disorders of bone growth and development. Our laboratory has demonstrated that many of these mutations, which occur in either the extracellular, transmembrane or kinase domains of these receptors, and most often occur as single point mutations, result in constitutive activation of the receptor's tyrosine kinase activity. We are currently investigating the changes in the signal transduction potential of these mutant receptors in an effort to determine the molecular etiology of these syndromes as well as potential strategies for therapeutic intervention. More recently, the laboratory has become interested in the feedback inhibition of the FGFR pathway by members of a gene family called sprouty, and a transmembrane domain protein called Sef.

Selected Publications

Neilson, K.M., and Friesel, R., Constitutive Activation of Fibroblast Growth Factor Receptor-2 by a Point Mutation Associated with Crouzon Syndrome. J. Biol. Chem. 270:26037-26040, 1995.

Yang, C.Q. and Friesel, R., Identification of a receptor-like protein tyrosine phosphatase expressed during Xenopus development. Dev. Dyn. 212:403-412, 1998.

Friesel, R. and Maciag, T., Fibroblast growth factor prototype release and fibroblast growth factor receptor signaling. Thromb. Haemost., 82(2):748-754, 1999.

Chong, L.D., Latimer, E., Kyun-Park, E., Friesel, R. and Daar I.O., FGF Receptor-Mediated Rescue of xEphrinB1-induced Cell Dissociation in Xenopus Embryos. Mol. Cell. Biol. 20(2):724-734, 2000.

Tsang, M., Friesel, R., Kudoh, T., and Dawid, I.B. Identification of Sef, a Novel Modulator of FGF Signaling. Nat.Cell Biol., 4(2):165-169, 2002.

Kovalenko, D., Yang, X., Nadeau, R., Harkins, L. and Friesel, R. Sef Inhibits Fibroblast Growth Factor Signaling by Inhibiting FGFR1 Tyrosine Phosphorylation and Subsequent ERK Activation. J. Biol. Chem. 2003; 278:14087-14091.

Lab Photo

Left to Right: Michael Summers, Pei Yu Chen, Robert Nadeau (in rear), Dmitry Kovalenko, Olga Zubanova, Xuehui Yang, Lauren Graham, Robert Friesel