Bob Friesel, Ph.D.
Maine Medical Center Research Institute
81 Research Dr
Scarborough ME, 04103
Phone: (207) 396-8147
Robert E. Friesel, Ph.D. is Senior Scientist, Director of Basic Science, and Director of the Center for Molecular Medicine at Maine Medical Center Research Institute. Dr. Friesel received his Ph.D. in Biochemistry and Molecular Biology from the George Washington University School of Medicine in 1989. He did postdoctoral training at the National Institutes of Heath in the Laboratory of Molecular Genetics at the National Institute of Child Health and Human Development from 1989-1990. Dr. Friesel was a staff scientist at the Holland Laboratory of the American Red Cross from 1990-1998. He is a member of the graduate faculty at the University of Maine, and an adjunct member of the faculty of the University of Southern Maine.rnDr. Friesel’s research has been funded by the National Institutes of Health since 1991. He is currently principal investigator of an NIH R01 grant, and an NIH Center of Biomedical Research Excellence (COBRE) grant in Vascular Biology in its ninth year awarded by the National Center for Research Resources. Dr. Friesel has served on numerous national and international peer review committees and advisory boards. Currently, Dr. Friesel serves on the Steering Committee for the National COBRE Conference and is a member of a peer review committee for the Founders Affiliate of the American Heart Association.rnrnrn
Dr. Friesel’s career has concentrated on growth factor-mediated mechanisms of angiogenesis, tissue remodeling, and development. These studies include several approaches such as transgenic and knockout mouse models, cell and molecular biology, in vitro and in vivo imaging, and proteomics. Dr. Friesel’s laboratory is investigating the molecular basis of blood vessel growth regulation by tyrosine kinase receptors (RTK) and the mechanisms by which RTK signaling is regulated. These studies have identified new targets for therapeutic intervention in vascular disease and cancer. rnAnother area of research interest of this laboratory is skeletal development and remodeling. This research is focused on understanding normal mechanisms of skeletal development and the molecular consequences of mutations in fibroblast growth factor receptor genes which cause inherited disorders such as dwarfism and craniosynostosis. Several growth factor signaling pathways regulate skeletal and craniofacial development, and we are investigating the mechanism by which these pathways regulate one another.
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. rnTsang, 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.rnMood, K., Friesel, R. and Daar, I. SNT/1FRS2 Mediates Germinal Vesicle Breakdown Induced by an Activated FGF Receptor 1 in Xenopus Oocytes. J. Biol. Chem, 277:33196-33204, 2002. rnKovalenko, D., Yang, X., Nadeau, R.J., Harkins, L.K. and Friesel, R., Sef Inhibits Fibroblast Growth Factor Signaling by Inhibiting FGFR1 Tyrosine Phosphorylation and Subsequent ERK Activation. J. Biol. Chem., 278: 14087-14091, 2003.rnYang, X., Kovalenko, D., Nadeau, R.J., Harkins, L.K., Mitchell, J., Zubanova, O., Chen, P-Y and Friesel, R. Sef Interacts with TAK1 and Mediates JNK Activation and Apoptosis. J. Biol. Chem., 279: 38099-38102, 2004.rnLindner, V., Wang, Q., Conley, B.A., Friesel, R.E. and Vary, C.P. Vascular Injury Induces Expression of Periostin: Implications for Vascular Cell Differentiation and Migration. Arterioscler. Thromb. Vasc. Biol., 25:77-83, 2005.rnPyagay, P., Heroult, M., Wang, Q., Lehnert, W., Belden, J., Liaw, L., Friesel, R. and Lindner, V. Collagen Triple Helix Containing1 (Cthrc1), a Novel Secreted Protein in Injured and Diseased Arteries Inhibits Collagen Expression and Cell Migration. Circ. Res., 96:261-268, 2005.rnYang, X., Webster, J.B., Kovalenko, D., Nadeau, R.J., Zubanova, O., Chen, P.-Y. and Friesel, R. Sprouty Genes are expressed in Osteoblasts and Inhibit FGF-mediated Responses. Calcif. Tissue Intl., 78:233-240, 2006.rnKovalenko, D, Yang, X., Chen, P.-Y., Nadeau, R.J., Zubanova, O., Pidgeon, K. and Friesel, R. A Role for Extracellular and Transmembrane Domains of mSef in mSef-mediated Inhibition of FGF Signaling. Cellular Signaling, 18(11):1958-1966, 2006.rnDuarte M, Kolev V, Soldi R, Kirov A, Graziani I, Marta-Oliveira S, Kacer D, Friesel R, Maciag T, Prudovsky I: Thrombin induces rapid PAR1-mediated non-classical FGF1 release. Biochem. Biophys. Res. Comm., 350(3):604-609, 2006. rnNadeau, R.J., Toher, J., Yang, X., Kovalenko, D., and Friesel, R. Regulation of Sprouty Stability by Mammalian Seven-in-Absentia Homolog 2. J. Cell. Biochem., 100:151-160, 2007.rnO’Neill, C.F., Urs, S., Cinelli, C., Lincoln, A., Nadeau R.J., Leon, R., Toher, J., Mouta-Bellum, C., Friesel, R., and Liaw, L. Notch2 Signaling Induces Apoptosis and Inhibits Human MDA-MB-231 Xenograft Growth. Am. J. Pathol., 171:1023-1036, 2007.rnNikopoulis, G., Duarte, M., Bellum, S., Kubu, C., Friesel, R., Maciag, T., Prudovsky, I., and Verdi, J. Soluble Jagged1 Attenuates Lateral Inhibition Allowing for Clonal Expansion of Neural Crest Stem Cells. Stem Cells, 25:3133-3142, 2007.rnConnerney, J., Andreeva, V., Leshem, Y., Mercado, M.A., Yang, X., Friesel, R., and Spicer, D.B. Twist homodimers promote increased FGF-responsiveness and craniosynostosis. Developmental Biology, 318:323-334, 2008.rnYang, X., Harkins, L.K., Zubanova, O., Harrington, A., Kovalenko, D., Nadeau, R.J., Chen, P.Y., Toher, J.L., Lindner, V., Liaw, L., and Friesel, R. Overexpression of Spry1 in Chondrocytes Causes Attenuated FGFR Ubiquitination and Sustained ERK Activation Resulting in Chondrodysplasia. (Developmental Biology, in press, PMID 18582454).
Front Row: Qing He, Yan Gong, Lindsey Gower
Back Row: Xuehui Yang, Robert Friesel, Ruth Leon