Patricia M.-J. Lievens
Role: Postdoctoral fellow
Platform: Neuroscience and Brain Technologies
Patricia Lievens graduated with honours in Biological Sciences at the University of Siena (Italy) in 1989. From 1990 to 1992 she conducted a research on transcription factors involved in myeloid differentiation supervised by Stuart Orkin, in the Department of Pediatric Oncology of Children’s Hospital at the Harvard Medical School of Boston (USA). Here she learned the basics of molecular biology and contributed to the cloning of the transcriptional repressor CCAAT Displacement protein (CDP). Back to Italy she pursued her studies until 1994 in the laboratory of Sergio Ottolenghi, in the Division of Human Genetics at the University of Milano. In 1995 she obtained a research contract at the Neurological Institute “C. Besta” of Milano to work on prion protein (PrP) diseases under the supervision of Fabrizio Tagliavini. Here she studied the genetic Gestmann-Sträussler-Sheinker disease, mainly contributing to the characterization of the biochemical properties and composition of PrP amyloid structures. In 2001 she moved to the University of Verona where she started a new project on Fibroblast Growth Factor Receptors (FGFRs) focusing on cellular and biochemical changes associated with mutated forms of FGFRs causing chondrodysplasias. The research was carried out with Elio Liboi in the Division of Biochemistry of the Department of Morphological and Biomedical Sciences. In 2007 she accomplished her PhD in Biology and Molecular and Cellular Pathology with a thesis on the characterization of the early secretory pathway of FGFRs biosynthesis.
Currently, she is a postdoctotal fellow at the Italian Institute of Technology (IIT) working with Alexander Dityatev on projects addressing the role of FGFRs and palmitoylation in neuronal plasticity and designing molecular tools to control adhesive interactions between neurons.
Patricia Lievens has a strong experimental background in molecular and cellular biology and biochemical techniques.
- Kochlamazashvili G, Henneberger C, Bukalo O, Dvoretskova E, Senkov O, Lievens P. M-J., Westenbroek R, Engel AK, Catterall WA, Rusakov DA, Schachner M, Dityatev A. The extracellular matrix molecule hyaluronic acid regulates hippocampal synaptic plasticity by modulating postsynaptic L-type Ca(2+) channels. Neuron 67, 116-128 (2010)
- Lievens P. M.-J., Zanolli E., Garofalo S., and Liboi E.. Cell adaptation to activated FGFR3 includes Sprouty4 up regulation to inhibit the receptor-mediated ERKs activation from the endoplasmic reticulum. FEBS Lett. 583, 3254-3258 (2009)
- Lievens P. M.-J., De Servi B., Garofalo S., Lunstrum G. P., Horton W.A. and Liboi E.. Transient dimerization and interaction with ERGIC-53 occur in the fibroblast growth factor receptor 3 early secretory pathway. Int. J. of Biochem. & Cell Biol. 40, 2649-59 (2008)
- Lievens P. M.-.J., Roncador A. and Liboi E. K644E/M FGFR3 mutants activate Erk1/2 from the Endoplasmic Reticulum through FRS2a and PLCg-independent pathways. J. Mol. Biol. 357, 783-792 (2006)
- Lievens P. M.-J., Mutinelli C., Baynes D. and Liboi E. The kinase activity of fibroblast growth factor receptor 3 with activation loop mutations affects receptor trafficking and signaling. J. Biol. Chem. 279, 43254-43260 (2004).
- Lievens P. M.-J. and Liboi E. The thanatophoric dysplasia type II mutation hampers complete maturation of FGF receptor 3, which activates STAT1 from the endoplasmic reticulum. J. Biol. Chem. 278, 17344-17349 (2003).
- Tagliavini F., Lievens P. M.-J., Trinchant C., Warter J.M., Mohr M., Perini F., Salmona M., Rossi G., Giaccone G., Piccardo P., Ghetti B., Bugiani O., Beavis R.C., Frangione B., Prelli F. N- and C-Terminal fragments of the Prion Protein participate in amyloid formation in Gerstmann-Sträussler-Scheinker disease with Ala to Val substitution at codon 117 (Alsatian family). J. Biol. Chem. 276, 6009-6015 (2001).
- Piccardo P., Dlouhy S. R., Lievens P. M.-J., Young K., Bird T. D, Nochlin D, Dickson D.W, Vinters H. V., Zimmermann T.R., Mackenzie I. R, Kish S. J, Ang L. C., De Carli C.,Pocchiari M., Brown P., Gibbs C. Jr., Gajdusek D.C., Bugiani O., Tagliavini F. and Ghetti B. Phenotypic varability of Gerstmann-Sträussler-Scheinker disease associated with prion protein heterogeneity. J. Neuropathol. Exp. Neurol. 57, 979-988 (1998).
- Jiménez-Huete A., Lievens P. M.-J., Vidal R., Piccardo P., Ghetti B., Tagliavini F., Frangione B. and Prelli F. Endogenous proteolytic cleavage of normal and disease-associated isoforms of the human prion protein in neurol and non-neural tissues. Am. J. Pathol. 153, 1561-1572 (1998).
- Tagliavini F., McArthur R. A., Canciani B., Giaccone G., Porro M., Bugiani M., Lievens P. M.-J., Bugiani O., Peri E., Dall'Ara P., Rocchi M., Poli G., Forloni G., Bandiera T., Varasi M., Suarato A., Cassutti P., Cervini M.A., Lansen J., Salmona M. and Post C. Effectiveness of anthracyclines against experimental prion disease in syrian hamsters. Science 276, 1119-1122 (1997).
- Lievens P. M.-J., Donady J. J., Tufarelli C. and Neufeld E. J. Repressor activity of CCAAT Displacement protein in HL-60 myeloid leukemia cells. J. Biol. Chem. 270, 12745-12750 (1995).
- Neufeld E.J., Skalnik D.G., Lievens P. M.-J., Orkin S.H. Human CCAAT displacement protein, a repressor of developmentally-regulated gene expression, is the homolog of the Drosophila homeodomain protein, Cut. Nature Genetics 1, 50-55 (1992).