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Fabienne Maurer

    Fabienne Maurer received her PhD in Plant Biochemistry and Molecular Biology from the University of Neuchâtel (Switzerland) in 1995. As a junior postdoc, she moved to biomedical research, studying mRNA stability in the context of fibrinolysis first at Monash University in Melbourne (Australia) and then at the Friedrich Miescher Institute in Basel. Fabienne joined the Department of Medical Genetics in 2001 and has since been involved in a series of research projects covering various topics, starting from eye genetics in the mouse to cellular stress signalling in type 1 diabetes and mouse pharmacogenetics.  

Research summary

Pharmacogenetic analysis of the cardiovascular response in mice

Little is currently known about inherited susceptibility factors determining an individual's response to common drugs. Inbred mouse strains will be examined to identify naturally occurring genetic variations influencing cardiovascular responses to common β-adrenergic and β-blocking drugs. Following the establishment of basal and drug- dependent cardiovascular phenotypes in several lines, the most discriminative pairs of strains (i.e. presenting extreme and easily scorable phenotypes) will be further analyzed by standard genetic approaches (F2 or backcross) with the ultimate goal of identifying polymorphisms in new and previously unsuspected susceptibility genes. These results have potentially wide ramifications as they should open up onto a whole new field of functional, physiological or pharmacological projects and will eventually allow for the testing of the orthologous human regions for their involvement in the corresponding cardiovascular response.

(C. Berthonneche and F. Maurer, in collaboration with T. Pedrazzini and H. Abriel)


Representative Publications (Complete list of publications (PubMed))

Hersch M., Peter B., Kang H.M., Schüpfer F., Abriel H., Pedrazzini T., Eskin E., Beckmann J.S., Bergmann S., Maurer F., 2012. Mapping genetic variants associated with beta-adrenergic responses in inbred mice. PLoS ONE 7(7) pp. e41032.

Berthonneche C. , Peter B. , Schupfer F. , Hayoz P. , Kutalik Z. , Abriel H. , Pedrazzini T. , Beckmann J.S. , Bergmann S. , Maurer F., 2009. Cardiovascular response to beta-adrenergic blockade or activation in 23 inbred mouse strains. PLoS ONE 4(8) p. e6610.

Bustamante M. , Tasinato A. , Maurer F. , Elkochairi I. , Lepore M.G. , Arsenijevic Y. , Pedrazzini T. , Munier F.L. , Schorderet D.F., 2008. Overexpression of a mutant form of TGFBI/BIGH3 induces retinal degeneration in transgenic mice. Molecular Vision 14 p. 1129-1137.

Sarre A., Gardier S., Maurer F., Bonny C., Raddatz E., 04-2008. Modulation of the c-Jun N-terminal kinase activity in the embryonic heart in response to anoxia-reoxygenation: involvement of the Ca(2+) and mitoK (ATP) channels. Molecular and Cellular Biochemistry.

Cardozo A. K. , Buchillier V. , Mathieu M. , Chen J. , Ortis F. , Ladriere L. , Allaman-Pillet N. , Poirot O. , Kellenberger S. , Beckmann J. S. , Eizirik D. L. , Bonny C. , Maurer F., 2007. Cell-permeable peptides induce dose- and length-dependent cytotoxic effects. Biochimica et Biophysica Acta 1768(9) p. 2222-34.

Kristensen O. , Guenat S. , Dar I. , Allaman-Pillet N. , Abderrahmani A. , Ferdaoussi M. , Roduit R. , Maurer F. , Beckmann J.S. , Kastrup J.S. , Gajhede M. , Bonny C., 2006. A unique set of SH3-SH3 interactions controls IB1 homodimerization. EMBO Journal 25(4) p. 785-797.

Schorderet D. F. , Manzi V. , Canola K. , Bonny C. , Arsenijevic Y. , Munier F. L. , Maurer F., 2005. D-TAT transporter as an ocular peptide delivery system. Clinical and Experimental Ophthalmology 33(6) p. 628-35.

Beckmann J.S. , Maurer F. , Delorenzi M. , Falquet L., 2005. On ubiquitin ligases and cancer. Human mutation 25(6) p. 507-12. 

Beckmann J.S. , Maurer F. , Delorenzi M. , Falquet L., 2004. Ubiquitin ligases as cancer genes. Nature Reviews Cancer. Online Correspondence

Hirt L. , Badaut J. , Thevenet J. , Granziera C. , Regli L. , Maurer F. , Bonny C. , Bogousslavsky J., 07-2004. D-JNKI1, a cell-penetrating c-Jun-N-terminal kinase inhibitor, protects against cell death in severe cerebral ischemia. Stroke 35(7) p. 1738-43.

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