Markus Rüegg

Markus Rüegg is a Swiss neurobiologist and professor at the Biozentrum of the University of Basel.
Life
Markus Rüegg studied biochemistry at the University of Zurich and graduated with a PhD in the field of Neurobiology. In 1989 he went as a postdoctoral fellow to conduct research at the Department of Neurobiology at Stanford University School of Medicine. In 1992 he was appointed as Assistant Professor to the Biozentrum, University of Basel. Since 1998 he is a Professor of Neurobiology and teaches and conducts research at the Biozentrum of the University of Basel.
Work
Rüegg studies the molecular processes important for the formation and function of the neuromuscular system. A major part of his investigations involve the characterization of the extracellular and intracellular signaling pathways. Markus Rüegg has successfully developed new approaches for the therapy of merosin-deficient congenital muscular dystrophy, a serious genetic disease. In addition, his research group has recently demonstrated that the multi-protein complex mTORC1 is an important regulator of muscle growth and autophagy, a cellular self-cleaning process. These findings may help to counteract pathological muscle degradation and to develop new therapy strategies.
Awards and honors
*2000 Robert Bing Prize of the Swiss Academy of Medical Sciences
*2013 Chairperson, Scientific Advisory Board of the “ Swiss Foundation for Research on Muscle Diseases ” (SSEM)
*2000 - 2007 Council Member of the der Swiss Society for Neuroscience
*2014 Member of the Research Committee of the European Neuromuscular Centre (ENMC)
Notable publications
Full publication list
*Ruegg, M.A., Tsim, K.W., Horton, S.E., Kröger, S., Escher, G., Gensch, E.M., and McMahan, U.J. (1992). The agrin gene codes for a family of basal lamina proteins that differ in function and distribution. Neuron 8, 691-699.
*Moll, J., Barzaghi, P., Lin, S., Bezakova, G., Lochmuller, H., Engvall, E., Muller, U., and Ruegg, M.A. (2001). An agrin minigene rescues dystrophic symptoms in a mouse model for congenital muscular dystrophy. Nature 413, 302-307.
*Bentzinger, C.F., Romanino, K., Cloetta, D., Lin, S., Mascarenhas, J.B., Oliveri, F., Xia, J., Casanova, E., Costa, C.F., Brink, M., Zorzato, F., Hall, M.N., and Rüegg, M.A. (2008). Skeletal muscle-specific ablation of raptor, but not of rictor, causes metabolic changes and results in muscle dystrophy. Cell Metab 8, 411-424.
*Meinen, S., Lin, S., Thurnherr, R., Erb, M., Meier, T., and Ruegg, M.A. (2011). Apoptosis inhibitors and mini-agrin have additive benefits in congenital muscular dystrophy mice. EMBO Mol Med 3, 465-479.
*Castets, P., Lin, S., Rion, N., Di Fulvio, S., Romanino, K., Guridi, M., Frank, S., Tintignac, L.A., Sinnreich, M., and Ruegg, M.A. (2013). Sustained Activation of mTORC1 in Skeletal Muscle Inhibits Constitutive and Starvation-Induced Autophagy and Causes a Severe, Late-Onset Myopathy. Cell Metab 17, 731-744.

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