Prof. Dr. Tobias B. Huber
Tobias B. Huber is a Professor of Medicine, Heisenbergprofessor, Co-Director of the Center of Systems Biology, and Senior Attending Physician at the University Medical Center, Freiburg. Huber`s main research interests are in understanding the molecular mechanisms underlying glomerular disease. His team identified several key molecular mechanisms of podocyte biology and progressive glomerular disease. Specifically, his work identified signalling programs that regulate podocyte cell survival, endocytosis, cytoskeletal organization and polarity, providing novel insight of how podocytes contribute to glomerular diseases. The latest research of Huber’s team in Freiburg includes the study of mTor-autophagy signalling networks in glomerular disease and kidney aging. Tobias B. Huber received numerous awards including the Young Investigator Award of the American Society of Nephrology and the American Heart Association in 2012 (considered the world wide highest recognition for renal researchers younger than 45 years of age).
- Hartleben, B., Godel, M., Meyer-Schwesinger, C., Liu, S., Ulrich, T., Kobler, S., Wiech, T., Grahammer, F., Arnold, S.J., Lindenmeyer, M.T., Cohen, C.D., Pavenstadt, H., Kerjaschki, D., Mizushima, N., Shaw, A.S., Walz, G., and Huber, T.B. 2010. Autophagy influences glomerular disease susceptibility and maintains podocyte homeostasis in aging mice. J Clin Invest 120:1084-1096.
- Godel, M., Hartleben, B., Herbach, N., Liu, S., Zschiedrich, S., Lu, S., Debreczeni-Mor, A., Lindenmeyer, M.T., Rastaldi, M.P., Hartleben, G., Wiech, T., Fornoni, A., Nelson, R.G., Kretzler, M., Wanke, R., Pavenstadt, H., Kerjaschki, D., Cohen, C.D., Hall, M.N., Ruegg, M.A., Inoki, K., Walz, G., and Huber, T.B. 2011. Role of mTOR in podocyte function and diabetic nephropathy in humans and mice. J Clin Invest 121:2197-2209.
- Liu, S., Hartleben, B., Kretz, O., Wiech, T., Igarashi, P., Mizushima, N., Walz, G., and Huber, T.B. 2012. Autophagy plays a critical role in kidney tubule maintenance, aging and ischemia-reperfusion injury. Autophagy 8:826-837.
- Grahammer, F., Haenisch, N., Steinhardt, F., Sander, L., Roerden, M., Arnold, F., Cordts, T., Wanner, N., Reichardt, W., Kerjaschki, D., Ruegg, M.A., Hall, M.N., Moulin, P., Busch, H., Boerries, M., Walz, G., Artunc, F., and Huber, T.B. 2014. mTORC1 maintains renal tubular homeostasis and is essential in response to ischemic stress. Proc Natl Acad Sci U S A.
- Godel, M., Grahammer, F., and Huber, T.B. 2015. Thrombospondin type-1 domain-containing 7A in idiopathic membranous nephropathy. N Engl J Med 372:1073.
Membrane Trafficking in Ageing and Disease
Increasing age causes progressive deterioration of tissues and organs, leading to impaired tissue function, increased organismal vulnerability to infection, and death. Hence ageing is recognized as a prime disease factor. Improving health in the elderly will be crucial to deal with the enormous socio-economic challenges arising as a consequence of increased life expectancy. Membranes are at the center of cellular biology, compartmentalizing cells into functional distinct sub-compartments and constituting scaffolds for signal initiation and propagation. Hence, it is not surprising that deregulated membrane trafficking emerges also as key processes in ageing and disease. By combining model organisms, such as C.elegans and mouse, with mammalian cell culture, advanced molecular biology and protein biochemistry, and ‘omics’ approaches we aim at characterizing deregulated membrane trafficking in ageing and disease. This will allow a functional understanding of underlying biological processes which can be employed to design strategies promoting healthy ageing.