Cluster of Excellence –
University of Freiburg

Prof. Dr. Tobias Huber

Prof. Dr. Tobias Huber

Department of Nephrology, University Medical Center Freiburg

+49 761 270 35590

Our team initiated a Glomerular Research Programm for the analysis of signalling networks regulating glomerular diseases. This platform includes various transgenic mouse models and invertebrate models to identify different aspects of glomerular diseases. We truely believe in the inestimably value of scientific cooperation and many of our projects involve close local, national and international collaborations.                   

Glomerular kidney diseases are of major public health importance not only because of their high prevalence, but also because they are a major independent risk factor for cardiovascular morbidity and mortality. Despite the crucial importance of the kidney both as a target and as determinant of human disease, knowledge of the molecular networks underlying glomerular development, regeneration and diseases is very limited. Our studies aim to elucidate molecular programs that will help to formulate therapeutic interventions that delay the onset and progression of glomerular diseases.

Our research focuses on four main topics:

1.) Mechanisms of glomerular development.

2.) Slit diaphragm signalling and Neph1-Nephrin protein biology.

3.) Signalling networks regulating kidney regeneration and glomerular aging.

4.) mTor signalling in polycystic kidney disease.

10 selected publications:

  • Thrombospondin type-1 domain-containing 7A in idiopathic membranous nephropathy.
    Godel M, Grahammer F, Huber TB. (2015).
    N Engl J Med 372(11):1073
  • Calciphylaxis.
    Zhou Q, Neubauer J, Kern JS, Grotz W, Walz G, Huber TB. (2014).
    Lancet 383(9922):1067
  • mTORC1 maintains renal tubular homeostasis and is essential in response to ischemic stress.
    Grahammer F, Haenisch N, Steinhardt F, Sander L, Roerden M, Arnold F, Cordts T, Wanner N, Reichardt W, Kerjaschki D, Ruegg MA, Hall MN, Moulin P, Busch H, Boerries M, Walz G, Artunc F, Huber TB. (2014).
    Proc Natl Acad Sci U S A. 111(27):E2817-26.
  • AKT2 is essential to maintain podocyte viability and function during chronic kidney disease.
    Canaud G, Bienaime F, Viau A, Treins C, Baron W, Nguyen C, Burtin M, Berissi S, Giannakakis K, Muda AO, Zschiedrich S, Huber TB, Friedlander G, Legendre C, Pontoglio M, Pende M, Terzi F. (2013).
    Nat Med 19(10):1288-96
  • FAN1 mutations cause karyomegalic interstitial nephritis, linking chronic kidney failure to defective DNA damage repair.
    Zhou W, Otto EA, Cluckey A, Airik R, Hurd TW, Chaki M, Diaz K, Lach FP, Bennett GR, Gee HY, Ghosh AK, Natarajan S, Thongthip S, Veturi U, Allen SJ, Janssen S, Ramaswami G, Dixon J, Burkhalter F, Spoendlin M, Moch H, Mihatsch MJ, Verine J, Reade R, Soliman H, Godin M, Kiss D, Monga G, Mazzucco G, Amann K, Artunc F, Newland RC, Wiech T, Zschiedrich S, Huber TB, Friedl A, Slaats GG, Joles JA, Goldschmeding R, Washburn J, Giles RH, Levy S, Smogorzewska A, Hildebrandt F. (2012).
    Nat Genet 44(8):910-5
  • Autophagy plays a critical role in kidney tubule maintenance, aging and ischemia-reperfusion injury.
    Liu S, Hartleben B, Kretz O, Wiech T, Igarashi P, Mizushima N, Walz G, Huber TB. (2012).
    Autophagy 8(5):826-37
  • Role of mTOR in podocyte function and diabetic nephropaty in humans and mics.
    Gödel M, Hartleben B, Herbach N, Lu S, Debreczeni-Mór A, Liu S, Lindenmeyer MT, Rastaldi MP, Hartleben G, Wiech T, Fornoni A, Nelson RG, Kretzler M, Wanke R, Pavenstädt H, Kerjaschki D, Cohen CD, Hall MN, Rüegg MA, Inoki K, Walz G, and Huber TB (2011). 
    J Clin Invest. 121(6):2197-209.
  • Autophagy influences glomerular disease susceptibility and maintains podocyte homeostasis in aging mice.
    Hartleben B, Godel M, Meyer-Schwesinger C, Liu S, Ulrich T, Kobler S, Wiech T, Grahammer F, Arnold SJ, Lindenmeyer MT, Cohen CD, Pavenstadt H, Kerjaschki D, Mizushima N, Shaw AS, Walz G, Huber TB. (2010).
    J Clin Invest 120(4):1084-96
  • Podocin and MEC-2 bind cholesterol to regulate the activity of associated ion channels.
    Huber TB, Schermer, B, Müller, RU, Höhne, M, Bartram, M, Calixto, A, Hagmann, H, Reinhardt, C, Koos, F, Kunzelmann, K, Shirokova, E, Krautwurst, D, Harteneck, D, Simons, M, Pavenstädt, H, Kerjaschki, D, Thiele, C, Walz, G, Chalfie, M, Benzing, T (2006). 
    Proc Natl Acad Sci USA 103(46):17079-86
  • Combined heterozygosity of CD2AP, Fyn and Synaptopodin leads to Focal Segmental Glomerulosclerosis.
    Huber TB, Kwoh C, Wu H, Godel M, Blumer KJ, Miner JH, Mundel P, Shaw AS. (2006).
    J Clin Invest 116(5):1337-45
  • Molecular basis of the functional podocin-nephrin complex: mutations in the NPHS2 gene disrupt nephrin targeting to lipid raft microdomains.
    Huber TB, Simons M, Hartleben B, Sernetz L, Schmidts M, Gundlach E, Saleem MA, Walz G, Benzing T. (2003).
    Hum Mol Genet 12(24):3397-405
  • Nephrin and CD2AP associate with phosphoinositide 3-OH kinase and stimulate AKT dependent signaling.
    Huber TB, Hartleben B, Kim J, Schmidts M, Schermer B, Keil A, Egger L, Lecha RL, Borner C, Pavenstadt H, Shaw AS, Walz G, Benzing T. (2003). 
    Mol Cell Biol 23(14):4917-28
  • Bigenic mouse models of focal segmental glomerulosclerosis involving pairwise interaction of CD2AP, Fyn, and synaptopodin.
    Huber TB, Kwoh C, Wu H, Asanuma K, Godel M, Hartleben B, Blumer KJ, Miner JH, Mundel P, Shaw AS. (2006).
    J Clin Invest 116(5):1337-45.