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Michael Köttgen

Prof. Dr.
Michael Köttgen

Department of Medicine IV
Phone: 0049-761-270-32990

www.nephrolab.org/groups/michael-koettgen

CV

  • 1997-1998 Residency, Department of Medicine, Medical Center – University of Freiburg
  • 1998-2004 Postdoctoral Fellow, Institute of Physiology and Department of Medicine, University of Freiburg
  • 2004-2009 Postdoc - Research Associate, Department of Biological Chemistry, Johns Hopkins University, Baltimore, USA
  • 2010 Adjunct Professor, Department of Medicine, Johns Hopkins University, School of Medicine, Baltimore, USA
  • Since 2010 Full Professor (W3), Department of Medicine IV, Medical Center – University of Freiburg

Focus of research

  • Molecular pathogenesis of hereditary kidney disease
  • Signal transduction

Selected publications

  • Hofherr A, Köttgen M. Polycystic kidney disease: Cilia and mechanosensation revisited. Nat Rev Nephrol 12, 2016; 318-319.
  • Hofherr A, Wagner CJ, Watnick T, Köttgen M. Targeted rescue of a polycystic kidney disease mutation by lysosomal inhibition. Kidney Int. 2016; 89,949-955.
  • Hofherr A, Wagner C, Fedeles S, Somlo S, Köttgen M. N-glycosylation determines the abundance of the transient receptor potential channel TRPP2. J Biol Chem. 2014; 289, 14854-14867.
  • Wegierski T, Steffl D, Kopp C, Tauber R, Buchholz B, Nitschke R, Kuehn EW, Walz G, Köttgen M. TRPP2 channels regulate apoptosis through the Ca2+ concentration in the endoplasmic reticulum. EMBO J. 2009; 28, 490-499.
  • Woodward OM, Köttgen A, Coresh J, Boerwinkle E, Guggino WB, Köttgen M. Identification of a urate transporter, ABCG2, with a common functional polymorphism causing gout. Proc Natl Acad Sci USA. 2009; 106,10338-10342.

Research methods

  • Drosophila genetics
  • Live imaging - electrophysiology
  • Genome editing