Prof. Dr. rer. nat.

Ursula Klingmüller

Deutsches Krebsforschungszentrum

Born in 1964

Professional Background

  • Since 2011 Professor for Systems Biology of Signal Transduction at the University of Heidelberg
  • Since 2007 Head of the Division Systems Biology of Signal Transduction at the German Cancer Research Center (DKFZ) in Heidelberg
  • 2006 Refusal of a call for a professorship in Quantitative Systems Biology from Chalmers University of Technology in Gothenburg/Sweden
  • Venia legendi in Cell Biology at the University of Heidelberg
  • 2003 – 2007 Leader of the Theodor Boveri Junior Research Group at the German Cancer Research Center (DKFZ) in Heidelberg
  • 2003 Refusal of a call for a professorship from the Technical University of Aachen
  • 2000 Habilitation and Venia legendi in Molecular Biology and Genetics at the University of Freiburg
  • 1996 – 2003 Group leader of a Hans-Spemann Junior-Group at the Max Planck Institute of Immunobiology in Freiburg
  • 1993 – 1996 Postdoctoral Fellow at the Whitehead Institute for Biomedical Research in Cambridge/USA
  • 1992 – 1996 Postdoctoral Fellow at the Harvard Medical School in Boston
  • 1992 PhD as Dr. rer. nat at the University of Heidelberg
  • 1983 – 1988 Studies and Diploma in Biology at the University of Heidelberg

Memberships (Selection)

  • 2016 Appointment to the German Ethics Council
  • German Society for Cell Biology
  • German Society of Proteome Research
  • German Society for Lung Research
  • Executive Committee of the Assistance Measures of the Federal Ministry of Education and Research for “Artificial Liver” and “LiSyM”
  • Scientific Council of the Centre for Systems Biology in Groningen/Netherlands
  • Scientific Council BREAST in Dublin/Ireland
  • Chair of the Executive Women of the German Cancer Research Center (DKFZ) in Heidelberg
  • Board of Trustees of the German Cancer Research Center (DKFZ) in Heidelberg (2007 – 2015)

Publications (Selection)

  • Klingmüller, U., Lorenz, U., Cantley, L. C., Neel, B. G., and Lodish H. F.. Specific recruitment of SH-PTP1 to the erythropoietin receptor causes inactivation of JAK2 and termination of proliferative signals. Cell (1995), 80:729-738
  • Swameye, I., Müller, T. G., Timmer, J., Sandra, O., and Klingmüller, U., Identification of nucleocytoplasmic cycling as a remote sensor in cellular signaling by data-based dynamic modeling. Proc. Natl. Acad. Sci. USA (2003), 100:1028-33
  • Becker, V., Schilling, M., Bachmann, J., Baumann, U., Raue, A., Maiwald, T., Timmer, J., and Klingmüller, U., Covering a Broad Dynamic Range – Information Processing at the Erythropoietin Receptor. DOI: 10.1126/science.1184913. Science (2010), 328(5984):1404-8
  • Bachmann, J., Raue, A., Schilling, M., Boehm, ME., Kreutz, C., Kaschek, D., Busch, H., Gretz, N., Lehmann, WD., Timmer, J., Klingmüller, U. Division of labor by dual feedback regulators controls JAK2/STAT5 signaling over broad ligand range. Molecular Systems Biology (2011) 7:516
  • Mueller, S., Huard, J., Waldow, K., Huang, X., D'Alessandro, L.A., Bohl, S., Borner, K., Grimm, D., Klamt, S., Klingmüller, U.*, Schilling, M*. T160-phosphorylated CDK2 defines threshold for HGF dependent proliferation in primary hepatocytes. Molecular Systems Biology (2015) 11:795. (* equal last authors)