Persönlicher Status und Werkzeuge

Dr. Klaus Richter

Heisenberg-Stipendiat (DFG)

TUM Junior Fellow 

AG Klaus Richter 



Contact Details

Business card at TUMonline

Academic Career and Research Areas

Dr. Klaus Richter (b. 1973) conducts research in the area of cellular signal transduction and the influence of molecular chaperones. This interaction plays a role in many diseases, such as the activation of oncogenic kinases, the misregulation of gene expression, the loss of anchoring structures of muscle cells or in cellular protein aggregation, which occurs during the development of neurodegenerative diseases. We investigate concepts about the interaction of these proteins in model systems such as C.elegans, yeast, or mammalian cells. We want to reveal how the disease patterns develop and how better regulation of the chaperone interaction could have a positive effect.


Dr. Klaus Richter studied biochemistry at the University of Regensburg and graduated at the Technical University of Munich. Here, he devoted himself to the ATP hydrolysis of the chaperone Hsp90. This was followed by a time at Northwestern University Chicago, where Mr. Richter investigated the regulation of the heat shock response in the model organism C. elegans. Building on these results, Mr. Richter founded his junior research group at the TU Munich.

  • Curriculum Vitae


  • Heisenberg-Fellowship (2017)
  • DAAD-Fellowship (2004)
  • DAAD-Fellowship (1997)

Key Publications (all publications)

Eckl, J., Daake, M., Schwartz, S. & Richter, K. Nucleotide-free sB-Raf is preferentially bound by Hsp90 and Cdc37 in vitro. (2016), J. Mol. Biol. 428(20):4185-4196.


Haslbeck, V., Eckl, J.M., Drazic, A., Rutz, D.A., Lorenz, O.R., Zimmermann, K., Kriehuber, T., Lindemann, C., Madl, T. & Richter, K. The activity of protein phosphatase 5 towards native clients is modulated by the middle- and C-terminal domains of Hsp90. (2015), Sci Rep. 5:17058, 1-16.


Papsdorf, K., Kaiser, C.J., Drazic, A., Grötzinger, S.W., Haeßner, C., Eisenreich, W. & Richter, K. Polyglutamine toxicity in yeast induces metabolic alterations and mitochondrial defects. (2015), BMC Genomics 16-662, 1-18.


Papsdorf, K., Sacherl, J. & Richter, K. The balanced regulation of Hsc70 by DNJ-13 and UNC-23 is required for muscle functionality. (2014), J Biol Chem. 289, 25250-25261.


Kaiser, C.J., Grötzinger, S.W, Eckl, J.W., Papsdorf, K., Jordan, S. & Richter, K. A network of genes connects polyglutamine toxicity to ploidy control in yeast. (2013), Nat Commun 4, 1571.