Postdoc Position: Protein Homeostasis in Ageing and Disease

Cellular Stress Responses in Ageing-Associated Diseases, CECAD Research Center, University of Cologne, Joseph-Stelzmann-Str. 26, D-50931 Cologne, Germany

LOCATION: Cologne is a vibrant city with a highly international academic research environment. CECAD forms a focal point of ageing research in Europe bringing together researchers and clinicians at the University of Cologne with researchers at the new Max Planck Institute for Biology of Ageing in a unique research venture.


We are seeking highly motivated POSTDOC candidates for our ERC-funded team investigating the fundamental role of protein homeostasis mediated by the ubiquitin system and autophagy. We are using both genetic and biochemical approaches primarily in the C. elegans but also in mammalian systems to investigate proteolytic networks in ageing and disease.

The ubiquitin/proteasome system (UPS) is a major proteolytic route functioning in a cellular network that maintains the proteome during stress and ageing. Degradation of damaged proteins is mediated by the 26S proteasome upon attachment of ubiquitin. Another proteolytic system supporting protein homeostasis is the autophagy-lysosome pathway that degrades proteins inside activated autophagosomes. An age-related impairment of either of these systems causes enhanced protein aggregation and affects lifespan, suggesting functional overlap and cooperation between UPS and autophagy in stress and ageing. The ultimate goal of the proposed research is to assemble a global picture of stress-induced proteolytic networks critical for ageing and age-related diseases. 

Applicants should have a solid background in molecular biology and experience in cell biology, genetics, or biochemistry. Postdoc candidates should have demonstrated outstanding performance by high impact publications. Beside creativity and strong motivation we expect good communication skills and the ability for teamwork. The successful applicant will join an enthusiastic and collaborative group where a multidisciplinary approach is pursued.

The Salary for this full-time position will be based on the rules of the German civil service (TV L -13). 
Pathogenesis of Human Mitochondrial Diseases Is Modulated by Reduced Activity of the Ubiquitin/Proteasome-System. Segref A, Kevei E, Pokrzywa W, Schmeisser K, Mansfeld J, Livnat-Levanon N, Ensenauer R,  Glickman MH, Ristow M, Hoppe T* (2014). Cell Metab. (in press)
 DNA damage in germ cells induces an innate immune response that triggers systemic stress resistance. Ermolaeva M, Segref A, Dakhovnik A, Ou H-L, Schneider J, Utermöhlen O, Hoppe T, Schumacher B. (2013). Nature, 501, 416-20.
The myosin chaperone UNC-45 is organized in tandem modules to support myofilament formation in C. elegans. Gazda L, Pokrzywa W, Hellerschmied D, Löwe T, Forné I, Mueller-Planitz F, Hoppe T*, and Clausen, T (2013). Cell, 152, 183-95.
The Machado-Joseph disease deubiquitylase ATX-3 couples longevity and proteostasis. Kuhlbrodt K, Janiesch PC, Kevei E, Segref A, Barikbin R, and Hoppe T* (2011). Nat. Cell Biol. 13, 273-81.
CDC-48/p97 coordinates CDT-1 degradation with GINS chromatin dissociation to ensure faithful DNA replication. Franz A, Orth M, Pirson PA, Sonneville R, Blow JJ, Gartner A, Stemmann O, Hoppe T* (2011). Mol Cell. 44, 85-96.
The ubiquitin-selective chaperone CDC-48/p97 links myosin assembly to human myopathy. Janiesch  PC, Kim J, Mouysset J, Barikbin R, Lochmüller H, Cassata G, Krause S, and Hoppe T* (2007). Nat Cell Biol. 4, 379-90.
*corresponding author

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About Universität zu Köln

Institut für Genetik, Arbeitsgruppe Prof. Dr. Thorsten Hoppe CECAD Cluster of Excellence in Ageing Research Protein Homeostasis in Ageing and Disease

More about Universität zu Köln

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