Hoppe, Thorsten - assoc. RG 76

Accumulation of damaged proteins is associated with age-related neurodegeneration in Alzheimer’s and Parkinson’s patients. The maintenance of protein homeostasis, or proteostasis, involves the degradation of misfolded and damaged proteins, and is essential for cellular function, organismal growth, and ultimately viability. Sustaining proteostasis is not only a long-term challenge for individual cells but also for entire organisms, since damaged proteins accumulate with stress and aging. Not all tissues are equally susceptible to the toxicity of protein aggregates, suggesting tissue-specific differences in proteostasis pathways.

The ubiquitin/proteasome system (UPS) is a major proteolytic route functioning in a cellular network that maintains the proteome during stress and aging. Another proteolytic system supporting proteostasis 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 aging. The ultimate goal of our research is to assemble a global picture of stress-induced proteolytic networks critical for aging of multicellular organisms.

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• Center for Molecular Medicine Cologne (CMMC)
• Institute for Genetics (Univ. of Cologne)
• CECAD Research Center