Archiv Jochen-Kalden-Förderprogramm
Overview of completed projects
Role of extracellular vesicles as biological shuttle system for inter-kingdom communication and organ crosstalk
Term: 01.07.2021 – 31.03.2025
Both host environmental components as well as host cells release Extracellular vesicles (EVs) who are increasingly recognized for their immune-stimulatory properties and their potential role as biological shuttle system for inter-kingdom communication. Within this project, we will elucidate the role of extracellular vesicles as communication system and the impact of such vesicles on the pathogenesis of immune-mediated inflammatory diseases.
Prof. Dr. Claudia Günther
Cell-cell communication through miR containing exosomes, autophagy and circulating factors in rare glomerular diseases
Term: 01.04.2021 – 31.12.2024
I investigate rare glomerular diseases with different cell culture models, transgenic zebrafish models, podocyte specific knockout models, innovative techniques, interdisciplinary collaborations and patient material to cover multidimensional aspects of the disease in a patient centered manner. Cell-cell signaling through miRs, exosomes, autophagy and circulating factors are investigated to learn more about pathomechanisms of rare glomerular diseases that might translate into novel therapeutic targets in the future.
Direct lineage reprogramming as a heuristic approach to identify key players in human neurogenesis
Term: 01.07.2021 – 28.02.2025
This IZKF grant will be essential to realize my vision of using direct lineage reprogramming for the identification of novel regulators of human neurogenesis. My data provide evidence for the exciting opportunity to identify new potential molecular targets to enhance and navigate human neurogenesis for improving reprogramming and understanding developmental neurogenesis. We will study putative new neurogenesis key players during direct lineage reprogramming and early human brain development.
The role of lysosomal dysfunction within glial cells in Parkinson’s disease
Term: 16.02.2021 – 15.11.2024
Recent studies suggest that glial dysfunction significantly contributes to neurodegeneration in Parkinson’s disease (PD). Since lysosomal degradation is important for glial cell function, we aim to analyse the molecular consequences of lysosomal dysfunction within different glial cell lines. A better understanding of glial regulation and lysosomal turnover will help to unravel molecular mechanisms in PD and might facilitate the identification of novel therapeutic strategies in PD.
