Date: October 2020
Meet our lab team at the DGFN 2020 in Berlin/online:
Catherine Meyer-Schwesinger is going to moderate the plenary lecture 3 with T. Benzing: "Single Cell Approaches in Medicine" by N. Rajewsky (Berlin) on Saturday, October 3rd, 2020, 09:45 - 10:15 a.m..
The following posters are awaiting you on Saturday, October 3rd, 2020, 2:00 - 3:30 p.m.:
• “Urinary extracellular vesicles mirror the glomerular proteostasis” (P206)
• “ADAM10-mediated ectodomain shedding is an essential driver of podocyte damage” (P212)
• “Investigations of the role of ubiquitin ligase 3A in the turnover of the podocyte surface antigen THSD7A in membranous nephropathy” (P213)
And we are very proud and happy that our dear colleague Dr. rer. nat. Wiebke Sachs will receive the doctoral award (Rainer-Greger-Promotionspreis) for her doctoral thesis "Characterization of the physiological and pathophysiological role of the proteasome in glomerular cells" on Saturday, October 3rd, 2020 10:15 - 10:30.
We are looking forward to a lively discussion with you!
Date: August 2020
Don't miss our new publication in JASN:
In a cell organelle called the lysosome cellular material is degraded via lysosomal enzymes. The lysosomal storage disorders mucolipidosis (ML) type II and III are caused by the missorting of lysosomal enzymes to the extracellular space instead of to the lysosomes. MLII and MLIII exhibit different disease severity. Patients with MLII exhibit severe lysosomal dysfunction resulting in multisystemic symptoms and early death, while MLIII patients exhibit moderate lysosomal dysfunction resulting in an attenuated clinical progression. In a few ML cases renal involvement has been described leading to the question whether this was coincidental or the result of lysosomal dysfunction.
To investigate the effect of lysosomal dysfunction on glomerular cells a MLII mouse model was generated and validated as well as compared to an established MLIII model. Both, MLII and MLIII mice, showed enlarged lysosomes in renal cells while renal morphology and function remained normal. The dysfunctional lysosomal degradation was distinctly compensated in MLII and MLIII mice. The lysosomal dysfunction in MLIII mice was compensated by enhancing the proteasomal protein degradation system, whereas MLII mice compensated the dysfunctional lysosomal protein degradation by the downregulation of protein synthesis.
Date: July 2020
Our team is growing further:
Lisa Schebsdat joined us in March after finishing her 9th semester at the university of Hamburg. In the following year she will have a closer look into the activity of the proteasome and immunoproteasome in renal diseases, especially the membranous nephropathy. In order to do so, she will work with activity-based probes, generated by scientists of the university in Leiden, NL.
Date: March 2020
And two more - our newest scientific PhD students:
We are happy that our team is growing further:
Lukas Heintz studied biochemistry and molecular biology. During his master's thesis at Kiel university he worked on (metallo)proteases and established CRISPR-based techniques of endogenous tagging. Now he will start working on the differential role of the immuno-proteasome in glomerular cells.
Sarah Frömbling finished her master's thesis as well at the university of Kiel. She worked on the optogenetic manipulation of second messenger levels in the intestine of the fruit fly to evaluate the associated host microbe homeostasis. On her PhD project she will investigate the role of UCH-L1 in membranous nephropathy.
Date: January 2020
We are happy to welcome a new scientific PhD student:
We are happy to welcome our new scientific PhD student Karen Lahme who joined us after her master studies in biology at the university in Brunswick (Braunschweig). In her master thesis she investigated the Influence of Willebrand factor on the adherence of pneumococci. In the upcoming years she is going to work on her PhD project on the differential influence of the proteasome and lysosome system in glomerular cell injury.