The role of calcium mediated actin rearrangement (CaAR) in podocyte function
We have identified a fundamental ability of mammalian cells to reset their actin cytoskeleton in response to calcium influx (Calcium mediated Actin Rearrangement - CaAR). Calcium, actin and a key regulator of CaAR, the formin INF2, have been implicated in injury of podocytes, the cells responsible for ultrafiltration in the kidney. In this proposal we therefore want to establish the molecular basis and physiological relevance of CaAR for the function of podocytes. We will use a combination of live cell imaging and genetic perturbations in cultured cells and mouse models, with a particular focus on the role and biochemical interactions of INF2.
Medical Clinic of Internal Medicine D (Nephrology and Rheumatology)
Phone: +49 (0) 251 83 47-516
Principal investigator: B 10