![](/fileadmin/einrichtung/sfb_1009/4Projekte/Projekt_B/10/CaAR_2.jpg)
© R. Wedlich-Söldner
![](/fileadmin/einrichtung/sfb_1009/4Projekte/Projekt_B/10/CaAR_3.jpg)
© R. Wedlich-Söldner
![](/fileadmin/einrichtung/sfb_1009/4Projekte/Projekt_B/10/CaAR_5.jpg)
© R. Wedlich-Söldner
We have characterized a large panel of mutants in the calcium-regulated actin nucleator inverted formin 2 (INF2) that cause the kidney disease “focal segmental glomerulosclerosis” (FSGS) and the neurological disorder Charcot Marie Tooth disease (CMT). While all CMT linked INF2 mutations result in complete activation of the formin, many FSGS-linked mutations mediate partial INF2 activation. We will now characterize the actin regulatory network in podocytes during recovery from plasma membrane damage and characterize the consequences of INF2 deletion in mice on glomerular morphology, function and repair.
Research area: Cell biology, clinical nephrology
Prof. Dr. Roland Wedlich-Söldner
Prof. Dr. Hermann Pavenstädt
Funding period: July 2016 - June 2024
Original articles
Skryabin BV, Kummerfeld DM, Gubar L, Seeger B, Kaiser H, Stegemann A, Roth J, Meuth SG, Pavenstädt H, Sherwood J, Pap T, Wedlich-Söldner R, Sunderkötter C, Schwartz YB, Brosius J, Rozhdestvensky TS (2020) Pervasive head-to-tail insertions of DNA templates mask desired CRISPR-Cas9-mediated genome editing events. Sci Adv. 6(7):eaax2941