WCN26-5398 CLINICAL PROFILE ANDHISTOLOGICAL PATTERNS OF STERIOD RESISTANT NEPHROTIC SYNDROME IN CHILDREN

alone, led to increased cell motility and accelerated focal adhesion turnover.Notably, motility of double knockdown podocytes lacked directionality and was accompanied by a significant reduction of Cdc42 activity especially at the cell edge.Mechanistically, the loss of Cdc42 activity in double knockdown podocytes was linked to enhanced degradation of the Cdc42-activating protein ARHGEF7, which was rescued by knockdown of the E3 ubiquitin ligase CBL-b.Furthermore, in double knockdown podocytes, ARHGEF7 was not properly localized in focal adhesions, which was rescued by re-expressing either GIT1 or GIT2.Conclusion: GIT1 and GIT2 cooperatively maintain the ARHGEF7-Cdc42 signaling axis, highlighting a previously unrecognized mechanism regulating Rho GTPase activity and cytoskeletal organization in podocytes.I have no potential conflict of interest to disclose.I did not use generative AI and AI-assisted technologies in the writing process.