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Insulin-activated store-operated Ca entry via Orai1 induces podocyte actin remodeling and causes proteinuria

Nat Commun. 2021-11; 
Ji-Hee Kim, Kyu-Hee Hwang, Bao T N Dang, Minseob Eom, In Deok Kong, Yousang Gwack, Seyoung Yu, Heon Yung Gee, Lutz Birnbaumer, Kyu-Sang Park, Seung-Kuy Cha
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Catalog Antibody … permeation and blocking steps, the slides were incubated with goat anti-synaptopodin (1:40 dilution; sc21537, Santa Cruz Biotechnology), rabbit anti-Orai1 (1:100 dilution, NBP1-46470, Novus, Littleton, CO, USA), and rabbit anti-Flag-tag (1:20 dilution; A00170, GenScript) at 4 … Get A Quote

摘要

Podocyte, the gatekeeper of the glomerular filtration barrier, is a primary target for growth factor and Ca signaling whose perturbation leads to proteinuria. However, the effects of insulin action on store-operated Ca entry (SOCE) in podocytes remain unknown. Here, we demonstrated that insulin stimulates SOCE by VAMP2-dependent Orai1 trafficking to the plasma membrane. Insulin-activated SOCE triggers actin remodeling and transepithelial albumin leakage via the Ca-calcineurin pathway in podocytes. Transgenic Orai1 overexpression in mice causes podocyte fusion and impaired glomerular filtration barrier. Conversely, podocyte-specific Orai1 deletion prevents insulin-stimulated SOCE, synaptopodin depletion, and pro... More

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