{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ni J"],"funding":["Bundesministerium für Bildung und Forschung","European Research Council","Deutsche Forschungsgemeinschaft","NIDDK NIH HHS","National Institute of Diabetes and Digestive and Kidney Diseases"],"pagination":["24406-24417"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5114397"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["291(47)"],"pubmed_abstract":["MAGI-1 is a multidomain cytosolic scaffolding protein that in the kidney is specifically located at the podocyte slit diaphragm, a specialized junction that is universally injured in proteinuric diseases. There it interacts with several essential molecules, including nephrin and neph1, which are required for slit diaphragm formation and as an intracellular signaling hub. Here, we show that diminished MAGI-1 expression in cultured podocytes reduced nephrin and neph1 membrane localization and weakened tight junction integrity. Global magi1 knock-out mice, however, demonstrated normal glomerular histology and function into adulthood. We hypothesized that a second mild but complementary genetic insult might induce glomerular disease susceptibility in these mice. To identify such a gene, we uti"],"journal":["The Journal of biological chemistry"],"pubmed_title":["MAGI-1 Interacts with Nephrin to Maintain Slit Diaphragm Structure through Enhanced Rap1 Activation in Podocytes."],"pmcid":["PMC5114397"],"funding_grant_id":["R01 DK103022","616891","CRC 1140","STOP-FSGS 01GM1518C","R01 DK104712","Heisenberg program","1 R01 DK104712–01A1"],"pubmed_authors":["Ni J","Huber TB","Li J","Chan A","Johnson RI","Campbell KN","Bao S","Zhu B","Kaufman L","Smith CM","Grahammer F","D'Agati VD","Vadaparampil J","He JC"],"additional_accession":[]},"is_claimable":false,"name":"MAGI-1 Interacts with Nephrin to Maintain Slit Diaphragm Structure through Enhanced Rap1 Activation in Podocytes.","description":"MAGI-1 is a multidomain cytosolic scaffolding protein that in the kidney is specifically located at the podocyte slit diaphragm, a specialized junction that is universally injured in proteinuric diseases. There it interacts with several essential molecules, including nephrin and neph1, which are required for slit diaphragm formation and as an intracellular signaling hub. Here, we show that diminished MAGI-1 expression in cultured podocytes reduced nephrin and neph1 membrane localization and weakened tight junction integrity. Global magi1 knock-out mice, however, demonstrated normal glomerular histology and function into adulthood. We hypothesized that a second mild but complementary genetic insult might induce glomerular disease susceptibility in these mice. To identify such a gene, we uti","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Nov","modification":"2026-05-29T20:29:56.219Z","creation":"2026-04-08T06:11:11.022Z"},"accession":"S-EPMC5114397","cross_references":{"pubmed":["27707879"],"doi":["10.1074/jbc.M116.745026"]}}