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Phenotype Image Detail
Caption Selective depletion of Prkci from mouse podocytes causes focal segmental glomerulosclerosis. Periodic acid-Schiff staining and immunohistochemistry for nephrin and synaptopodin in Prkcitm1Kido/Prkcitm1.1Kido Tg(Nphs1-cre)33Mska/0 (cKO) and control kidneys at P0, P10 and P21 show that mutant mice develop segmental to global glomerulosclerosis. Boxed regions are enlarged to show an irregular pattern of nephrin staining in mutant podocytes. Loss of podocytes (arrows) and occasional adhesion of glomeruli to Bowman's capsules (arrowheads) reveal the development of focal segmental glomerulosclerosis. Consistent with massive proteinuria in mutant mice at birth, PAS staining reveals occasional hyaline droplets, representing reabsorbed urinary protein, in the proximal renal tubules at P0. Bars, 50 um.
Copyright This image is from Hirose T, PLoS ONE 2009;4(1):e4194, and is displayed under the terms of the Creative Commons Attribution 4.0 International License. J:144995
Symbol Name
Prkcitm1.1Kido protein kinase C, iota; targeted mutation 1.1, Yoshiaki Kido
Prkcitm1Kido protein kinase C, iota; targeted mutation 1, Yoshiaki Kido
Tg(Nphs1-cre)33Mska transgene insertion 33, Taiji Matsusaka
Allelic Composition Genetic Background
involves: C57BL/6 * C57BL/6N * DBA/2

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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB), Gene Ontology (GO)
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