α-Actinin-4-Mediated FSGS: An Inherited Kidney Disease Caused by an Aggregated and Rapidly Degraded Cytoskeletal Protein (original) (raw)
Figure 5
In Vivo Phenotype
Electron micrographs from Actn4 wild-type (A) and _Actn4_K228E/K228E mice (B–D). As shown, _Actn4_K228E/K228E mice were found to have abnormalities that were typically focal, with some areas of podocyte foot process effacement (B), as well as areas that appeared essentially normal (C). Bottom image ([D] using tannic acid counterstaining) illustrates electron-dense deposits observed in several podocyte cell bodies in _Actn4_K228E/K228E mice. No such deposits were observed in wild-type or heterozygous mice.