Mutations in the α-actinin-4 gene ACTN4 cause an autosomal dominant human kidney
disease. Mice deficient in α-actinin-4 develop a recessive phenotype characterized by
kidney failure, proteinuria, glomerulosclerosis, and retraction of glomerular podocyte foot
processes. However, the mechanism by which α-actinin-4 deficiency leads to glomerular
disease has not been defined. Here, we examined the effect of α-actinin-4 deficiency on the
adhesive properties of podocytes in vivo and in a cell culture system. In α-actinin-4-deficient …