Mice deficient in α-actinin-4 have severe glomerular disease
J. Clin. Invest. Claudine H. Kos, et al. 111:1683 doi:10.1172/JCI17988 [Go to this article.]

Figure 7
(a) Results of a representative chemotaxis assay. Lymphocytes were incubated with varying concentrations of SDF-1 as shown. Base-line movement is greater in the Actn4^–/– cells, as well as in the Actn4^–/– cells stimulated with 1 nmol and 10 nmol SDF-1. (b) Summary of all four sets of pairwise comparisons. Shown is the average increase in cell count in Actn4^–/– expressed as a fraction of the cell count of Actn4^+/+ cells. (c) Western blot analysis of lymphocyte lysates from Actn4^+/+, Actn4^+/–, and Actn4^–/– mice using an anti–α-actinin-4 antibody. Antibody to total ERK-1 and -2 served as a protein loading control.