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 2
(a) Targeting construct. The construct used was originally designed for the development of a knock-in model. A neomycin resistance cassette is 438 bp from the 3′ end of exon (Ex) 8 of Actn4. (b) Genotyping assay. A PCR fragment amplified from wild-type genomic DNA does not digest with EarI. The targeted allele has an EarI site, allowing simple genotyping. The two left-hand lanes show this assay in two wild-type mice; the middle five lanes show amplification and digestion products of heterozygous mice. The final lane is derived from a mouse homozygous for the targeted allele. (c) Northern blot analysis of Actn4 expression in mice homozygous for the wild-type allele (+/+) and for the targeted allele (–/–). Rehybridization of membrane with β-actin as a control for RNA loading is shown below. (d) Western blot of kidney lysates using anti–α-actinin-4 antibody. The same pattern was seen with lung, liver, brain, and spleen. No difference was seen in the expression of α-actinin-1 (not shown).