Skip to main content
. 2010 Jun 1;285(32):24487–24493. doi: 10.1074/jbc.M110.136820

FIGURE 1.

FIGURE 1.

Targeting the Timp4 gene. A, the targeting construct was produced by cloning genomic BglII-HindIII and EcoRI-Acc65I fragments of the murine Timp4 gene into pKO Scrambler 921, which contains neomycin (neo) and thymidine kinase (tk) cassettes. The mutant allele lacks the first three exons. B, Southern blot analysis of genomic DNA after EcoRI digestion, hybridized with a 5′-probe, showing the 5.7-kb wild-type and the 4.9-kb mutant fragments. C, the histogram shows quantification of Northern analysis (see supplemental Fig. 1) of adult cardiac tissue revealing a lack of Timp4 mRNA in homozygous mice, and 50.7% reduction of Timp4 mRNA in heterozygous mice (mean ± S.E.; *, p < 0.001 versus Timp4+/+). D–F, Taqman RT-PCR analysis of RNA for Timp1, Timp2, and Timp3 in hearts of Timp4+/+ and Timp4−/− mice. Values were normalized to 18 S rRNA and are expressed as mean ± S.E.; n = 4–6 for each group.