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Heparin cofactor II inhibits arterial thrombosis after endothelial injury
Li He, Cristina P. Vicente, Randal J. Westrick, Daniel T. Eitzman, Douglas M. Tollefsen
Published in Volume 109, Issue 2
J Clin Invest. 2002; 109(2):213–219 doi:10.1172/JCI13432
This article Copyright © 2002, The American Society for Clinical Investigation
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Figure 1

Targeted disruption of the murine HCII gene. (a) Restriction map of the HCII locus and design of a replacement vector. The boxes represent exons 1–4 of the HCII gene. The thick lines represent genomic DNA; the thin lines, vector DNA. The targeting vector was constructed by insertion of the neomycin phosphotransferase gene (neo) between the EcoRI and BamHI sites of the HCII gene. (b) Southern blots of genomic DNA isolated from the tails of 4- to 6-week-old mice and digested with SacI. The restriction fragments were detected with probes (5′-probe and 3′-probe) that hybridized with sequences external to the genomic DNA present in the targeting vector. (c) Northern blot of total liver RNA obtained from adult mice. The blot was first hybridized with a cDNA probe containing sequences present in exons 2–4 of the HCII gene. It was then stripped and rehybridized with a probe containing sequences present in the neo cassette. (d) Western blot of mouse plasma probed with goat anti-human HCII IgG. The 68-kDa and 72-kDa bands represent two glycoforms of HCII that are present in normal mouse plasma (22). HCII genotypes (+/+, +/–, and –/–) are indicated in panels b–d.

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