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. 2009 Jan 19;206(1):153–167. doi: 10.1084/jem.20081202

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© 2009 Li and Eckhardt

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 1. — Eμ deletion and V_H gene insertion in an Igh^a locus. (A) Targeting strategy. WT^b, WT Igh^b locus. Thick vertical bars show exons for DQ52, J_H1-4, and the first two exons of Cμ. Sμ, μ switch region; shaded oval, Eμ; B, BamHI; H, HindIII; WT^a, unmodified Igh^a locus. Shaded boxes (5′H and 3′H) show regions of homology with targeting vector. Targeting vector: LoxPNeo^R, loxP-flanked neomycin resistance gene (white arrowheads indicate loxP sites), B1-8V_H promoter region (shaded), and coding sequences (thick vertical lines). neo^RV_HΔ^a: Igh^a allele after homologous recombination. V_HΔ^a, modified Igh^a allele after neo^R gene deletion. (B) Southern blot of liver DNA from WT (WT^a/WT^b) and mouse heterozygous for modified Igh^a allele before neo^R deletion (neo^RV_HΔ^a/WT^b). (C) Southern blot of liver DNA from WT^a/WT^b, neo^R V_HΔ^a/WT^b, and heterozygous mutant mice after neo^R deletion (V_HΔ^a/WT^b).