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. 2006 Jun 7;26(23):6269–6281. doi: 10.1523/JNEUROSCI.4212-05.2006

Figure 4.

Figure 4.

Generation of mice lacking NP2 or NPR and mice lacking multiple neuronal pentraxins. Mice lacking NP2 (A) and NPR (B) were generated through homologous recombination in ES cells with a targeting strategy. C, Alteration of genomic XhoI restriction fragment lengths in wild-type and recombined ES cells or BH1 in wild-type, heterozygous, and homozygous null NP2 mice. D, Alteration of genomic BglII restriction fragment lengths in wild-type, heterozygous, and homozygous null NPR mice. E, F, Alterations in NP2 and NPR message size and abundance in wild-type, heterozygous, and homozygous mice is shown in Northern blots. G, Chromatography of solubilized wild-type brains on taipoxin columns greatly enriches NP1, NP2, and NPR. H, Similar chromatography of solubilized brain from single, double, and triple KO mice shows the lack of the respective neuronal pentraxins. I, Loss of NPR in single, double, and triple KO mice shown by immunoprecipitation. J, Quantification of the loss of NP1, NP2, and NPR by taipoxin chromatography in select single, double, and triple KO mice. Ab, Antibody; FT, flow through; SM, solubilized membranes; BH1, BamH1; Wt, Wild-type.