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. 2014 Jul;160(1):11–16. doi: 10.1016/j.imlet.2014.03.008

Fig. 1.

Fig. 1

Generation and characterization of siglec-F-deficient mice. (A) Schematic representation of Siglec-F locus, the gene targeting vector to introduce R114D mutation in exon 3 (that contains the sialic acid binding site) and the targeted allele, with the aim of generating siglec-FR114D ‘knock-in’ (KI) mice expressing full length protein that lacks the ability to bind sialic acid. The ‘knock-out’ (KO) allele was generated following a cross of siglec-FR114D mice with Bal1 cre mice to excise exons 6–9, in order to generate siglec-F−/− mice (Neo, neomycin; Pur, puromycin; Tk, thymidine kinase; FRT, neomycin resistance site; F3, puromycin resistance site). (B) Flow cytometric analysis of siglec-F on blood eosinophils (determined by SSc/Gr1mid expression) from WT, siglec-FR114D and siglec-F−/− mice. Top panels show representative histograms of siglec-F staining from unstained (gray line) and WT (dotted line) and siglec-F deficient (black line) mice. Lower panels present mean ± S.D. GeoMean of siglec-F fluorescence from 2 to 4 mice per group.