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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: Lupus. 2015 Sep 18;25(2):137–154. doi: 10.1177/0961203315603139

Figure 3.

Figure 3

The Lck-cre transgene itself accelerated the development of lupus nephritis in (NZB × NZW)F1 mice. (a) qPCR amplification curves are shown for a representative DNA sample from a non-transgenic (nTg) mouse carrying the floxed allele of exon 3 of ERα, an Lck-cre transgenic (Tg) mouse carrying the floxed allele of exon 3 of ERα, and a mouse homozygous for a constitutive knockout of exon 3 of ERα. The calculated efficiency of cre-mediated deletion of the floxed allele (b) in Lck-cre transgenic ERαfl/+and ERαfl/− mice is shown (N=4–6 mice per genotype per time point). Additionally the incidence of albuminuria (c) and survival (d) of Lck-cre transgenic and non-transgenic (NZB × NZW)F1 mice is shown, along with representative histological images (e, f) of kidneys collected at the time of sacrifice (N=30 mice per genotype per gender). Scale bars represent 50 µm.