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Several murine models show no correlation between histopathologic injury and bacterial load.
Some studies in murine models show that the eggs are responsible for a predominantly Th2 response.
Evidence from murine models show that deregulated β-catenin signaling in basal stem cells or luminal progenitors induces breast tumors.
Studies in murine models show that partial depletion of Dicer and Drosha accelerates cellular transformation and tumorigenesis.
A large number of different and unrelated murine models show clinical and/or histological features akin to human SLE [ 4].
Not all of these murine models show the same results, and Tribouillard-Tanvier et al (2009) suggest that this may be attributable to the animal model used [ 15].
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Moreover, studies in murine models showed that activation of intestinal GLP-1 cells improves glycemic and insulin response [ 47].
Other transgenic murine models showing that overexpression of S100A4 causes metastasis have also been developed (Ambartsumian et al, 1996).
In addition, three different Mecp2-deficient murine models showed variably skewed XCI favorably inactivating the mutant allele and correlating with phenotypic severity [ 10, 11].
Research using murine models showed that denatured forms of the recombinant outer membrane porin proteins OmpC, OmpF, and OmpL from Salmonella enterica ssp.
Experiments in murine models showed that targeted delivery of minute amounts (picograms) of an IFNγ-GCNGRC fusion product (called IFNγ-NGR) to tumor vasculature could be a valuable strategy for uncoupling antitumor activity and counter-regulatory mechanisms [ 83].
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