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The overlap between the model systems was slight.
The genes that were common between the model systems may be of particular interest for further study.
We report here the major alterations to glycan-associated gene expression that are associated with each of the model systems and that are common between the model systems.
Another obvious difference between the model systems is the amount of genetic variation.
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While these studies are useful and often informative, they also entail assumptions of functional conservation between the model system and the species of interest that may not necessarily be true (Gallego Romero et al., 2012).
We next investigated whether certain gene expression changes were common between two or more of the model systems.
The difference between these model systems and the NOD model of type 1 diabetes perhaps indicates that the role of the therapeutic DC in this model is to deliver high levels of IL-4 to critical areas of disease activity, such as the PLN.
Because VN1203 pathogenicity is likely partially regulated by dysregulation of immune signaling and hypercytokinemia, the observed commonalities between the three model systems strongly suggest a role for airway epithelium in VN1203 pathogenesis.
Nevertheless, there are also many important differences between the two model systems (specificity numbers in the ancestral populations, number of positively selected amino acid sites, and competitive interaction, for instance).
The variability of tumor incidence with regard to individual Cre-drivers does differ somewhat between the two model systems, most likely caused by the contrasting causative oncogenic events (ie, Ptch loss vs. forced Smo overexpression).
However, there were some differences observed between the two model systems.
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