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H. pylori type I-strains are not fully virulent in mouse models, since they neither inject CagA, nor does VacA induce immunomodulation in murine T cells [8].
As discussed above, a substitute for Scarb1 attenuated models could be the Pdzk1−/− mouse models, since Pdzk1−/− mice have a 95% liver specific reduction in SCARB1 protein levels and do not have fertility abnormalities.
This is not necessarily a limitation of these early mouse models since humans also show a transient increase in breast cancer risk after a term pregnancy.
This makes it adequate for monitoring the oxygenation of subcutaneous lesions such as FsaR tumours, particularly in mouse models since the skin overlying the tumours (<200 μm) is thinner than human skin.
This study supports a critical role of mouse tau in propagation of tau pathology in mouse models since, in tau knockout mice, no propagation of oligomeric tau was observed.
More future studies are needed to explain the regional lymph node involvement in mouse models since there are basic differences between human and mouse mammary tissue in epithelium-stroma microenvironment.
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Preclinical studies of prostate cancer (CaP) have employed a genetically engineered mouse model, since there is no naturally occurring CaP in rodents.
This is somewhat difficult to establish in the mouse model since the ability of the wild-type adenovirus to replicate is limited [53].
We consider this to be an advantage of our mouse model since ectopic expression of Dlx5 is at near physiological levels in Col2a1-Dlx5t19 hemizygotes.
This animal model was chosen instead of the mouse model, since a H. pylori type I-strain is instable in the mouse and rapidly switches off the cag-T4SS.
However, Pkd1ΔC/ΔC appear to have a milder phenotype as compared to the complete null mouse model, since in Pkd1ΔC/ΔC lines analyzed more than 90% of Pkd1ΔC/ΔC mice survived to E15.5 and approximately 60% survived to day E16.5 (Table S1) on a pure C57BL/6 background, whereas complete null [40] mice die at day E12.5 in a C57BL/6 background (Chiaravalli, Wodarczyk, Germino and Boletta, unpublished).
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