As the mouse model used in our study is a whole body knock out model, we cannot exclude that non muscle cells might express collagen XXV within the embryonic limb.
The reason for these differences is currently unclear but may include the very different nature of the trinucleotide repeats studied (CAG/CTG versus CGG/CCG), and/or the difference between the human cells used here and the in vivo mouse model used in both previous studies.
There are several advantages for the mouse model used in this study.
In the mouse model used in this study (CPC Apc model [12]), one Apc allele is somatically inactivated in the epithelium from the distal ileum to the rectum.
The APP/PS1 mouse model used in our study possesses concurrent mutated forms of APP and Presenilin 1 (PS1), both identified separately in human Alzheimer diseases [1].
We use primate viruses, since we wish to filter out any species-specific effects that may result from the mouse model used for the gene expression data.
Thus, the correlation between gD2-antibody titers and protection against HSV-2 challenge may be an artefact of the mouse model used in this study.
The characteristics of the anaemia in the mouse model used here were very similar to the anaemia in trypanotolerant and susceptible cattle and suggest that the causes of the anaemia are similar in both species.
However, it should not be neglected that the mouse model used in our study was in the early stage of obesity with only mildly increased body weight and plasma Cho.
The AD mouse model used in this study (APPswe/PS1dE9-Line 85) co-expresses a chimeric mouse/human APP695 harboring the Swedish K670M/N671L mutations (Mo/HuAPPswe) and human PS1with the exon-9 deletion mutation (PS1dE9).
The neuroendocrine prostate tumors that arise in the mouse model used in the present study (CR2-TAg mice) have been previously characterized and shown to reproduce the stages of human tumor progression and metastasis [17], [18].
