Since Claudin-15 (Cldn15) was one of the earliest modified transcripts in Hnf4α colon null mice, we verified its status as a direct gene target for Hnf4α.
Our findings revealed a pronounced bias underlying SNP location in mice and we verified the same observations prospectively in human germ line DNA based on 1000 Genomes data (http://www.1000genomes.org, last accessed August, 2015) and acquired somatic mutations in human breast cancer (https://tcga-data.nci.nih.gov/tcga/dataAccess Matrix.htm, last accessed August, 2015).
Using RT-PCR of human and mouse cells, we verified that the two exon ZBTB42 was expressed and correctly spliced in human skeletal muscle, and murine C2C12 cells.
Only one of the eight northern-confirmed novel mouse transcripts we verified mapped to the regions surveyed by Cheng et al. [ 9] and it did not overlap a "transfrag", also consistent with our results (Fig. 3).
In combination with another mouse macrophage marker, F4/80 [32], we verified that these cells are macrophages and that a significant recruitment to the lungs appeared as early as 36 hours after introduction of the tumor cells into the circulation (Figure 3G).
For this reason, we verified that MBL-deficient mice responded to MCA occlusion with a similar perfusion deficit than WT mice by monitoring CBF with laser Doppler flowmetry.
We verified that the mouse targets for the most GC-rich human genes are much less GC-rich by an average of 6.9% (e.g., a human target that is 60% GC would only be 53% GC in the mouse).
Using the reference tables as bridges, we fetched the target genes in human one by one, and we verified whether the mouse or rat orthologs also corresponded to the candidate pre-miRNAs.
Next, we verified that Pink1−/− mice lacked functional Pink1 mRNA.
In the next experiment we verified that GluR2-cKO mice were indeed using an NMDAR-independent learning mechanism in context B (Fig. 8D).
