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This highly disease-specific group of mouse genes was combined with an extensive human coronary artery data set to identify a shared group of genes differentially regulated among atherosclerotic tissues from different species and different vascular beds.
And a few years later, both he and Smithies, then working at the University of Wisconsin, Madison, showed that targeting specific mouse genes was indeed possible.
Additional assignment of orthology between fly and mouse genes was based on experimental data.
To further delineate the sequence characteristics of different exonic groups, GC content for different groups of human and mouse genes was calculated with a self-written Matlab program.
To assess the potential of these genes to be involved in DSD, expression analysis of the orthologous mouse genes was performed on cDNA from purified somatic cells isolated from male and female mouse gonads at the time of sex differentiation.
The mean number of AS variants of mouse genes was 5.76 for those with 2∼3 promoters, 7.22 for those with 4∼5 promoters, however the mean number of AS variants increased to 10.16 for genes with 6∼ promoters (p<0.001 for genes with 2∼3 promoters versus genes with 4∼5 promoters; p<0.001 for genes with 4∼5 promoters versus those with 6∼ promoters; Wilcoxon Test).
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The mouse genes are generally in similar order to human genes, but blocks have often been transferred to other chromosomes.
The mouse genes are almost exactly the same as human genes, but experiments can be done on mice that could never be done on people.
About one-third of mouse genes are essential for embryonic growth; the mouse is never born if they are disabled from the start.
Similarly, the human homologs of the mouse genes were identified.
Repetitive elements from different exonic groups of human and mouse genes were outlined in Table 3.
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