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R26floxneoWnt4 heterozygous and homozygous mutant mice appeared normal and were fertile.
Overall, the general health of mutant mice appeared normal in a specific-pathogen-free (SPF) animal facility.
The motor phenotypes of mutant mice appeared later might be caused by secondary changes of the brain.
Although retinal function in young mutant mice appeared to be normal, from three months of age cone function in heterozygous Guca1a+/COD3 mice was significantly reduced.
Despite that approximately 90% of striatal neurons were ablated, the motor performance of the mutant mice appeared to be comparable to that of control mice in stationary thin rod and rotating rod tests.
In addition, conventional histological analyses revealed that the choroid plexus, from which the CSF is secreted, of p23-ST1 micent mice appeared normal when compared to that of control mice (Fig. 2B).
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By the age of 1 year, Muc16 homozygous mutant mice appear normal.
Given that Cdc42−/− mice have more preselection DP thymocytes, T cell development in mutant mice appears to be impeded at early stage of positive selection.
Spp1−/− mutant mice are grossly normal [46] and the RGC projection pattern in the LGNs of P4 Spp1−/− mutant mice appears equivalent to WT. Reduced SPP1 does not cause the segregation defect.
Although all of these phenotypic hallmarks are shared between RXRs and Notch mutant mice, they also exhibit certain differences; for example disease progression of the RXRs mutant mice appears to be milder, it affects primarily ear skin and later to a lesser extent dorsal skin.
To see if MELK is important in healthy mice, Wang et al. genetically engineered mice to delete the MELK gene and found that these mutant mice appear normal.
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