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The pathogenesis underlying the hairlessness in the knockout mice is so far unknown.
Nonetheless, these findings might help to explain why the phenotype of the ΔARE mice is so much more severe than that of the TTP KO mice [ 13].
Similarly, the phenotype of PISD homozygous knock-out mice is so severe that embryos die at day 8 to 10 of embryonic development.
However, the phenotype of the Lrsam1 mutant mice is so mild that it is of questionable utility as a disease model, and similar findings in genes such as Hint1 highlight the challenges of creating valid mouse models of axonal neuropathies.
If the history of house mice is so intimately determined by humans, then the genetics of house mice may be useful to answer human historical questions; for example, the details of human affiliations in the Iron Age are sometimes imprecise - might house mice be able to indicate associations between Iron Age people from different geographical areas?
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I am sorry the field mice are so frightened of losing what they hold so dear.
The Littles' biggest problem was that mice were so badly treated in children's books.
Some mice are so inbred, a result of many generations of brother-sister mating, that they carry the same versions of each gene from both parents.
In the first case, researchers at an American Chemical Society conference reported that they were zeroing in on the gene that may explain why mice are so partial to sweets.
Still, if mice are so well cared for, why did the Alternatives Research and Development Foundation sue the Agriculture Department to include them under the Animal Welfare Act?
Knockout mice are so precious and expensive that they are kept in pathogen-free conditions, which requires them to be housed at vast expense in climate-controlled rooms and attended by every comfort known to animal husbandry.
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