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In mice, the development of the first digit relies on Hoxd13 but not Hoxd12, whereas the other digits need both.
In Nkx2.5−/−Nkx2.6−/− double knockout mice, the development of pharynx is totally abolished.
Although no short term memory deficiencies were observed in knock-in mice, the development of brain histopathology was similar to that of human patients.
Despite the severe defect of pro-B cells in Egr-2 cTg mice, the development of B cells in Egr-2 cKO mice is normal.
While significantly higher levels of CIC were seen in FcRγ−/− mice, the development of high-titred tissue IC deposits was delayed as compared to wt mice.
In mice, the development of Th17 cells is driven by the transcription factor retinoic acid-related orphan receptor γt (RORγt).
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Atkinson describes all the important technological milestones — stored memory, the first mouse, the development of touch screens — but this is more art book than technical manual.
In the Shh mutant mouse, the development of many embryonic structures, including the limb, is severely compromised.
In the Shh−/− mutant mouse, the development of many embryonic structures, including the limb, is severely compromised.
These mice are also more resistant than wild-type mice to the development of colitis [139].
One significant breakthrough in generating humanized mice was the development of NOD-scid Il2rg − / − mice, which are double homozygous for the severe combined immunodeficiency (SCID) mutation and interleukin-2Rg (Il-2Rg) allelic mutation (gamma c null) (Ito et al., 2002).
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