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Foxn1Δ/Δ mutant mice generated in our laboratory were described previously [10].
VRK1 mutant mice generated by the gene trap method showed progressive germ cell loss and resulting infertility.
ATF2 mutant mice generated by different gene targeting approaches have demonstrated the importance of ATF2 for tissue development and integrity and for postnatal viability.
Because all these reports and reviews hinged on attribution of some biological significance to the phosphorylation state of APP Thr668, we investigated in vivo brain APP metabolism and Aβ levels in mutant mice generated by knocking into their genome an APP gene containing a non-phosphorylatable alanyl substitution at position 668.
Thus, since four recent and highly visible papers [2, 4,17; rev in 3] have emphasized the potential importance of APP Thr668 phosphorylation state in controlling brain Aβ levels, we investigated brain APP metabolism and Aβ levels in mutant mice generated by knocking into the mouse genome an APP gene containing a non-phosphorylatable alanine substitution at position 668 of APP.
First of all, the number of mutant mice generated over the past 10 years or so has increased dramatically, so much so that several high throughput methods are in progress that will generate a null allele for every single gene (http://www.knockoutmouse.org/ and http://www.eucomm.org/).
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The Ptbp1 mutant mouse generated and analysed here demonstrates how the absence of an RNA-binding protein, involved in splicing and RNA stability among other functions, can completely halt embryonic development.
Mutant mice were generated by standard blastocyst injection and backcrossed for six generations into the C57BL6 background.
GRβ geo /+ mutant mice were generated from an ES cell line (ESKN92) in which a βgeo reporter cassette had integrated into the GR gene, generating a transcriptional and translational fusion (23).
FKRP P448L mutant mice were generated by the McColl-Lockwood Laboratory for Muscular Dystrophy Research32,33.
To analyse Krt76 expression and function, we used Krt76 mutant mice (Krt76tm1a KOMP Wtsi) generated by the Wellcome Sanger Institute Mouse Genetics Project13,16,17 (Fig. 1a).
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