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The Irf3−/− mice were reported previously63.
Plxnd1+/o and Sema3E+/o mice were reported in ref. 29.
In previous studies, GlastCreER T2 mice were reported to selectively modify α-tanycytes without obvious recombination in β-tanycytes40.
Furthermore, Parp1−/− mice were reported to suffer from high energy expenditure and decreased body fat mass similar to ALS patients (for review see ref. 33).
Extensive fibrosis observed in the Lepob/ob/Sesn2−/− mouse liver was particularly striking because Lepob/ob mutant mice were reported to be very resistant to liver fibrosis3.
Male APP23 mice were reported to show slightly slower deposition of Aβ plaques compared to females [17], but these mice were 27 months old; thus, Aβ deposition was abundant.
The CIB1-deficent mice were reported previously [23].
For example, MyD88−/− mice were reported to be completely EAE resistant [21].
The reason why COX2+/−, but not COX2 KO mice were reported to be prone to obesity is not clear.
Recently, HPK1−/− mice were reported to have normal numbers of B220+ cells and B-cell/T-cell ratios in peripheral lymphoid organs [31].
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At 6 months of age, these mice were reported to exhibit cardiac hypertrophy and ventricular contractile dysfunction (Rivard et al., 2008).
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