GAP-43 −/− mutant mice have a comparable number of ipsilaterally and contralaterally projecting neurons growing in semicircular trajectories.
Accordingly, female FHM1 mutant mice have been shown to be more susceptible to CSD when compared to their male counterparts [119].
By P10, NP1/2 null mutant mice have an obvious defect in eye-specific segregation and refinement that the contralateral axons occupy the whole territory and the ipsilateral/overlap projection areas are significantly larger.
Tbr-1 mutant mice have been found to have reduced RELN expression, resulting in improper neuronal migration, particularly in Cajal-Retzius cells of the marginal zone.
Gelsolin homozygous mutant mice have normal embryonic development and longevity.
Consistent with the growth retardation, the Fto mutant mice have reduced serum levels of IGF-1.
Furthermore, both strains of SHIP mutant mice have a significantly lower hematocrit percentage compared to WT littermates (Table 1).
Consistent with this expression, some Asxl2 mutant mice have smaller, degenerating eyes compared to wild-type animals (data not shown).
Necropsy and histological analysis show that mutant mice have enlarged hearts and may have impaired heart function.
Raldh1 mutant mice have been generated and are viable, suggesting that they are not devoid of β-cells [32].
The mutant mice have fewer mature B cells in the BM and spleen and mount sub-optimal TD-antigen responses.
