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The myostatin knockout mouse exhibits a 2 3 fold increase in skeletal muscle mass due to a combination of hyperplasia and hypertrophy [6].
Unlike the retina in the homozygous (rds−/−) mouse, which fails to form OSs and undergoes fairly rapid apoptotic photoreceptor cell death, the retina in the heterozygous (rds+/−) mouse exhibits a classic, well-defined adRP phenotype characterized by early onset rod degeneration and late onset cone degeneration.
The retinal vasculature of the Vldlr-/ mouse exhibits a developmental increase in "neo" vessels which are absent from control retinas (Fig. 1) suggesting the possibility that these vessels arise as a result of the increase in retinal VEGF and that the nanoceria can inhibit their development.
In collaboration with Kanasaki et al., we found that the Comt-deficient pregnant mouse exhibits a preeclampsia phenotype similar to that found in human preeclampsia, including hypertension, proteinuria and vascular and placental lesions; and the mouse preeclampsia-like phenotype is reversed by administration of 2-ME[27].
RGMa and RGMb, although primarily expressed in the central nervous system during mouse embryonic development[38], [39], are detectable in skeletal muscle after birth.[39] The RGMa knockout mouse exhibits a partially penetrant failure in cephalic neural tube closure,[39] while an RGMb deficient mouse has not been reported.
This mouse exhibits a phenotype similar to type 2 diabetes mellitus owing to hyperphagia and disrupted metabolism of adipocytes.
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The skin of RASSF9−/− mouse exhibited a significant epidermal thickening.
A LIPHlpd1 Knock Out mouse exhibited a complex multifactorial phenotype including retarded hair growth [12].
The PRAKO mouse, like the PRKO mouse, exhibited a infertility phenotype.
After an initial swimming period, the mice exhibits an immobility behavior considered a depression-like response.
Depletion of p120 in conditional knockout mice exhibits an inflammatory response underlying epidermis [ 12, 13].
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