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While Dkk1 heterozygous mice are normal and fertile, mice double heterozygous for Dkk1 and the BMP inhibitor Noggin show head defects similar to those of Dkk1 homozygous mutants (del Barco Barrantes et al., 2003).
Importantly, the liver samples from the treated mice are normal without degeneration or fibrosis.
Another possible reason why Muc16 homozygous mutant mice are normal might be the functional compensation by mesothelin in the mesothelia.
Muc16 homozygous mutant mice are normal and fertile, and do not display abnormal phenotypes by 1 year of age.
This result cannot be satisfactorily explained by the locomotion defects in the knockout mice because the same mice are normal in the cued experiment.
In contrast, COMP knock-out mice are normal in all growth parameters with only mild growth plate disturbances and flattening of the articular cartilage surface only found with exercise [16].
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Transgenic mice were normal in behavior and fertility.
These data indicate that the overall somatic development during embryonic and postnatal stage of ChR2 ET/TC -transfected miChR2 ET/TC -transfected
Memory functioning in the Tg2576 mice was normal (ie, ∼100% of control) at 3, 6, and 9 months of age, but it was significantly impaired in 12-month-old mice (n=9/group).
Hematopoiesis in cathepsin G-/ mice is normal, and the mice have no overt abnormalities in blood clotting.
In addition, axonal innervation of the auditory and somatosensory cortex in p75NTR knockout mice is normal.
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