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Mice homozygous for the Nrarp tm1Grid mutant allele (henceforth referred to as Nrarp−/− mice) were viable and fertile.
As expected, because both male and female H3mm7−/− mice were viable and indistinguishable from control mice, H3mm7 was not necessary during development.
Smac-deficient mice were viable and normal.
These mice were viable, with no apparent morphological defects.
ACE2-deficient mice were viable, fertile, and lacked any gross structural abnormalities.
Although these triple knock-out mice were viable and had normal brain anatomy, they exhibited a number of behavioral defects.
Syntaxin-1BOpen mice were viable but succumbed to generalized seizures at 2 to 3 months of age.
ErbB2-deficient conditional mutant adult mice were viable and displayed no overt phenotype, but physiological analysis revealed a phenotype consistent with dilated cardiomyopathy [14, 15].
OGR1 KO mice were viable and fertile.
M-CyldΔ9 mice were viable and normal in appearance.
TPH2KO and DKO mice were viable and normal in appearance.
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