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Mice lacking Siglec-E are viable, exhibit no apparent developmental defect and reproduce normally (McMillan et al., 2013).
They also pointed out that hormonal deprivation, such as ovariectomy, kills a large percentage of hormone dependent mammary tumors, whereas the normal mammary epithelia remain viable, only exhibiting slower growth and metabolic rates [ 49].
The Acvr1 R206H/+ knock-in mouse model sheds light on many important questions about the cellular targets of the FOP mutation, including those that could only be addressed in viable chimeras exhibiting the classic FOP phenotype.
The viable cells exhibit Annexin V /PI ; early apoptotic cells exhibit Annexin / PI ; late apoptotic cells or necrotic cells exhibit Annexin V /PI.
Surprisingly, transgenic mice bearing a modified VEGFR1-TK −/− locus expressing a VEGFR1 truncated protein lacking tyrosine kinase activity are viable and exhibit normal blood vessel formation during development; however, such mice exhibit defects in VEGF-A-dependent macrophage migration [ 85].
The viable cells exhibited a green fluorescence (acridine orange staining) whereas apoptotic cells exhibited an orange-red nuclear fluorescence (ethidium bromide staining) by intercalation of ethidium bromide into DNA damage in apoptotic cells.
The cells in contact with CHN HYA GO composite scaffolds remained viable and exhibited a high growth potential.
The heat pipe PV/T hybrid system is viable and exhibits the potential and competitiveness over the other conventional BIPV/T systems.
These knockout (KO) mice are viable and exhibit different phenotypes.
αB-R120G heterozygous and homozygous mice were viable and exhibited no obvious phenotype at birth.
Lmna−/− mice are viable, but exhibit growth retardation from 2 3 weeks of age, and stop growing after ∼4 weeks.
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