Sentence examples for mice exhibit developmental from inspiring English sources

In contrast, mSirT1-deficient cells are p53-hyperacetylated and have elevated p53-dependent apoptosis, whereas, mSirT1 knock-out mice exhibit developmental defects [11], [14].

Whereas Tcf1-null mice display attenuated T cell differentiation [39], Lef1-null mice exhibit developmental defects in teeth, hair follicles, mammary glands and the brain [36], [40].

SPL null mice exhibit developmental defects, lymphocyte trafficking defects and death within 1 2 months after birth.

FUT1-deficient mice exhibit developmental defects, including fewer and smaller glomeruli and a thinner olfactory nerve layer, suggesting that fucosylation contributes to OB development.

Akt1-/; Akt3-/ mice die during embryonic development at embryonic day 12, and Akt1-/; Akt3+/- mice exhibit developmental abnormalities in multiple organs that result in the death of 90% of mice shortly after birth [ 9].

mice exhibit severe developmental abnormalities and no increased tumour formation, whereas p53 K.O.mice show no developmental defect but early appearance of tumours (for review see [ 9]).

Previous reports have shown that CXCR4-null mice exhibit multiple developmental defects and die perinatally [3], [4], [29].

These mice exhibit normal developmental angiogenesis, but impaired neonatal arteriogenesis in the heart, kidney, and hindlimb.

We have previously reported that germ-line cartilage-specific PPARγ KO mice exhibit early developmental defects and exhibit accelerated spontaneous OA phenotype during adulthood.

Atf3 knockout mice exhibit no developmental abnormalities [ 71] unless challenged with LPS or another stress stimulus, resulting in an overt susceptibility to endotoxic shock and death [ 70].

However, these mice exhibit severe developmental deficits and die around 3 weeks after birth, implying that the reduction in ultrasonic vocalization might not represent specific effects of FoxP2 on mouse vocalizations (Groszer et al. 2008).