Sentence examples for mutant mice all from inspiring English sources

These mutant mice all show the characteristic cellular ICL-inducing agent sensitivity, but only partially recapitulate the developmental abnormalities, anaemia and cancer predisposition seen in individuals with FA.

While Tyro3 −/−, Axl −/−, and Gas6 −/− single mutant mice all displayed wild-type number of cCasp3+ Acells.02 cells per tubule cross-section– Mertk −/− mice displayed nearly 20 times more.

In the testis of 5 month old mutant mice, all the analyzed genes had significant reduction in mRNA levels, with the exception of NQO1 and catalase, which were unaltered (Fig.  5G).

Despite elevated auditory thresholds, the Tecta mutant mice all exhibit an enhanced tendency to have audiogenic seizures in response to white noise stimuli at low sound pressure levels (≤84 dB SPL), revealing a previously unrecognised consequence of Tecta mutations.

Although an explanation for the observed seizure sensitivity is thus far lacking, it should be noted that the Tecta mutant mice all carry mutations that are known to cause deafness in humans, and the affected patients might also be abnormally sensitive to certain sound stimuli.

On cholate diet, mutant mice of all strains lose weight (p<0.001 for all comparisons of mice on control versus cholate diet, except p<0.01 for F1 females; Figure 2b).

Cholate-fed mutant mice of all strains had higher sALP levels as compared to cholate-fed WT mice (p<0.001 for all comparisons; Figure 3c and d).

Mice lacking one or both copies of p53 as well as mutant p53 mice all display increased susceptibility to UVB-induced skin cancer and greatly decreased apoptosis in response to UVB.

However, similar to the Cry2−/− mutants, the circulating osteoclast activity marker TRAP5b was significantly lowered in plasma of double mutant mice at all times (Figure 4F), suggesting lowered osteoclast-dependent bone degradation.

Although the entire sectioned brain was analyzed for vascular leakage, the majority of blood vessel leakage was detected in the cerebellar lobules (6 9Cb), cerebral cortex (M2), hippocampus (CA1, CA2), and midbrain of mutant mice at all disease stages (Table 1).

The amount of hair-cell loss was similar in both the wild-type and the heterozygous mutant mice at all ages.