Sentence examples for mutant mice indicating from inspiring English sources

Although strong immunoreactivity with an otoferlin-specific antibody was detected in cochlear hair cells of wildtype mice, no expression was detected in mutant mice, indicating that the missense mutation has a severe effect on the stability of the protein and potentially its localization.

However, the greatest defect in lung bacterial clearance was observed in TLR4lps-d/TLR9−/− double mutant mice, indicating that both TLR4 and TLR9 are required for optimal clearance.

However, no difference in the ratio of TUNEL-positive cells was apparent between control and mutant mice, indicating that increased cell death does not substantially contribute to impaired cerebellar size (Fig. S2).

In addition, the magnitude of potentiation induced by these monoamines significantly correlated with each other in the mutant mice, indicating that a subpopulation of sandy mice has marked hypersensitivity to both serotonin and dopamine.

Similar reduction of GAP43 mRNA detection and augmentation of ScMAS staining were observed in cortical extracts from doubly mutant mice, indicating that these alterations could take place in the absence of microglial cell priming by HS oligosaccharides.

However, at five months of age there was a marked reduction in the thickness of the outer nuclear layer (ONL) in both heterozygous and homozygous mutant mice, indicating a loss of photoreceptor nuclei.

ManNAc treatment appeared to ameliorate the hyposialylation status of mutant mice, indicated by a lectin histochemistry pattern similar to that of wild-type mice, with improved sialylation of both nephrin and podocalyxin, as well as reduced albuminuria compared with untreated mutant mice.

The ability to reverse age deterioration in the mutant mice indicates that the cells that divide to replenish tissues don't simply die when their telomere clock expires, says DePinho.

In vitro, mutant E155G GCAP1 results in a reduced sensitivity of cyclase activity to Ca2+ inhibition [22], and the elevated levels of cGMP seen in the retinae of the Guca1aCOD3 mutant mice indicate that the mutant GCAP1 is having a similar effect in vivo, so the delay in recovery is presumably a consequence of these elevated levels of cGMP.

Recent data from human studies in distinct leukodystrophies and some forms of MS together with investigations in myelin mutant mice indicate that a primary glial injury can be causative for neuroinflammation of substantial pathological and clinical relevance [1], [3], [4], [23], [24], [25].

Studies in experimental angiogenesis models and in mutant mice indicate that several integrins play key roles in regulating angiogenesis.