Sentence examples for mutant mice indicate from inspiring English sources

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.

The similarities between the phenotypes of the receptor- and ligand-null mutant mice indicate that the CSF-1R is the only receptor for CSF-1.

In addition, evidence from RB family mutant mice indicate that retinoblastoma might arise from fully differentiated retinal cells that had previously exited the cell cycle (Ajioka et al., 2007).

Furthermore, the reduced size of pyramidal neurons and the lesser complexity of dendritic arborizations in MeCP2 mutant mice indicate that MeCP 2 is involved in maturation and the maintenance of neurons, including dendritic integrity and synaptogenesis [ 66, 67].

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.

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.

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.

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.