Sentence examples for mutant mouse brains from inspiring English sources
At first glance, the touch-sensing region looked normal, but on closer inspection the team noticed some subtle but persistent differences in the mutant mouse brains.
Total Thr668Ala mAPP in knock-in mutant mouse brains was identical in levels and distribution except that, as expected, there was no detectable phospho-mAPP (Fig. 5).
We gratefully thank Vassilis Pachnis and Maria Grigoriou (NIMR London, UK) for the kind gift of Lhx6 cDNA, John Rubenstein (UCSF, CA) for the kind gift of Dlx1 cDNA, and both John Rubenstein and Stewart Anderson (Weill Cornell Medical Center, NY) for Dlx1/2 double mutant mouse brains.
Our further findings highlight a reduced PTRH2-mediated signaling in mutant mouse brains as molecular correlates for the observed phenotype (Fig. 5F and G).
In contrast, Lmo1 expression was greatly expanded ventrolaterally to encompass nearly the entire volume of the GEs in mutant mouse brains (Fig. 3D).
Remarkably, in the triple mutant mouse brains (APP/PSEN1/GD3S−/−), the concentration of GT1aα was elevated and as expected there was no expression of GQ1bα.
Although bulk analysis suggested overall metal accumulation in CLN6 disease, loss of the ER to cytoplasmic metal importer, Zip7, would ultimately drive metal mislocalization to the ER, as previously observed for Zn in Cln6 mutant mouse brain [ 15], and may induce deficiencies of bioavailable metals elsewhere in the cell.
We detected a reduction in both integrin-mediated signaling as determined by pFAK and Bcl-2 expression and an increase in pERK in Ptrh2-mutant mouse brains.
Our data suggest that the elevated cholinergic-specific ganglioside, GT1aα, in the triple-mutant mouse brains (APP/PSEN1/GD3S−/−) may contribute to diminished plaque formation and, concomitantly, functional recovery in these mice.
Recent phenotypic characterization of Sez-6 null-mutant mouse brain has revealed a role for Sez-6 in specifying dendritic branching patterns of cortical neurons [4].
This study sets out to compare and contrast the astrocyte reaction in two unrelated experimental designs both resulting in marked chronic astrogliosis and natural motoneuron death in the wobbler mutant mouse and brain damage in the context of transplantation of xenogeneic embryonic CNS tissue into the striatum of newborn mice.
