Sentence examples for mutant neurons lacking from inspiring English sources

Interestingly, while in Drosophila mutant neurons lacking OR83b, OR22a/b and OR43a were highly degraded with trace quantities detected only in the cell body [5], [57], we did not observe any enhancement of OR1 or OR2 protein levels upon co-expression of OR7, either in whole cell lysates or in the membrane fraction of the expressing cells.

Neurons lacking MeCP2 have a significantly reduced rate of RNA synthesis; however, re-expressing MeCP2 in mutant neurons rescues the nuclear size phenotype in vitro [ 71] and in Mecp2 mice [ 72].

Combined with the lack of major anatomic defects in neurons lacking functional MeCP2, this suggests that a lack of MeCP2 does not result in irreversible damage to neurons.

The hypothesis is that serotonergic neurons lack the feedback mechanisms of dopaminergic neurons to release dopamine adequately [12, 13].

With the exception of the photoreceptors, all neurons lack dendrites.

The lack of changes in tau protein in PSEN1 mutant neurons indicates that a simple lack of carboxypeptidase processivity does not lead to altered tau proteostasis.

The C. albicans SC5314 strain, the C. albicans SAP null mutants sap1 3 triple mutant (lacking SAP1 3), sap4 6 triple mutant (lacking SAP4 6), sap9 single mutant (lacking SAP9), sap10 single mutant (lacking SAP10) and sap9,10 double mutant (lacking both SAP9 and SAP10), as well as the parent strain CAI4 (URA-) were used in these experiments [42], [43], [44].

Notably, in vivo analyses of chic05205 and chic221 mutant neurons produced contradictory results (abundant filopodia in embryonic motoraxons, lack of filopodia in pupal mushroom body neurons) [36], [37].

The neuronal architecture of minocycline-treated mutant neurons was significantly rescued compared with non-treated mutant neurons (Fig. 3A).

Lack of MECP2 also leads to impaired mitochondrial function in mutant neurons.

As rpm-1 mutant interneurons lack the presynaptic defects observed in rpm-1 mutant motorneurons, we reasoned that the postsynaptic GLR-1 trafficking defects in the rpm-1 mutant neurons might instead be due to a cell-autonomous requirement for RPM-1 activity.