Sentence examples for effects of a mutant from inspiring English sources
The precise location of this insertion along the sequence allows us to explain the deleterious effects of a mutant in this region and suggests new functional studies.
To better understand the mechanism of the dominant negative activity on the negative regulation of TSHα gene expression, we examined the effects of a mutant TR (Mf-1) from a RTH patient [28], on histone modifications of the TSHα promoter in the absence or presence of T3 using adenovirus-GFP control as well as adenovirus encoding wild-type TRβ or Mf-1 in α-23 cells (Figure 6A).
In a final example, we examined the effects of a mutant kinesin, Kif3B, on LR patterning.
In the mouse model, we describe here, we successfully abolished TWINKLE protein expression, whereas other models and human patients have phenotypes caused by dominant negative effects of a mutant TWINKLE protein expressed against a background of wild-type TWINKLE.
To determine if the Pias1 effect on Gli proteins was related to their SUMOylation, we analyzed the effect of a mutant form of Pias1 lacking its E3 ligase activity, Pias1-C350S [29], [30], on Gli1 transcriptional activity.
The other is the effect of a mutant on the colocalization of GluA1 with a marker, in particular with transferrin endocytosed by the transferrin receptor.
Unfortunately, as a single mannosyltransferase is responsible for both branching of the mannan core and elongation of the mannose cap, it is not possible to separate these functions and study the effect of a mutant exclusively disrupted in mannan core branching.
In cells, Ndel1 depletion by siRNA also mimics the effects of Dyn2 K44A), a mutant with reduced GTPase activity, while overexpression of Ndel1 impacts on GluR1 distribution in a similar way to enhancing Dyn2 activity.
Both reviewers however also felt that knowledge about the effects of a phosphomimetic mutant would further strengthen your conclusion, and in addition being useful to distinguish whether phosphorylation of Munc18 is not only required but also sufficient to trigger the high release probability state.
We have compared this with the effect of expressing a mutant form which is defective in PCNA-binding, but which retains the secondary cyclin CDK-inhibitory site.
