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The lower saliva pH observed in the ΔF508 mouse suggests that the ΔF508 CFTR mutation compromises the HCO3− secretion mechanism.
These results suggest that the L642Q mutation compromises the binding of NEDD1 to γ-tubulin in vivo, and that the additional mutations in the triple L642Q/L649Q/L656Q mutant have an additive effect, although the individual mutants did not disrupt binding (Figure 5A).
10.7554/eLife.04686.024 Figure 7. N255K uncoupling mutation compromises the microtubule interface, with accompanying orientational disorder of the motor domain.
Thus, our present in vivo and in vitro data indicate that the R952H mutation compromises the participation of KCC2 in the formation and maturation of cortical dendritic spines.
It is illustrated that expression of truncated CASQ2DEL (G112 + 15X) and CASQ2R33Q mutations can alter myocyte Ca2+ signaling through two distinctly different mechanisms: 39 CASQ2DEL mutation disrupts the polymerization of calsequestrin required for high-capacity Ca2+ binding, whereas CASQ2R33Q mutation compromises the ability of calsequestrin to control the RyR2 channel activity.
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Furthermore, the E897K mutation compromised the effect of NLK on AR activity more so than the K720A mutation.
The nucleophile mutation compromised the centrepiece of the catalytic mechanism and consequently had a much greater effect on activity than in previous handicap-recover experiments.
Introduction of Δphx1 mutation compromised the long-lived phenotypes of Δpka1 and Δsck2 mutants that are devoid of pro-aging kinases of nutrient-signalling pathways, and of the Δpyp1 mutant with constitutively activated stress-responsive kinase Sty1.
However, the accumulating of mutations compromise the efficacy of NA inhibitors.
Since fga loss-of-function mutations compromise the entire fga locus, the expression of both FgaA and FgaB is affected in these mutants.
However, all of these mutations compromised the transcriptional activation of a tested target gene.
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