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In the mouse infection model, each of the knockout mutants was able to establish successful infections in the bladder and kidneys by day one post-infection.
As shown in Figure 5, external application of 100 µM Cd2+ switched the slowly activating voltage-dependent conductance into an instantaneous linear leak K+ current, and none of the three double mutants was able to suppress or even reduce the effect of Cd2+.
To test if the ΔMovam7 mutants was able to form functional appressoria, appressorium assay was performed and results showed that the ΔMovam7 mutant was unable to form appressoria on the host leaves, whereas plenty of appressoria were found in 52 and 71% of the hyphal tips of the control at 24 and 48 hours post infection (Figure 8C).
As a consequence, none of these 3 mutants was able to dimerize.
Neither of the mutants was able to mediate TBP ubiquitination in vitro.
Neither of the mutants was able to interact with wild-type TRIM32 in the Y2H system (Fig. 5C).
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All these mutants were able to accelerate the rate of insulin precipitation.
Genetic studies in C. elegans reveal that Moco-biosynthetic mutants are able to survive if Moco is provided through the microbial diet.
Unexpectedly, this latter was able to inhibit a GH11 enzyme, but not GH12, whereas the mutants were able to modulate the inhibition capacity.
The TREX1 D18N and V201D mutants are able to bind both metals in the active site, but with inter-metal distances that are larger than optimal for catalysis.
Interestingly, the mutants were able to grow and to produce macedocin at considerably higher concentrations of NaCl compared to the wild-type (up to 4.0% w/v).
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com