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Since disrupting cpdA restored TM and T3SS function in the ΔfimL mutant, we predicted that ΔfimL mutants would have decreased levels of cAMP.
An ideal inhibitor for patients harboring JAK mutants would have to preferentially target the mutant JAK and spare signaling by the wild-type JAK.
It was initially thought that the mrs2-10 and sel1-10 mutants would have an advantage over wildtype in elevated magnesium sulfate soils, but this was not the case.
Therefore, only the experimentally determined, high-resolution structures of Sec61-RNA complex (and corresponding mutants) would have been appropriate for such quantitative estimations.
It is possible that MSUC triggered by unsynapsed autosomes, such as chromosome V in zim-2 mutants, would have a greater impact on the germline transcriptome.
We predicted that these mutants would have Trx-reductase activity, similar to results with the mammalian enzyme with an analogous mutant [reported by us (DOI 10.1021/bi400658g)].
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So what they've learned is that if you put the pupae in the freezer for a while, you can get a butterfly that is genetically normal but which has the same markings as a mutant would have.
If the intermediate one-point mutants (at least one of them) have larger fitness value than the two-point mutant would have in the absence of epistasis then the effect would be strong.
In contrast, we have found many autophosphorylation sites of TRPM7 basally phosphorylated in mammalian cells and in combination with our in vitro analysis of TRPM7 mutants, it seems unlikely that the TRPM7 S1512A/S1568A mutant would have significantly reduced incorporation of phosphate in living cells.
As σS seems to have a role in autoinducing its own transcription, it follows that if SACOL1828 were to inhibit the activity of the σS protein, then a SACOL1828 mutant would have higher sigS expression, as a result of an increase in free σS protein.
However, the atl mutant would have extending PGN fragments at its surface, which would be easily detected by PGRP-SA, inducing an immune response.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com