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In such works we can find the definition of the operators, what operators are more expensive, what generate more equivalent mutants and so.
It was reported that two disease-linked mutations prolonged S-phase from 12 h to 22 h when overexpressed in COS-7 cells [5]; however similar effects were not observed in all disease mutants and so this was not investigated in further detail.
Therefore, replication timing was altered in rpd3 mutants, and so was the nucleosomal organization around origin regions.
Our model remains that WT cells ingest lower volumes of fluid than mutants, and so their growth is arrested by the conventional starvation response unless high levels of nutrients are present (as supplied by HL5 medium with 10% FBS).
One possible concern is that Caton et al. (1982) mapped antigenic sites largely by selecting monoclonal-antibody escape mutants, and so these sites might be biased towards being more mutationally tolerant.
We refer the reviewers to the revised manuscript for the full text, but here is the most relevant portion: One possible concern is that Caton et al. (1982) mapped antigenic sites largely by selecting monoclonal-antibody escape mutants, and so these sites might be biased towards being more mutationally tolerant.
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(I can't keep from imagining conspiracies to blackmail the famously fence-straddling justice, plots to slip microscopic mind-control robots into his morning oatmeal, schemes to kidnap and replace him with a shapeshifting mutant, and so on).
Comparative studies can be used with two or more samples, such as active vs inactive, diseased vs healthy, treated vs untreated, wild type vs mutant, and so on.
Another ablation-induced failure in retraction can phenocopy mys mutants, and does so by targeting amnioserosa cells in the same region where the mutant fails to adhere to the germ band.
SEM and phalloidin-stained preparations of the early postnatal cochlea revealed that hair-bundle structure was severely disrupted in both the v2J and the av3J mutants, and less so in the av6J mutants.
It will be interesting to test whether iron homeostasis is dysregulated in bkr and gnz mutants and, if so, this could provide a context to begin to understand the molecular relationships between different pathways that alter early forebrain development.
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