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In S. cerevisiae, the dmc1 mutant shows almost complete absence of meiotic recombination [11], [15], [16].
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The ΔP3 mutant showed almost 50% residual activity at temperatures up to 338K and became inactive at 343K.
The bipD mutant showed almost no escape from phagosomes within RAW 264.7 cells up to 6 h p.i.; similar results have been observed for a B. pseudomallei bipD mutant within J774.2 murine macrophage-like cells [9].
The mutant showed almost the same activity as the wild-type with regard to PNP-α l-Ara f, but there was a significant reduction in the hydrolysis rate when the mutant was incubated with debranched arabinan (Fig. 7).
All sensor-loop mutants show almost exclusively holotoxins when mixed with TcA WT), but practically no holotoxins with TcA(L2422E).
All mutants showed almost the same final cell density.
Fed and starved odr-1(n1933) mutants showed almost normal migration and dispersion after conditioning at both 23 and 17 °C (Fig. 6A,B).
In fact, these double mutants showed almost completely reversed stereoselectivities toward substrate 2 with good conversion, thereby providing a pair of practically useful, enantiocomplementary counterparts to wild-type OYE 2.6.
In contrast, although odr-3(n1605) mutants showed almost normal thermotactic plasticity after conditioning at 17 °C, they showed abnormal thermotactic plasticity after conditioning at 23 °C; starved odr-3(n1605) mutants conditioned at 23 °C migrated to higher-temperature region, similar to aho-3(nj15) mutants (Fig. 6A,B).
The mutant channel shows almost 10-fold slower inactivation than wild-type (N = 9 for CACNA1HWT, N = 7 14 for CACNA1HM1549V, p < 0.001 across all voltages studied, Mann Whitney rank sum test).
While the wildtype showed a reduction of CFUs of approximately 75%, the carolacton treated and untreated mutant cells showed almost no difference in the amount of colony forming units.
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