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Indeed, this single mutation lowered the methanol concentration for which the initial rates of alcoholysis and hydrolysis are equal from 2 M in CAL-A down to 0.3 M in its mutant, while the exceptional stability of the parental enzyme toward alcohol and temperature was conserved.
At 24 h, no bacteria were recovered from the Δppk2 mutant, while the WT showed 5×107 CFU of bacteria.
These results showed that apoptosis was enhanced in myoblasts of the tw mutant while the number of dividing cells was not altered.
Accelerated nuclear accumulation of p65 was observed in the alanine mutant, while the aspartic acid mutation displayed slowed nuclear translocation kinetics.
RbcL was rapidly degraded by subtilisin in samples of the mutant, while the RbcL degradation was clearly delayed in wild-type extracts with bound microcystin (Fig. 6B and C).
The cecum was significantly distended in the mutant while the antrum, small intestine, and colon appeared to be partially distended (Figure 2B) compared to those of the WT control mouse (Figure 2A).
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In the proband, direct sequencing of the NOTCH3 cDNA obtained by retrotranscription of the residual mRNA detected only the 2898A allele (mutant), while in the heterozygous parents, the C2898 allele (wild-type) appeared to be predominant (Fig 2B).
The simulations in Wang et al. preserve the large structural change observed in the mutant while probing the role of wild-type side chain chemistry in that context.
These results suggest that the albumin fusion did not significantly change the catalytic efficiency of the BChE mutant while extending the plasma half-life.
Inclusion of reactive nitrogen species in the form of 1 mM acidified sodium nitrite severely impeded growth of the hfq mutant while leaving the wild type unaffected.
The production of tensidol B on CYA was absent in the Δ laeA mutant, while in the D15 mutant, which contains a point mutation in the laeA gene, tensidol B was still produced.
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