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Physiological characterization of each mutant demonstrated that the growth and metabolites accumulation properties of these mutations exhibited significant change upon pathway engineering.
Non-catalytic Cys286 was identified as the only site of modification, but further mutagenesis studies using the C286Q mutant demonstrated that this site was not responsible for inhibition of EhTrxR by Auranofin.
Studies with the NS2A mutant demonstrated that it was unable to produce a larger form of NS1 (Nsuggestingesthat thet the mutation had been selected to eliminate a ribosomal frame-shift "slippage site" in NS2A.
Surprisingly, analyses of the hydA1-1 and hydA2-1 single mutants, as well as the HYDA1 and HYDA2 rescued hydA1-1 hydemonstrated demonsthated that both hydrogenases are able to catalyze H2 production from either fermentative or photosynthetic pathways.
Sequencing of cDNA from cells infected with this last mutant demonstrated that the parental mutant sequence was retained and that genotypic revertants to the wild-type as well as new mutant sequences were generated.
Infection of an ATHB12 T-DNA insertion mutant demonstrated that ATHB12 is necessary for complete symptom development.
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However, SMX had no effect on nuc-1 mutants, demonstrating that animals maintain a functional folate cycle.
Here we show that the lack of both Gadd45a and p21 dramatically accelerates the development of autoimmunity observed in each individual single-gene disruption mutant, demonstrating that these genes play nonredundant roles in the immune response.
A recent study of a similar α-hemolysin mutant demonstrates that this mutant toxin is capable of inducing an apoptotic host response [47].
The qRT-PCR data obtained with the rofA::aad9 ΔmsmR mutant demonstrates that MsmR is a potent activator of prtF2 transcription (Table 4).
The wild-type and Q766H forms of the enzyme restored viability of the yeast double deletion mutant, demonstrating that the human proteins – even the Q766H mutant in the catalytic domain – were catalytically active in yeast cells.
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