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Thus, gp150-specific monoclonal antibodies (mAbs) increase MuHV-4 infection of GAG-deficient cells [8] and gp150− mutants are almost completely GAG-independent: they infect GAG+ cells normally, infect GAG− cells much better than the wild-type does, and largely resist inhibition by soluble heparin.
In contrast, the T171D and T171E phosphomimic mutants are almost exclusively nuclear throughout the cell cycle.
Sarcomeric structures in mutants are almost entirely absent and only rare triads are observed.
The limb phenotypes of the Wnt5a mutants and the Ror2/Vangl2 double mutants are almost identical [ 17].
Binding affinities for Thr-179, Ser-182 and Thr-186 mutants are almost identical to those shown elsewhere (9).
The interactions of the PLP cofactor with the protein in the wild type and T254 mutants are almost identical.
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On the other hand, the change in cell length in the double mutants was almost the same as that in the single mutants.
Although the saccharification efficiencies were nearly similar, due to the high cellulase activity the required amount of enzyme from mutants was almost threefold lower than the wild-type.
The growth of all the mutants was almost similar in terms of dry cell mass and thus the specific bikaverin production by Mut-4 was also highest reaching 317 mg bikaverin g−1 dry cell weight against just 6.5 mg bikaverin g−1 dry cell weight by the parent.
Another remarkable difference between the two data sets was observed in the N6 subtype, where the proportion of mutants was almost 20 times higher in the Ottenby than the NCBI data set (Table 2).
Our genetic data show that the early-flowering phenotype of brm mutants is almost, but not completely reverted in a ft background (Figure 1C), suggesting that FT mostly contributes to the early-flowering phenotype of brm.
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