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Moreover, the optimum pHs of the G276K, G276Y, and G276N mutants were lower than that of the wild type.
As expected, the caspase activities in both the cmp1Δ and crz1Δ mutants were lower than that in wild-type cells (Fig. 4B).
However, the numbers of infective juveniles produced on all mutants were lower than that on the wild type (Fig. 4B), and no infective juveniles were produced on purL−.
The expression levels of both F857-L mutants were lower than the wild type constructs, but no significant difference in the S1/S2 cleavage was observed (Fig. 3b, lane 9 12).
Consistent with this, the transcription levels of CaMCA1 in cmp1Δ and crz1Δ mutants were lower than that in the wild-type cells, while the transcription levels of CaMCA1 in the CaMCA1-introduced cells were similar to that in the wild-type cells (Fig. 4C).
A similar trend was observed in Mexican lime where the populations of xopAF single and xopAF, avrGf1 double mutants were lower compared to Xcaw12879 and XcawΔ avrGf1 respectively.
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The activities of the Lys172Glu and Lys144Glu mutants were lowered slightly but the Asc Ka values were similar compared with the native ACCO.
Overall autophagy levels in lkb1 mutants are lower compared to those of wt siblings: while expression of autophagy related proteins is progressively upregulated following yolk depletion in wt larvae, induction of autophagy in lkb1 mutants is strongly attenuated.
The rate of emergence of phage-resistant mutants was lower for phage phT4A when compared with phage ECA2 and phage cocktail phT4A/ECA2.The results indicate that in addition to the efficacy, the potential development of phage-resistant mutants must also be considered in the design of phage cocktails.
It is noteworthy that the fertilization success rate of the mutants was lower than that of the controls, suggesting there may be some defects in the mutant oocytes that affected their fertilization.
In addition, the level of GLR-1 in the cell bodies of ire-1 mutants is lower than that in wild-type cell bodies, suggesting that much of the ER-trapped receptor in ire-1 mutants is removed by ERAD [74], [75].
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