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Moreover, the two former variants displayed a remarkable resistance to trypsin degradation.
The resulting variants displayed a higher specific activity (from 1.5-to 4-fold) than the parental enzyme.
Mediator release assays using rat basophil leukemia cells showed that these variants displayed a 1 × 105-fold reduced allergenic potency as compared to wild-type protein.
We tested whether any of the 16 missensesense variants displayed a unique spectrum of base-pair substitutions when compared to wild-type or the msh2 null.
The N83A and Q84A variants displayed a 150 250-fold decrease in kcat/ KAcCoA., while the kcat /KKIV parameters are relatively unchanged.
Both R126W and P509S variants displayed a similar level of ability to bind substrates when compared with wild-type, indicating that mitochondrial client protein sequestration is not compromised in the folding cycle.
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Both variants displayed an altered substrate preference profile, with reduced ligand binding capacity.
We thus observed that the AT3Q55 oligomers progressively decreased from the beginning and disappeared completely at 30 h, whereas the two other variants displayed an approximately constant level of oligomers over the entire incubation time (Fig. 1B).
Such SMK variants display a "constitutively OFF" behavior both in vitro and in vivo.
All CPY* deletion variants display a similar pattern, except two (Figures 1C and S1).
UV treated cells expressing DinB variants, display a number of DNA damage-induced mutants that are, for the most part, equivalent to the level of mutants found both in ΔdinB carrying the DinB(D103N) variant, which is unable to synthesize DNA, and to cells without DinB (Fig. 7).
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CEO of Professional Science Editing for Scientists @ prosciediting.com