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An initial test on a melittin-based mutant seems to support this hypothesis.
In apparent controversy, the Cx26R75A mutant seems to fold correctly and exhibits detergent resistance [26].
Consequently, the transient ubiquitination (detectable only at 1 min of ligand stimulation) observed for the Y1136F mutant seems to be sufficient to activate ERKs.
However, the phospho-mimic BicDS103D mutant seems to have slightly less hyperphosphorylated BicD than the phosphorylation defective mutants BicDS103F and BicDS103A (Figure 2B and 2A, lanes 5 7).
While the Chk1D469A mutant seems to be as checkpoint-deficient as cells with no Chk1 at all, they survive better than the chk1 null strain.
Specifically, the KIR mutant seems to enhance both periosteal apposition and endosteal resorption, as evidenced by significant increases in Tt.Ar.
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Although this scaffolding function was shown to be independent of CaMKIIα kinase activity toward Rpt6-S120, proteasomes containing the Rpt6-S120D mutant seemed to be more resistant to detergent extraction in hippocampal neurons (Djakovic et al., 2012).
However, under oxygen-limited conditions, NAD regeneration via respiratory pathways is restricted, and ADH2A-deficient mutant seemed to regenerate NAD by accumulating more glycerol at the expense of the decreased xylitol yield.
The RMSD values for the mutant seem to be slightly higher compared to those for the wild-type.
Both wild type Hfq and the mutant seem to bind cfa in a similar way but with different affinity (see binding assay below, right panel).
A few additional points came up during the discussion among the reviewers and may be worthy of consideration: 1) the ADDA mutant seem to form oligomers by size exclusion chromatography in Figure 2A and native gel electrophoresis in Figure 5 figure supplement 1A.
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CEO of Professional Science Editing for Scientists @ prosciediting.com