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The mutations are predicted to result in elevated NOTCH2 signaling.
The mutations are predicted to result in an increase in NOTCH2 signaling.
More mutations are predicted than in the core, seemingly in order to optimise the network of complementary interactions between polar and charged groups.
The majority of the mutations are predicted to cause an up-regulation of the pathway; hence they are gain-of-function mutations.
The pathogenic HIST1H1E mutations are predicted to result in a product that is less effective in neutralizing negatively charged linker DNA because it has a reduced net charge, and in DNA binding and protein-protein interactions because key residues are truncated.
We find that qualitative effects of individual mutations are predicted quite well (Fig. S4).
Both mutations are predicted to confer amino acid changes but their impact on gene function is unknown.
Therefore, if flavonoids are essential for plant survival, loss of function mutations are predicted to persist only in the late genes of the ABP [14].
Nearly all of these indel mutations are predicted to create frameshift mutations although a few frame-preserved mutations are also observed.
Both mutations are predicted to result in changes in single amino acid residues in the TNF domain of the protein: p.D316G and p.T338M.
Based on previous report [43] these mutations are predicted to disrupt DNA-binding ability of the paired-type homeodomain such as AmphiVent1.
More suggestions(15)
mutant are predicted
transfer are predicted
mutations are summarized
mutations are associated
mutations are known
mutations are seen
mutations are observed
mutations are spread
mutations are detected
mutations are mapped
mutations are kept
mutations are located
mutations are replicated
mutations are implicated
mutations are termed
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