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Alternatively, different parasite binding variants may be associated with CM1, CM2, and adult CM.
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Novel promoter variants may be investigated by examination of known transcription binding sites or by in vitro transfection experiments [ 39– 42].
Akin to the functional classification of coding variants, non-coding variants may be recognized as, for example, disrupting transcription factor binding sites.
In many cases, the relevant genetic variants may be rare and difficult to find.
Recombinant allergen variants with reduced IgE binding capacity may be used as component in such vaccines, as they may induce fewer treatment side effects than materials currently in use.
The WRKY genes encoding the variant domain patterns might be functional, because 10 genes with a total of seven heptapeptide variants and two zinc-finger motif variants have sequenced ESTs, although the DNA binding capacity may be reduced [ 48].
Genetic variants that create or destroy an miRNA binding site may be the casual cis-acting eQTLs.
We demonstrated that Rab21 and Rab5 have similar but not identical binding profiles towards APPL1 variants, which may be explained by their sequence divergence.
RAVEN combines phylogenetic footprinting with scanning of all sequence variants for transcription factor binding sites that may be differentially affected by the variation.
Thus, as in P-gp32, these distinct polarities within the binding cleft may be one possible explanation for the results obtained by Clark et al.54 in which, although using the R482G variant, several substrates appear to bind to distinct locations (Fig. 12A).
These variations in binding may be explained by the differential adhesion properties of the variant surface proteins (PfEMP1) expressed by each parasite line or the expression levels of PfEMP1.
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