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Molecular analyses, even using long concatenated sequences, fail to provide consistent statistical support to any of these (compounded by the fact that taxon sampling makes a considerable difference) suggesting the phylogenetic models are breaking down [11], [33].
This explains why these sequences fail to survive despite having a high replication rate.
Because these sequences fail to align, we cannot call variants in them.
A number of sequences fail to cluster into any group (black in Figure 3), but remain independent of classic eukaryotic lipid phosphatases and PFAs.
Although there is significant sequence identity shared between the regions, the lengths of the sequences fail to show the entire shared orthology.
In our analysis based on PYD protein sequences alone, a number of sequences fail to cluster with either human NLRP7 or NLRP2, suggesting that they represent intermediate forms of the gene (e.g. the NLRP2-like macaque XR 010180.1).
Similar(51)
Inhibition was sequence-specific, since a scrambled control oligonucleotide or mismatched or scrambled target sequences failed to inhibit CAT expression.
Indeed, uncorrelated random paired sequences failed to induce long-term plasticity.
Both sequences failed to demonstrate transcriptional regulatory function in vitro and in vivo in MCF7 cells.
However, the isolated NES sequences failed to induce nuclear export when inserted into the Rev(1.4 -GFP vector (Table 1.4 -GFP
A recent study of gorilla gestural sequences failed to find evidence of syntactic organisation or corresponding semantic content [39].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com