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Using these data, we show that domain proximities calculated from a domain-domain interaction network do, indeed, imply phenotype similarities of diseases.
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In other words, domain proximity implies phenotype similarity.
In other words, semantic similarity of genes implies phenotype similarity of diseases that the genes are associated.
The fact that there is discordance with regards these actual or implied phenotypes in humans and the mouse phenotype described here most probably reflects differences in the nature of the mutations involved.
Using phenotype patterns to generate secondary phenotype predictions implies that phenotypes that co-occur often with each other, are likely to always co-occur.
The lack of an evident phenotype in vitro upon gene disruption may, alternatively, imply that a phenotype can only be revealed in vivo through host-parasite interactions, perhaps that involve the 'conserved' C-terminal domains.
These results imply that the phenotype caused by GMR-GAL4-driven c- Myb is cell-autonomous.
For some organisms, many of the strains were sequenced to identify the fraction of gene contents that can imply the specific phenotype of each strain.
They also imply that the phenotypes in llg1 and lre, together spanning the developmental spectrum of fer phenotypes, could have largely resulted from diminished FER localization to its proper functional location in the cell membrane, thus mimicking loss of FER.
Or, do diazotrophic phenotypes imply additional endo-hydrogenase function(s), e.g. chemiosmotic work associated with membrane ion translocation [28] not undertaken by exo-hydrogenase?
These two phenotypes imply that myosin II activity is required for both uropod formation and lamellipodial protrusion in T cells, as previously suggested [3], [63].
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