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This process involves ubiquitin modifications and various new molecules not considered as yet in this complex pathway.
Modulation of the substrate specificity of enzymes of this complex pathway is therefore likely to enable metabolic engineering efforts of these alkaloids.
Since this complex pathway is crucial to cell functions such as growth, proliferation, and survival, inhibition of this pathway would be postulated to inhibit leukemia initiation and propagation.
Further studies are required to assess DDAH sequence variation and its influence on DDAH activity and serum ADMA levels both in individuals with and without diabetes to increase understanding of this complex pathway in normal and pathogenic conditions.
The random occurrence of this complex pathway regulation in males and females is highly unlikely and perhaps underlines a commonality of connectivity between the mTOR pathway, dietary energy consumption and gonadal transcription.
More than 200 target genes joined in this complex pathway.
Currently, the molecular mechanisms of this complex pathway are not fully understood.
Many advances have occurred in elucidating the genes and the genetic modules involved in this complex pathway [ 14, 16].
This complex pathway has several known metabolic interactions, such as MTRR maintaining MTR in an active state.
Further studies for a better understanding of this complex pathway orchestration of HGF-induced migration will be necessary, of course.
This complex pathway enables the VEGFs to have numerous effects, including increasing vascular permeability (thereby augmenting tumour stroma formation), endothelial cell proliferation, endothelial cell survival and tube formation.
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