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The scores of the designed sequences have a much higher overlap with Pfam than the random sequences, even those generated at a 55% identity level (R55 sequences).
However, based on our previous analysis with IlluminaBeadChip technology, which discovered highly consistent DNAm changes that are continuously acquired throughout long-term culture [ 13, 14, 19], we would have anticipated a much higher overlap between the two replicates.
However, comparative ChIP-seq studies between mouse and human for other transcription factors have demonstrated much higher overlap of target genes (≥50%), even when the individual binding sites were not well conserved [ 38, 46].
This is mainly due to the fact that there is a much higher overlap of top predicted groups between diagnosis-based models and prior expenditures status compared to that between the demographic model and prior status (area b in Figure 1).
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Much higher overlaps might be anticipated in repeated analysis of samples derived from same individuals.
This information complements the observed much higher curation overlap between HPRD and BioGRID compared to the other pairs of source PPI datasets discussed by Turinsky et al. in [ 12].
Most importantly, we have discovered that the degree of overlap between sets of regulatory proteins predicted from gene expression and proteomic data is much higher than the overlap between the experimental sets themselves (52% vs. 17%).
Compared to Figure 3, we observe a much higher degree of overlap among subtypes.
The percentage of overlapping pathways was much higher than that of overlapping genes illustrated in Figure 1, indicating that the in vitro system perturbed by TNT could reflect more biological truth for an in vivo system from a mechanism related pathway view.
Comparison of the pathways generated from SCNA-genes in our data and genes affected by copy number changes in two published datasets (Stark and Hayward [14] and Gast et al. [13]) revealed a high level of overlap, much higher than we expected based on the number of commonly affected genes (see Fig. 4).
These overlaps, much higher than those observed within or across tumour types, further confirm tumour specificity of the observed methylation changes that accompany xenografting.
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