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However, while Myc binding sites are frequently proximal to altered H3 methylation sites, peaks of Myc binding can also be found several kb away.
In general, transcription factor binding sites are frequently lost and gained [ 71].
Since it is well-known that binding sites are frequently lost in one or more lineages (Doniger and Fay, 2007), we now present a method for calculating PMM score distributions under a theoretical model that allows sites to be lost independently in any lineage.
This type of results i.e., moderate E-Scores and low P-scores but high %-presence, was also obtained for the SMEENK_TP53 ChIP-Chip data and indicates that TP53 binding sites are frequently seen in promoters albeit at low numbers for each promoter.
Notably, miR-181 binding sites are frequently distributed in the 3′-UTRs of many inflammatory cytokines, including IL-1α and TNF-α; surprisingly, no miR-181 binding sites have been found in the 3′-UTRs of anti-inflammatory cytokines such as IL-10 and TGF-β.
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Their DNA binding sites were frequently found in putative promoter regions of cluster 9 genes (see Additional file 3, B for examples).
Finally, high-throughput microarray and ChIP-seq data from lung and skin cancer cells (39, 49) revealed that p63-promoter-binding sites are frequently targeted by mutant p53, indicating that direct influence on p63 is one of the distinctive mechanisms of mutant p53 GOF.
Consistent with the recent reports of the increased LTR7 transcription in hESC (Kelley and Rinn 2012; Santoni et al. 2012; Xie et al. 2013; Lu et al. 2014), transcriptional activity of the LTR7-embedded human-specific NANOG-binding sites was frequently observed in hESC (fig. 1).
Several other SNP sites are frequently heterozygous.
Taken together, these results suggest that CTCF-A binding sites are more frequently involved in active gene transcriptional regulation than the two other types of sites.
They find that transcription-factor binding sites are, on average, less frequently methylated in cell types that express those transcription factors, suggesting that binding-site methylation often results from a passive mechanism that methylates sites not bound by transcription factors.
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