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Furthermore in HeLa cells, high resolution mapping of MBD2 binding sites indicated that MBD2 only associated the methylated region close to the TATA-box, whereas the unmethylated region, including the pS2 ERE, was not targeted by this repressor.
Notably, a small nucleosome occupancy peak at the binding sites indicated that a tiny fraction of binding sites resided on nucleosomes.
The same analysis for the proximal repressor binding sites indicated that genes associated with proximal repressor sites in Pattern 3 (P_3) had significantly lower expression in the GM12878 cell line.
In silico prediction of putative transcription factor binding sites indicated that of the four transcription factor binding sites potentially affected by the deletion, some are predicted to involve proteins not expressed in the breast.
Bioinformatic analysis of the promoter region SNPs for altered transcription factor binding sites indicated that the mutant alleles of all promoter and 5-UTR SNPs are likely to both introduce new transcription factor binding sites and prevent binding of some transcription factors compared to their respective common alleles (TESS).
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Comparison of these proteins' in vitro binding sites with their in vivo binding sites indicates that PBM-derived specificitiesificanies caccuratelyely reflect in vivo DNA sequence specificities.
The increase in binding affinity at lower pH was greater for the Ubx optimal binding site than for other DNA binding sites, indicating that subtle sequence alterations in DNA binding sites may influence pH-dependent behavior.
The widespread distribution of intronic AREs and their particular association with HuR and HuR binding sites indicates that more than half of human genes can be regulated post-transcriptionally by AREs.
The structure of the binding sites indicates that lipid ligands are anchored within them with their hydrophobic tails oriented towards the core of the protein and their polar headgroups bound to charged sidechains at the mouth of the pockets.
Interestingly, the UCH L1 promoter revealed c-Myc and E2F binding sites indicating that UCH L1 might be playing a role in proliferation via these molecules.
However, when considering the down-regulated genes compared to no-change genes, there was also a slight enrichment of STAT1 permuted binding sites, indicating that some of the observed effects may be non-specific (FIGURE S7C).
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