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The MTLD contains all of the ligands binding to MTLs and sheds light on the side effects through anticipation of their multiple functions as well as the similarities in the binding site of multiple targets.
This has been reported to be the binding site of multiple proteins, which dynamically interact, and participate in the regulation of physiological events (for review, see Giepmans).
The same region was also DNaseI-hypersensitive and the predicted binding site of multiple transcription factors, including NFKB, PU.1, POU2F2 and MYC (http://genome.ucsc.edu/cgi-bin/hgTrackUi hgsid=174313571&c=chr15&g=wgEncodeReg).ucsc.edu/cgi-bin/hgTrackUi hgsid=174313571&c=chr15&g=wgEncodeReg
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It also sheds light on the side effects of drugs through anticipation of their multiple functions and similarities in the binding sites of multiple targets.
Therefore, equivalent analyses were performed after excluding genes with binding sites of multiple categories.
Simultaneously detecting the binding sites of multiple TFs, including SUMOylated TFs, is therefore a difficult task.
To examine this, we compared the clustering of binding sites of multiple factors studied by ChIP-seq across cell types.
However, it also contains the origin of replication and the binding sites of multiple transcription factors [ 3].
ACSL1-eRNA, ∼10 kb upstream of ACSL1, overlapped with the binding sites of multiple transcription factors shown previously to regulate the inflammatory response, including sub-units of NF-κB (RelA/p65) and AP-1 (c-fos, c-jun) [2].
We analysed the genome-wide binding sites of multiple factors, including CTCF, ELF1, ETS1, FOSL2, GABPA, REST, EP300, SIN3AK20, SIX5,SP1, TAF1, TCF12, USF1, YY1, ZBTB33, FOXA1, ATF3, BCL33, and RNA polymeraseII(POL2) using ENCODE ChIP-Seq data from human A549 cells [ 15].
Some more recent models have used binding sites of multiple TFs observed through ChIP-Seq [ 11- 13], but they estimate TF binding affinity only for the cell type used in ChIP-Seq, and therefore, cannot predict gene expression in other cell types.
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