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The higher stability of promoters versus enhancers could be due in part to the intimate functional connection promoters have with the first exon of protein coding genes, which are highly stable features of vertebrate genomes (Lindblad-Toh et al., 2011).
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Further studies of promoter methylation and 3' UTR evolution will be needed to uncover the underlying mechanisms of the connection between promoter methylation level and the number of miRNA target sites.
But each year, faster Internet connections and promoters stepping up their game have allowed more people to be indoctrinated into this cult.
However, we found no connection between promoter hypermethylation in cancer and the presence of intragenic L1s.
Analysis of this data allowed for the comprehensive identification of the connections between promoter nucleosome positioning patterns and various transcription-dependent properties.
This has been used to infer a genome-wide DHS/enhancer-promoter connection set.
These data show a connection between MGMT promoter methylation and the hypermutator phenotype in temozolomide-treated GBM.
As such, we built the regulatory block for each gene based on distal-DHS-promoter connection map (denoted as DHS-based regulatory block in this study).
For example, 1538 (of 3391) heart enhancers assigned to at least one heart gene could not be retrieved from this distal-DHS-promoter connection map.
To fully understand the connections between gene promoters and gene expression, we analyzed thousands of promoter sequences using our Kappa Index of Coincidence method and a specialized Optical Character Recognition (OCR) neural network.
Although the distal-DHS-promoter connection map was established on the basis of an extensive panel of cells, this map does not cover the entire regulatory-element-promoter landscape for all tissues and cell lines.
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