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Genes with differential histone modification islands were used for network analysis.
The genes possessing differential histone modification islands were sorted by their expression levels (Fig. 3a).
However, the differential histone modification islands were detected at specific chromatin domains and genes colocalized with these islands could be regarded as potential candidates responsible for the maintenance of HIV-1 latency.
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The genomic distribution of differential histone islands was also analysed and most of islands were located in the promoter regions where the percentage of downregulated histone modification islands was greater than that of the upregulated ones (Fig. 2c).
The differential histone modification islands that were domains with dominantly enriched or depleted histone modification in the HIV-1 latency cells were defined by SICER 1.1 program.
Using a ChIP-based microarray approach, it was found that in prostate cancer and PC3 cell line around 5% of promoters (16% with CpG islands and 84% without CpG islands) were enriched with H3K27me3, a modification that marks inactive chromatin.
CpG islands were detected according to the criteria set by the UCSC genome browser which is a modification of [ 14].
The methylation of cytosine in CpG islands is a modification produced by DNMTs.
DNA methylation at CpG islands is the major epigenetic modification of mammalian genomes and is required for gene regulation and genome stability [ 2].
DNA methylation, occurring predominantly at CpG islands, is the most studied epigenetic modification and is frequently found within gene promoter regions.
Determination of methylation patterns in MGMT promoter CpG islands was based on the chemical modification of unmethylated (but not methylated) cytosine to uracil.
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