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Given that both marks are associated with gene repression, it has been suggested that they may cooperate with each other.
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While both these marks are associated with proximal promoters, only H3K4me1 is associated with distal enhancers [ 54].
Analysis of different chromatin marks in MeCP2−/y mice showed an increase in H3K4me3 and H3K9Ac in the region surrounding the miR-137 gene compared with WT mice (Szulwach et al., 2010); both histone marks are associated with an open chromatin state.
Both H3K9Me3 and H3K27Me3 marks are associated with gene silencing and have been implicated as drivers of other chromatin changes, including histone deacetylation and DNA methylation.
In addition, the presence of both H3K4me3 and H3K27me3 marks are associated with a 'poised' state that will become inactive or active following removal of either of the respective marks by histone demethylases.
To examine whether the hsi2-4-dependent changes in histone methylation marks are associated with both the Kan R and Kan S transgene loci, ChIP-qPCR analyses were performed on various regions of the endogenous GSTF8 gene and the GSTF8 LUC transgene in Kan R, Kan S, hsi2-4-Kan R and hsi2-4-Kan seedlingsgseedlings
By ChIP-seq and RNA-seq analysis, we demonstrate that histone Kbz marks are associated with gene expression and have physiological relevance distinct from histone acetylation.
Emerging evidence suggests that early alterations in epigenetic marks are associated with chronic lung diseases such as asthma, COPD, and IPF [30].
Others marks are associated with inactive chromatin (heterochromatin) and transcriptional repression, such as trimethylation of H3 lysine 9 (H3K9me3) or 27 (H3K27), or of H4 lysine 20 (H4K20me3).
Different methylation marks are associated with ISWI and CHD binding.
H3K4me3 and H3K36me3 are enriched on actively transcribed genes whereas H3K27me3 marks are associated with developmental repression of transcribed genes.
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