Sentence examples for marks of activation from inspiring English sources

The presence of both marks of activation (me3K4H3) and repression (me3K27H3) has also been defined as "bivalent mark" [23], [24] and has been reported to characterize a state of transcriptional competence.

The chromatin in primary progenitors and in myelinating cell lines was characterized by the presence of a transcriptionally competent histone code, composed of bivalent marks of activation (i.e. me3K4H3 and AcH3) and repression (me3K27H3).

We examined genome-wide enrichment sites for H3K4me3 and H3K27me3, marks of activation and repression, respectively.

For subtelomeres, the repressive marks H3K27me2/3 were found to be enriched along with two acetylations that are marks of activation, H2AK5ac and H3K14ac.

The two marks of activation (MOAs) examined, H3K4me3 and H3K9Ac, gave 79,412 and 52,511 unique peaks of enrichment, respectively (Model-based Analysis for Chip-seq [MACS], p ≤ 10-5, see Methods).

In contrast, one mark of activation, H3K4 trimethylation, is present but appears largely unchanged (Figures 5C, 6C and 7C), while H3K9 acetylation tracks gene activation for TOX and RASGRP1 but not for NOTCH2 (Figures 5E, 6E and 7E).

Specifically, various studies indicate that a number of key developmental and pluripotency genes are marked by bivalent marks of chromatin activation (H3K4me3) and repression (H3K27me3) that maintain genes in a "transcription-ready" state that allows rapid transcription activation upon differentiation of ESC [4], [5].

Also, H2A.Z-containing nucleosomes are often enriched with marks of transcriptional activation such as tri-methylated H3K4 [ 85].

JQ1 treatment in Tam-R cells eliminated the recruitment of BRD3/4 and WHSC1 to the ERα gene promoter, and dramatically reduced the level of H3K4me3 and H3K36me3, two histone marks of transcription activation.

We undertook an integrated pan-genomic analysis of the transcriptional responses to hypoxia in MCF7 breast cancer cells, employing total RNA-seq together with ChIP-seq for the hypoxia-inducible transcription factor (HIF) and for epigenetic marks of transcriptional activation (RNApol2 and histone H3K4me3).

However, our results described herein indicate the absence of CD34 on skeletal muscle satellite cells in vivo marks a state of activation dependent on muscle injury and not necessarily a hierarchy as initially predicted.