Background and objectives: Culture of blood CD34(+) cells with chromatin-modifying agents can lead to an increase in marrow repopulating cells and in the case of valproic acid increased erythroid cell colony formation
Chromatin immunoprecipitation for H3K9ac, H3K4me3 at Hoxb promoters after 0, 2 and 8 h in valproic acid (VPA)
This work attempts to explore the methylation profiles triggered by VPA treatment on human embryonic kidney cells (HEK 293) through a biochemical and computational approach
Heterochromatin was much more resistant to histone tail modification, changes in chromatin architecture and DNA damage
A chromatin immunoprecipitation (ChIP) experiment explored the interaction between the ALDH1A1 gene and AcH3
Regulation of chromatin arrangement during post-translation alterations of histones acetylation shows up as an essential mechanism to transform a diversity of environmental stimuli involving drugs of abuse into specific Treatment of ESCs with valproic acid leads to a pervasive genome-wide and time-dependent increase in H3K9ac, but this increase is selectively suppressed after 4 h in H3K4me3/H3K27me3 bivalent genes
the chromatin environment brought about by VPA treat-ment and inform the critical intersections of remodeling processes, such as changes in histone acetylation, linker histone expression, and locus-specic chromatin accessi-bility during early lineage commitment
VPA is a pleiotropic histone deacetylase (HDAC) inhibitor (HDI), which can modulate histone acetylation by preventing its deacetylation
Epigenetic modifications can be immediate or accumulate slowly, and may be passed on to daughter cells or to successive generations through mitotic or meiotic inheritance
For example, as an epigenetic modifier, it has a profound impact on the chromatin structure through