Vascular histone deacetylation by pharmacological HDAC inhibition [TSA, mouse, ChIP-seq]

ABSTRACT: HDAC inhibitors are thought to regulate gene expression by post-translational modification of histone as well as non-histone proteins. Often studied at single loci, increased histone acetylation is the paradigmatic mechanism of action, however, little is known of the extent of genome-wide changes of the mammalian genome when stimulated by the hydroxamic acids, TSA and SAHA. In primary human vascular endothelial cells we map the chromatin modifications, histone H3 acetylation of lysine 9 and 14 (H3K9/14ac) using chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq). Since acetylation mediated gene expression is often associated with modification of other lysine residues we also examined H3K4me3 and H3K9me3 as well as changes in CpG methylation (CpG-seq). G

ORGANISM(S): Mus musculus

SUBMITTER: Assam El-Osta 

PROVIDER: E-GEOD-54910 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress