Journal article
Vascular histone deacetylation by pharmacological HDAC inhibition
H Rafehi, A Balcerczyk, S Lunke, A Kaspi, M Ziemann, KN Harikrishnan, J Okabe, I Khurana, J Ooi, AW Khan, XJ Du, L Chang, I Haviv, ST Keating, TC Karagiannis, A El-Osta
Genome Research | COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT | Published : 2014
Abstract
HDAC inhibitors can regulate gene expression by post-translational modification of histone as well as nonhistone 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 in cells stimulated by the hydroxamic acids, TSA and SAHA. In this article, we map vascular chromatin modifications including 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 H3..
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Funding Acknowledgements
We thank Helen Kiriazis, Xiao-Ming Gao, Luciano Pirola, Andrew Siebel, and Prabhu Mathiyalagan for preparative assistance and Ross Lazarus for bioinformatics support. We also acknowledge grant and fellowship support from the Juvenile Diabetes Research Foundation International (JDRF), the Diabetes Australia Research Trust (DART), the National Health and Medical Research Council (NHMRC), and the National Heart Foundation of Australia (NHF). A.E.-O. and X.-J.D. are Senior Research Fellows supported by the NHMRC. This research was supported in part by the Victorian Government's Operational Infrastructure Support Program.