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Genome-wide mapping of HATs and HDACs in human CD4+ T cells

GSE15735 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by array 41 samples Submitted 2009/08/20 Platform GPL570Platform GPL9052
Summary
Histone acetyltransferases (HATs) and deacetylases (HDACs) function antagonistically to control histone acetylation. As acetylation is a histone mark for active transcription, HATs have been associated with active and HDACs with inactive genes. We describe here genome-wide mapping of HATs and HDACs binding on chromatin and find that both are found at active genes with acetylated histones. Our data provide evidence that HATs and HDACs are both targeted to transcribed regions of active genes by phosphorylated RNA Pol II. Furthermore, the majority of HDACs in the human genome function to reset chromatin by removing acetylation at active genes. Inactive genes that are primed by MLL-mediated histone H3K4 methylation are subject to a dynamic cycle of acetylation and deacetylation by transient HAT/HDAC binding, preventing Pol II from binding to these genes but poising them for future activation. Silent genes without any H3K4 methylation signal show no evidence of being bound by HDACs.
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Direct links to NCBI, no account and no request form: the whole study as GSE15735_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 41 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA129023 and SRA study SRP002112. Searching any of these in the dataset finder brings you back here.

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