ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR109/059/SRR10981259/SRR10981259.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR109/064/SRR10981264/SRR10981264.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR109/066/SRR10981266/SRR10981266.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR109/065/SRR10981265/SRR10981265.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR109/063/SRR10981263/SRR10981263.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR109/060/SRR10981260/SRR10981260.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR109/062/SRR10981262/SRR10981262.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR109/061/SRR10981261/SRR10981261.fastq.gzprimaryOK200GenomicsPathology and Cell Biology, Columbia Universityhttps://www.ebi.ac.uk/ena/browser/view/PRJNA603558Homo sapiensxref:PubMed:32315286FDA-approved global (panobinostat, vorinostat) and selective (romidepsin) histone-deacetylase (HDAC) inhibitors elicit metabolic reprogramming in concert with disruption of several Warburg-effect related super-enhancers Overall design: U87 and NCH644 cells were treated with panobinostat or romidepsin for 24h. Thereafter, cells were harvested and subjected to CHIP isolation. DNA was subsequently processed for CHIP sequencing.ENAfalseEpigenetic Targeting of the Warburg Effect by Inhibition of Histone-Deacetylases Leads to Activation of Oxidative MetabolismEpigenetic Targeting of the Warburg Effect by Inhibition of Histone-Deacetylases Leads to Activation of Oxidative Metabolism2025-09-242020-01-30PRJNA603558GSE144399960632315286