ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR290/023/SRR29029423/SRR29029423.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR290/026/SRR29029426/SRR29029426.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR290/022/SRR29029422/SRR29029422.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR290/024/SRR29029424/SRR29029424.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR290/025/SRR29029425/SRR29029425.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR290/021/SRR29029421/SRR29029421.fastq.gzprimaryOK200GenomicsMarikki Laiho Lab, Department of Radiation Oncology and Molecular Radiation Sciences, Johns Hopkins Universityhttps://www.ebi.ac.uk/ena/browser/view/PRJNA1111743Homo sapiensRibosome biosynthesis is essential for cancer growth and proliferation. This dependency is therapeutically exploitable by blocking the rate-limiting step, RNA polymerase I (Pol I) transcription. Here we investigated the effects of RNA Pol I inhibitor on binding of Pol I RPA1 and Pol II Rpb1 on genomic DNA. Overall design: We treated LNCaP prostate cancer cells with either DMSO vehicle or 1 microM BMH-21 for 6 hrs.xref:PubMed:40553690ENAfalseChIP-seq analysis of RNA polymerase I inhibitor effect on Pol I and Pol II bindingChIP-seq analysis of RNA polymerase I inhibitor effect on Pol I and Pol II binding2025-09-242025-05-15PRJNA1111743GSE267504960640553690