ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/080/SRR29208880/SRR29208880_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/084/SRR29208884/SRR29208884_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/082/SRR29208882/SRR29208882_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/086/SRR29208886/SRR29208886_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/088/SRR29208888/SRR29208888_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/080/SRR29208880/SRR29208880_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/081/SRR29208881/SRR29208881_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/089/SRR29208889/SRR29208889_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/086/SRR29208886/SRR29208886_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/089/SRR29208889/SRR29208889_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/087/SRR29208887/SRR29208887_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/083/SRR29208883/SRR29208883_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/085/SRR29208885/SRR29208885_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/083/SRR29208883/SRR29208883_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/085/SRR29208885/SRR29208885_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/084/SRR29208884/SRR29208884_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/088/SRR29208888/SRR29208888_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/087/SRR29208887/SRR29208887_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/081/SRR29208881/SRR29208881_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR292/082/SRR29208882/SRR29208882_2.fastq.gzprimaryOK200GenomicsTaatjes, Biochemistry, University of Colorado Boulderhttps://www.ebi.ac.uk/ena/browser/view/PRJNA1117577Homo sapiensCDK7 regulates RNA polymerase II (RNAPII) initiation, elongation, and termination through incompletely-defined mechanisms. Biochemical reconstitution of RNAPII transcription initiation showed that CDK7 inhibition suppressed RNAPII activity by blocking promoter escape and re-initiation and this was Mediator- and TFIID-dependent. These in vitro results were consistent with genomics and transcriptomics experiments in human cells CDK7 inhibition globally reduced transcription and increased RNAPII promoter-proximal pausing. Moreover, we observed termination defects in CDK7-inhibited cells unexpectedly, this coincided with rapid, widespread degradation of elongation and 3'-end processing factors. Collectively, these mechanistic insights further define how CDK7 kinase activity regulates RNAPII initiation, termination, and RNA processing. Overall design: Chromatin immunoprecipitation (ChIP-seq) of human RNA Polymerase II and RNA Polymerase II phosphomarks (p-Ser5, p-Ser2, and p-Ser7) under control and CDK7-inhibited conditions.xref:PubMed:40020069xref:PubMed:40570372xref:PubMed:39829884ENAfalseCDK7 inhibition suppresses RNA polymerase II re-initiation and triggers degradation of elongation and 3'-end processing factorsCDK7 inhibition suppresses RNA polymerase II re-initiation and triggers degradation of elongation and 3'-end processing factors2025-09-242024-12-21PRJNA1117577GSE2685319606398298844002006940570372