Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: Knockdown of CFIm25 or CFIm68 decreases RNA polymerase II pausing and transcription

PROVIDER: PRJNA390279 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5679910_1.fastq.gz	Fastqsanger.gz
	SRR5679910_2.fastq.gz	Fastqsanger.gz
	SRR5679911_1.fastq.gz	Fastqsanger.gz
	SRR5679911_2.fastq.gz	Fastqsanger.gz
	SRR5679912_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Homo sapiens

Project description:CDK9-dependent RNA polymerase II pausing controls transcription initiation

| PRJNA378674 | ENA

Knockdown of CFIm25 or CFIm68 decreases RNA polymerase II pausing and transcription

Project description:Transcription of eukaryotic protein-coding genes by RNA polymerase II (pol II) is highly regulated at initiation, elongation and termination and these steps are coordinated with co-transcriptional processing of the emerging pre-mRNA by capping, splicing, and cleavage and polyadenylation. Polyadenylation (Poly(A)) site recognition, which defines the end of the mRNA, relies on the cleavage and polyadenylation (CPA) complex. It was previously observed that knocking-down proteins of the CPA complex affects not only recognition of the poly(A) site but also results in increased pausing of pol II at the beginning of genes. This finding suggests that the CPA complex plays a role in regulating pol II turnover after transcription initiation. To explore this possibility, we knocked-down two subunits of the cleavage factor I (CFIm), CFIm25 and CFIm68, which are part of the CPA complex and involved in alternative polyadenylation, and performed pol II ChIP-seq. Surprisingly, we found that contrary to the effect of knocking down of other CPA factors, reduction of the level of CFIm25 or CFIm68 decreases pol II pausing and transcription genome-wide in HEK293 cells. These findings indicate that different subunits of the CPA complex have opposite effects on pol II pausing at the start of genes.

2019-06-20 | GSE99955 | GEO

Homo sapiens

Project description:Polymerase II pausing licenses cell-cycle progression (RNA-Seq)

| PRJNA393890 | ENA

The functional impact of RNA Polymerase II pausing across multiple mamamlian cell types

Project description:We analyzed the breadth and functional relationships of RNA Polymerase II pausing across many human and mouse cell types to understand what roles RNA Polymerase II pausing plays in gene regulation. We identified a novel association of H2A.Z at the TSS of increasingly paused genes. We knocked down H2A.Z to test whether H2A.Z positively or negatively affects RNA Polymerase II pausing to find that pausing globally increased upon knockdown.

2016-04-28 | GSE60872 | GEO

Effect of CFIm25 knock-out on RNA polymerase II transcription

Project description:Effect of CFIm25 knock-out on RNA polymerase II transcription

| PRJNA490093 | ENA

Homo sapiens

Project description:Polymerase II pausing licenses cell-cycle progression (ChIP-Seq)

| PRJNA393889 | ENA

Homo sapiens

Project description:The functional impact of RNA Polymerase II pausing across multiple mamamlian cell types

| PRJNA259708 | ENA

The PNUTS phosphatase complex controls transcription pause release

Project description:Gene expression is regulated by controlling distinct steps of the transcriptional cycle, including initiation, pausing, elongation, and termination. Kinases phosphorylate RNA Polymerase II and associated factors to control transitions between these steps and act as central gene regulatory nodes. Similarly, phosphatases that dephosphorylate these components are emerging as important regulators of transcription, though their roles remain less well understood. Here we discover that the PNUTS-PP1 phosphatase complex plays an essential role in controlling transcription pause release in addition to its previously described function in transcription termination. Transcription pause release by the PNUTS complex is essential for almost all RNA Pol II-dependent gene transcription, relies on its PP1 phosphatase subunit, and controls the phosphorylation of factors required for pause release and elongation. Together, this reveals an essential new role for a phosphatase complex in transcription pause release and shows that the PNUTS complex is essential for RNA Poll II-dependent transcription.

2024-06-28 | MSV000095177 | MassIVE

The pause-initiation limit restricts transcription activation in human cells

Project description:Eukaryotic gene transcription is often controlled at the level of RNA polymerase II (Pol II) pausing in the promoter-proximal region. Pausing Pol II limits the frequency of transcription initiation (‘pause-initiation limit’), predicting that the pause duration must be decreased for transcriptional activation. To test this prediction, we conducted a genome-wide kinetic analysis of the heat shock response in human cells. We show that the pause-initiation limit restricts transcriptional activation at most genes. Gene activation generally requires the activity of the P-TEFb kinase CDK9, which decreases the duration of Pol II pausing and thereby enables an increase in the productive initiation frequency. The transcription of enhancer elements is generally not pause-limited and can be activated without CDK9 activity. Our results define the kinetics of Pol II transcriptional regulation in human cells at all gene classes during a natural transcription response.

2019-07-10 | GSE123980 | GEO

Homo sapiens

Project description:Attenuation of RNA polymerase II pausing mitigates BRCA1-associated R-loop accumulation and tumorigenesis.

| PRJNA379324 | ENA