Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-Seq for validating the RNA expression of wild type and analog sensitive CDK12 and CDK13 in analog sensitive MV4 11 cell lines that generated by CRISPR HDR

ABSTRACT: RNA-Seq for validating the RNA expression of wild type and analog sensitive CDK12 and CDK13 in analog sensitive MV4 11 cell lines that generated by CRISPR HDR

PROVIDER: PRJNA593228 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10582175_1.fastq.gz	Fastqsanger.gz
	SRR10582175_2.fastq.gz	Fastqsanger.gz
	SRR10582176_1.fastq.gz	Fastqsanger.gz
	SRR10582176_2.fastq.gz	Fastqsanger.gz
	SRR10582177_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 10

Similar Datasets

RNA-Seq for validating the RNA expression of wild type and analog sensitive CDK12 and CDK13 in analog sensitive MV4;11 cell lines that generated by CRISPR HDR

Project description:We used Poly-A enriched RNA-Seq to validate CDK12, CDK13 anlalog senstive mutationsand their expression level in the cell lines that has analog sensitive mutations that were introduced by CRISPR HDR

2020-04-29 | GSE141366 | GEO

CDK13 cooperates with CDK12 to control global RNA polymerase II processivity

Project description:The RNA polymerase II (POLII) driven transcription cycle is tightly regulated at distinct checkpoints through cyclin dependent kinases (CDKs) and their cognate Cyclins. The molecular events underpinning transcriptional elongation and processivity and CDK-Cyclins involved remain poorly understood. Using CRISPR-CAS9 homology-directed-repair we generated analog-sensitive-kinase variants of CDK12 and CDK13 to probe their individual and shared biological and molecular roles. Single inhibition of CDK12 or CDK13 induced transcriptional responses associated with DNA-damage and cellular growth signaling pathways respectively, with minimal effects on cell viability. In contrast, dual-kinase inhibition potently induced cell death, which was associated with extensive genome-wide transcriptional changes including wide-spread use of alternative 3’ polyadenylation sites. At the molecular level dual-kinase inhibition resulted in the loss of POLII CTD phosphorylation and greatly reduced POLII elongation rates and processivity. These data define significant redundancy between CDK12 and CDK13, and identify both as fundamental regulators of global POLII processivity and transcription elongation.

2020-04-30 | PXD015453 | Pride

DRB-PRO-Seq for measuring Pol II transcriptional elongation rate alterations upon inhibition of analog sensitive CDK12 and/or CDK13

Project description:DRB-PRO-Seq for measuring Pol II transcriptional elongation rate alterations upon inhibition of analog sensitive CDK12 and/or CDK13

| PRJNA593231 | ENA

Identification of cellular CDK9 substrates using an analog-sensitive cell line

Project description:Analog-sensitive kinase technology allows for specific inhibition of a given kinase. Here we utilize an analog-sensitive CDK9 cell line to determine the impact of CDK9 inhibition on the phospho-proteome of human cells. Specifically, we aim to identify substrates of CDK9 in a quantitative way using stable isotope labeling by amino acids in cell culture (SILAC) followed by LC-MS/MS.

2019-11-11 | PXD014825 | Pride

Transcriptome wide analysis of differential gene expression and polyadenylation site usages caused by inhibition of CDK12 and/or CDK13 in MV4;11 cells (3’ Quant-seq)

Project description:We used 3' RNA-Seq to determine the effects of analog senstive CDK12, CDK13 and dual inhibition on gene expression and polyadenatltion site usages, and to test the redundancy between CDK12 and CDK13 in maintaining global transcrition on the tramcrotpomte level.

2020-04-29 | GSE141364 | GEO

DRB-PRO-Seq for measuring Pol II transcriptional elongation rate alterations upon inhibition of analog sensitive CDK12 and/or CDK13

Project description:We performed PRO-Seq to determine Pol II elongation rates by measruing the distance of Pol II travels during 25 minutes after Pol II being relased from DRB induced pausing. We allowed Pol II to release in the presence of 1-NM-PP1 or DMSO after DRB being wahsed out in order to assess the effects of CDK12 and/or CDK13 inhibtion on transcriptional elongation rates.

2020-04-29 | GSE141373 | GEO

Genome-wide map of Pol II and Ser2 phosphorylated Pol inoccupancy alteration on chromatin upon analog sensitive CDK12 and/or CDK13 inhibition (ChIP-Seq)

Project description:Genome-wide map of Pol II and Ser2 phosphorylated Pol inoccupancy alteration on chromatin upon analog sensitive CDK12 and/or CDK13 inhibition (ChIP-Seq)

| PRJNA593218 | ENA

Panicum virgatum strain:HDR | cultivar:HDR

Project description:Panicum virgatum HDR Resequencing genome sequencing

| PRJNA334737 | ENA

Identification of RSK substrates using an analog-sensitive kinase approach

Project description:RSK1 and RSK4 are two of the four members of the p90 ribosomal protein S6 kinases (RSK) family. These kinases are downstream kinases of mitogen-activated protein kinase 1 (ERK or MAPK1) in the ERK MAP kinase pathway. RSKs are implicated in fine tuning of cellular processes such as translation, transcription, proliferation, and motility. Previous work showed that pathogens such as Cardioviruses could hijack any of the four RSK isoforms to inhibit PKR activation or to disrupt cellular nucleocytoplasmic trafficking. In contrast, some reports suggest non-redundant functions for distinct RSK isoforms and Coffin-Lowry syndrome has only been associated with mutations in the gene encoding RSK2. In this work, we used the analog-sensitive kinase strategy to ask whether the cellular substrates of distinct RSK isoforms differ. We therefore compared the substrates of 2 of the most distant RSK isoforms: RSK1 and RSK4. We identified a series of potential substrates for both RSKs in cells, and validated RanBP3, PDCD4, IRS2 and ZC3H11A as substrates of both RSK1 and RSK4, and SORBS2 as a RSK1 substrate. In addition, using mutagenesis and inhibitors, we confirmed analog-sensitive kinase data showing that endogenous RSKs phosphorylate TRIM33 at S1119. Our data thus identify a series of potential RSK substrates and suggest that the substrates of RSK1 and RSK4 largely overlap and that the specificity of the various RSK isoforms likely depends on their cell- or tissue-specific expression pattern.

2024-02-06 | PXD047020 | Pride

Pol II and CTD Phosphorylation of ATP-analog sensitive Kin28 budding yeast

Project description:Pol II and CTD Phosphorylation of ATP-analog sensitive Kin28 budding yeast

| PRJNA325829 | ENA