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RNA polymerase II (RNAPII) ChIP-seq analysis evaluating effects of Cdk7 inhibitor THZ1 on responses of neonatal rat ventricular myocytes (NRVM) to adrenergic receptor agonist phenylephrine (PE)

ABSTRACT: RNA polymerase II (RNAPII) ChIP-seq analysis evaluating effects of Cdk7 inhibitor THZ1 on responses of neonatal rat ventricular myocytes (NRVM) to adrenergic receptor agonist phenylephrine (PE)

PROVIDER: PRJNA635293 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11854554.fastq.gz	Fastqsanger.gz
	SRR11854555.fastq.gz	Fastqsanger.gz
	SRR11854556.fastq.gz	Fastqsanger.gz
	SRR11854557.fastq.gz	Fastqsanger.gz
	SRR11854558.fastq.gz	Fastqsanger.gz

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RNA-seq analysis evaluating effects of Cdk7 inhibitor THZ1 on responses of neonatal rat ventricular myocytes (NRVM) to adrenergic receptor agonist phenylephrine (PE)

Project description:RNA-seq analysis evaluating effects of Cdk7 inhibitor THZ1 on responses of NRVM to adrenergic receptor agonist PE

2022-04-25 | GSE151253 | GEO

RNA polymerase II (RNAPII) ChIP-seq analysis evaluating effects of Cdk7 inhibitor THZ1 on responses of neonatal rat ventricular myocytes (NRVM) to adrenergic receptor agonist phenylephrine (PE)

Project description:RNA polymerase II (RNAPII) ChIP-seq analysis evaluating effects of Cdk7 inhibitor THZ1 on responses of NRVM to adrenergic receptor agonist PE

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RNA-seq analysis evaluating effects of Cdk7 inhibitor THZ1 on responses of neonatal rat ventricular myocytes (NRVM) to adrenergic receptor agonist phenylephrine (PE)

Project description:RNA-seq analysis evaluating effects of Cdk7 inhibitor THZ1 on responses of neonatal rat ventricular myocytes (NRVM) to adrenergic receptor agonist phenylephrine (PE)

| PRJNA635319 | ENA

A Comparison of Neonatal Rat Ventricular Myocytes Treated With Phenylephrine or PAMH

Project description:Neonatal rat ventricular myocytes cultured for 48 hours without stimulation, in the presence of twenty micromolar phenylephrine, or in the presence of one micromolar PAMH. Keywords = Rattus Keywords = Ventricular Myocytes Keywords = Cardiomyocytes Keywords = Hypertrophy Keywords = Phenylephrine Keywords = PAMH Keywords = 5-hydroxytryptamine Keywords = Pyridine Keywords: repeat sample

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LncRNA Chaer contributes to the transcriptome reprogramming during phenylephrine-induced hypertrophy in neonatal rat ventricular myocytes

Project description:We compared the transcriptome modified by siRNA-mediated cardiac hypertrophy associated epigenentic regulator (Chaer) with negative control siRNA treated neonatal rat ventricular myocytes with or without phenylephrine treatment. The results suggest that Chaer knockdown broadly blocks the phenylephrine-induced hypertrophic programming of the transcriptome. Transcripts profiles from neonatal rat ventricular myocytes with or without phenylephrine and with or without Chaer-specific siRNA compared to negative control siRNA

2016-06-30 | E-GEOD-82339 | biostudies-arrayexpress

Transcription profiling of neonatal rat ventricular myocytes treated with phenylephrine or PAMH

Project description:Neonatal rat ventricular myocytes cultured for 48 hours without stimulation, in the presence of twenty micromolar phenylephrine, or in the presence of one micromolar PAMH.

2008-06-16 | E-GEOD-925 | biostudies-arrayexpress

CDK7 inhibitor THZ1 induces the cell apoptosis of B-cell acute lymphocytic leukemia by perturbing cellular metabolism

Project description:Purpose:CDK7 is a potential drug target for the treatment of tumors. THZ1 is the first selective and covalent CDK7 inhibitor, which shows anti-tumor effects in various cancers by inhibiting cell proliferation and inducing apoptosis. However, whether THZ1 has an inhibitory effect on B-ALL cells and the underlying mechanism remains unclear. To address this question, we collected THZ1- and DMSO-treated cells for RNA sequencing Methods:Nalm6 cells were seeded at a density of 1× 10e6 cells/ml and treated with 500nm THZ1or DMSO for 24h. Results:THZ1 perturbed the cellular metabolic pathways of B-ALL cells in vitro.

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LncRNA Chaer contributes to the transcriptome reprogramming during phenylephrine-induced hypertrophy in neonatal rat ventricular myocytes

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THZ1 targeting CDK7 suppresses STAT transcriptional activity and sensitizes T-cell lymphomas to BCL2 inhibitors

Project description:Peripheral T-cell lymphomas (PTCL) are aggressive diseases with poor response to chemotherapy and dismal survival. Identification of effective strategies to target PTCL biology represents an urgent need. Here we report that PTCL are sensitive to transcription-targeting drugs, and, in particular, to THZ1, a covalent inhibitor of cyclin-dependent kinase 7 (CDK7). The STAT-signaling pathway is highly vulnerable to THZ1 even in PTCL cells that carry the activating STAT3 mutation Y640F. In mutant cells, CDK7 inhibition decreases STAT3 chromatin binding and expression of highly transcribed target genes like MYC, PIM1, MCL1, CD30, IL2RA, CDC25A and IL4R. In surviving cells, THZ1 decreases the expression of STAT-regulated anti-apoptotic BH3 family members MCL1 and BCL-XL sensitizing PTCL cells to BH3 mimetic drugs. Accordingly, the combination of THZ1 and the BH3 mimetic obatoclax improves lymphoma growth control in a primary PTCL ex vivo culture and in two STAT3-mutant PTCL xenografts, delineating a potential targeted agent-based therapeutic option for these patients.

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The CDK7 Inhibitor THZ1 Alters RNA Polymerase Dynamics at the 5’ and 3’ Ends of Genes

Project description:The t(8;21) is one of the most frequent chromosomal translocations associated with acute myeloid leukemia (AML). We found that t(8;21) AML were extremely sensitive to THZ1, which triggered apoptosis after only 4 hr. We used precision nuclear run-on transcription sequencing (PROseq) to define the global effects of THZ1 and other CDK inhibitors on RNA polymerase II dynamics. Inhibition of CDK7 using THZ1 caused wide-spread loss of promoter-proximal paused RNA polymerase. This loss of 5’ pausing was associated with accumulation of polymerases in the body of a large number of genes. However, there were modest effects on genes regulated by “super-enhancers”. At the 3’ ends of genes, treatment with THZ1 suppressed RNA polymerase “read through” at the end of the last exon, which resembled a phenotype associated with a mutant RNA polymerase with slower elongation rates. Consistent with this hypothesis, polyA site-sequencing (PolyA-seq) did not detect differences in polyA sites after THZ1 treatment. PROseq analysis after short treatments with THZ1 suggested that these 3’ effects were due to altered CDK7 activity at the 5’ end of long genes, and were likely to be due to slower rates of elongation.

2019-02-11 | GSE102243 | GEO

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