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The transcription factor c-Jun inhibits RBM39 to reprogram pre-mRNA splicing during genotoxic stress

ABSTRACT: The transcription factor c-Jun inhibits RBM39 to reprogram pre-mRNA splicing during genotoxic stress

PROVIDER: PRJNA802266 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17839202_1.fastq.gz	Fastqsanger.gz
	SRR17839202_2.fastq.gz	Fastqsanger.gz
	SRR17839203_1.fastq.gz	Fastqsanger.gz
	SRR17839203_2.fastq.gz	Fastqsanger.gz
	SRR17839204_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

The transcription factor c-Jun inhibits RBM39 to reprogram pre-mRNA splicing during genotoxic stress.

Project description:Genotoxic agents, that are used in cancer therapy, elicit the reprogramming of the transcriptome of cancer cells. These changes reflect the cellular response to stress and underlie some of the mechanisms leading to drug resistance. Here, we profiled genome-wide changes in pre-mRNA splicing induced by cisplatin in breast cancer cells. Among the set of cisplatin-induced alternative splicing events we focused on COASY, a gene encoding a mitochondrial enzyme involved in coenzyme A biosynthesis. Treatment with cisplatin induces the production of a short isoform of COASY lacking exons 4 and 5, whose depletion impedes mitochondrial function and decreases sensitivity to cisplatin. We identified RBM39 as a major effector of the cisplatin-induced effect on COASY splicing. RBM39 also controls a genome-wide set of alternative splicing events partially overlapping with the cisplatin-mediated ones. Unexpectedly, inactivation of RBM39 in response to cisplatin involves its interaction with the AP-1 family transcription factor c-Jun that prevents RBM39 binding to pre-mRNA. Our findings therefore uncover a novel cisplatin-induced interaction between a splicing regulator and a transcription factor that has a global impact on alternative splicing and contributes to drug resistance.

| S-EPMC9825188 | biostudies-literature

The transcription factor c-Jun inhibits RBM39 to reprogram pre-mRNA splicing during genotoxic stress

Project description:Gene expression and pre-mRNA splicing events were examined in human breast adenocarcinoma (MCF7) cells treated or not with cisplatin and various siRNAs.

2022-11-05 | GSE195842 | GEO

CHIP Analysis - c-Jun/ATF2

Project description:Identification of promoters bound by c-Jun/ATF2 during rapid large-scale gene activation following genotoxic stress

2010-06-05 | E-GEOD-1810 | biostudies-arrayexpress

CHIP Analysis - c-Jun/ATF2

Project description:Identification of promoters bound by c-Jun/ATF2 during rapid large-scale gene activation following genotoxic stress Keywords: other

2004-10-06 | GSE1810 | GEO

Genome-wide chromatin occupancy of RBM39 and MLL1 in T47D cells

Project description:We report high-throughput profiling of RBM39 and MLL1 chromatin occupancy in T47D cells. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of RBM39 and MLL1 in T47D cells. We found that more than 4500 regions were cofound by RBm39 and MLL1.

2021-04-13 | GSE144375 | GEO

Exceptional response of high-risk neuroblastoma to RBM39 degrader Indisulam (RNA-Seq)

Project description:Indisulam selectively bridges splicing factor RBM39 to DCAF15 for proteasomal degradation. However, clinical trials indicate that patient stratification based upon the mechanism of action of indisulam may be required to achieve the best response. Here we show that neuroblastoma, a MYC-driven cancer characterized by splicing dysregulation, requires RBM39 for survival, expresses high levels of DCAF15 among different solid tumor lineages, and is the most sensitive cancer lineage to indisulam that achieves therapeutic effect by specifically targeting RBM39 in neuroblastoma. Genetic depletion or proteasomal degradation of RBM39 by indisulam induces drastic splicing event changes in neuroblastoma cells. Through specifically targeting RBM39, indisulam induces exceptional tumor response in multiple high-risk neuroblastoma models. Collectively we demonstrate that high RBM39 dependency and high-level expression of DCAF15 provide indisulam a more efficacious therapeutic window to treating high-risk neuroblastoma.

2021-11-24 | GSE164505 | GEO

Exceptional response of high-risk neuroblastoma to RBM39 degrader Indisulam (ATAC-Seq)

2021-11-24 | GSE164504 | GEO

MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer [RBM39 RIP-seq]

Project description:RNA immunoprecipitation sequencing (RIP-seq) for the detection of RBM39 protein-binding RNA in SW480 cells.

2024-08-02 | GSE246656 | GEO

Global Regulation of Alternative RNA Splicing by the SR-Rich Protein RBM39

Project description:RBM39 is extensively involved in alternative splicing of RNA and helps regulate transcript levels. RBM39 may modulate alternative splicing similarly to U2AF65 by either directly binding to RNA or recruiting other splicing factors, such as U2AF65.

2016-09-13 | GSE86846 | GEO

Negative autoregulation of BMP dependent transcription by SIN3B splicing reveals a role for RBM39

Project description:We conducted RNASeq using mRNA extracted from C2C12 mouse myoblast cells transfected with non-targeting control (NTC) or RBM39 siRNA, to elucidate the effect of RBM39 on regulation of BMP4 pathway

2022-02-22 | GSE197107 | GEO

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