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Inhibition of a pathologic RBM39/MLL1 epigenomic regulatory complex with a dominant-negative peptides disrupts cancer cell transcription, proliferation and survival

ABSTRACT: Inhibition of a pathologic RBM39/MLL1 epigenomic regulatory complex with a dominant-negative peptides disrupts cancer cell transcription, proliferation and survival

PROVIDER: PRJNA716073 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14022709.fastq.gz	Fastqsanger.gz
	SRR14022710.fastq.gz	Fastqsanger.gz
	SRR14022711.fastq.gz	Fastqsanger.gz
	SRR14022712.fastq.gz	Fastqsanger.gz
	SRR14022713.fastq.gz	Fastqsanger.gz

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Inhibition of a pathologic RBM39/MLL1 epigenomic regulatory complex with a dominant-negative peptides disrupts cancer cell transcription, proliferation and survival

Project description:We report high-throughput profiling of RBM39 and MLL1 chromatin occupancy; H3K4me3 marks in T47D Control, T47D RBM39 KD and PME cells. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of RBM39, MLL1 and H3K4me3 in T47D and PME cells. We found that more than 4500 regions were cofound by RBM39 and MLL1.

2021-04-13 | GSE169277 | GEO

Inhibition of a pathologic RBM39/MLL1 epigenomic regulatory complex with a dominant-negative peptides disrupts cancer cell transcription, proliferation and survival.

Project description:Inhibition of a pathologic RBM39/MLL1 epigenomic regulatory complex with a dominant-negative peptides disrupts cancer cell transcription, proliferation and survival.

| PRJNA603517 | ENA

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

Inhibition of a pathologic RBM39/MLL1 epigenomic regulatory complex with a dominant-negative peptides disrupts cancer cell transcription, proliferation and survival.

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-04-13 | GSE144379 | GEO

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

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

| PRJNA603523 | ENA

Expression analysis on Mll1+/+ and Mll1-/- MEFs

Project description:Global analysis of H3K4 methylation defines MLL family member targets and points to a role for MLL1-mediated H3K4 methylation in the regulation of transcriptional initiation by RNA polymerase II A common landmark of activated genes is the presence of trimethylation on lysine 4 of histone H3 (H3K4) at promoter regions. The Set1/COMPASS was the founding member and the only H3K4 methylases in S. cerevisiae, however, in mammals at least six H3K4 methylases Set1A/B and MLL1-4 are found in COMPASS-like complexes capable of methylating H3K4. To gain further insight into the different roles and functional targets for the H3K4 methylases, we have undertaken a genome-wide analysis of H3K4 methylation pattern in wild-type Mll1+/+ and Mll1-/- mouse fibroblasts (MEFs). We found that Mll1 is required for the H3K4 trimethylation of less than 5% of promoters carrying this modification. Many of these genes, which include developmental regulators such as Hox genes show decreased levels of RNA polymerase II recruitment and expression concomitant with the loss of H3K4 methylation. Although Mll1 is only required for the methylation of a subset of Hox genes, Menin, a component of the Mll1 and Mll2 complexes, is required for the overwhelming majority of H3K4 methylation at Hox loci. However, the loss of MLL3/4 and/or the Set1 complexes have little to no effect on the Hox loci H3K4 methylation or expression levels in these MEFs. Together these data provide insight into redundancy and specialization of COMPASS-like complexes in mammals and provide evidence on a possible role for Mll1-mediated H3K4 methylation in the regulation of transcriptional initiation. Expression arrays were done with Mll1+/+ and Mll1-/- mouse embryonic fibroblasts. Four replicates were done (dyes were swapped). DNA was hybridized to Agilent Mouse Whole Genome Expression Arrays (4x44k).

2009-10-20 | E-GEOD-18261 | biostudies-arrayexpress

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.

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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

RBM39 organizes an m⁶A-dependent silencing complex to degrade Tat mRNA and maintain HIV-1 latency

Project description:To further elucidate the interaction between RBM39 and its partern proteins, Flag-tagged RBM39 were transfected into HEK293T cells. After transfection, RBM39 and RBM39-bound proteins were enriched using anti-Flag beads. Subsequently, the enriched proteins were separated by SDS-PAGE and analyzed by LC-MS/MS.

2025-10-31 | PXD064858 | Pride

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