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

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE197107 | GEO | 2022/02/22

REPOSITORIES: GEO

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

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

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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.

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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.

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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)

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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

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

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Identification of RBM39-dependent alternative splicing events in HeLa cells

Project description:We report a comprehensive analysis of alterations in gene expression and alternative splicing upon RBM39 depletion and rescue in HeLa cells.

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Identification and Quantification of Murine Mitochondrial Proteoforms Using an Integrated Top-Down and Intact-Mass Strategy

Project description:1) 144 intact-mass and top-down raw LC-MS and LC-MS/MS files (myoblast and myotube, 3 biological replicates, 6 fractions, 2 top-down MS/MS technical replicates and 2 MS1-only technical replicates) from 12% GELFrEE fractions of C2C12 mitochondrial extracts. 2) 12 intact-mass raw LC-MS files from unfractionated C2C12 mitochondrial extracts (myoblast and myotube, 3 biological replicates, 2 MS1-only technical replicates). 3) 12 bottom-up raw LC-MS/MS files from unfractionated C2C12 mitochondrial extracts digested with trypsin (myoblast and myotube, 3 biological replicates, 2 technical replicates).

2018-05-16 | MSV000082366 | MassIVE

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