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The splicing factor RBM25 controls MYC activity in Acute Myeloid Leukemia

ABSTRACT: The splicing factor RBM25 controls MYC activity in Acute Myeloid Leukemia

PROVIDER: PRJNA454907 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7109580_1.fastq.gz	Fastqsanger.gz
	SRR7109580_2.fastq.gz	Fastqsanger.gz
	SRR7109581_1.fastq.gz	Fastqsanger.gz
	SRR7109581_2.fastq.gz	Fastqsanger.gz
	SRR7109582_1.fastq.gz	Fastqsanger.gz

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The splicing factor RBM25 controls MYC activity in Acute Myeloid Leukemia

Project description:Cancer sequencing studies have implicated regulators of pre-mRNA splicing as important disease determinants in Acute Myeloid Leukemia (AML), but the underlying mechanisms have remained elusive. We hypothesized that “non-mutated” splicing regulators may also play a role in AML biology and therefore conducted an in vivo shRNA screen in a mouse model of CEBPA mutant AML. This led to the identification of the splicing regulator RBM25 as a novel tumor suppressor, and down-regulation of RBM25 increased proliferation and decreased apoptosis in human leukemic cell lines. Mechanistically, we could show that RBM25 controlled the splicing of key genes, including those encoding the apoptotic regulator BCL-x and the MYC inhibitor BIN1. Specifically, we demonstrated that RBM25 acts as a regulator of MYC activity and sensitizes cells to increased MYC levels. This mechanism also appears to be operative in human AML patients where RBM25 levels correlative inversely with MYC activity and clinical outcome.

2018-12-07 | GSE114027 | GEO

The splicing factor RBM25 controls MYC activity in acute myeloid leukemia.

Project description:Cancer sequencing studies have implicated regulators of pre-mRNA splicing as important disease determinants in acute myeloid leukemia (AML), but the underlying mechanisms have remained elusive. We hypothesized that "non-mutated" splicing regulators may also play a role in AML biology and therefore conducted an in vivo shRNA screen in a mouse model of CEBPA mutant AML. This has led to the identification of the splicing regulator RBM25 as a novel tumor suppressor. In multiple human leukemic cell lines, knockdown of RBM25 promotes proliferation and decreases apoptosis. Mechanistically, we show that RBM25 controls the splicing of key genes, including those encoding the apoptotic regulator BCL-X and the MYC inhibitor BIN1. This mechanism is also operative in human AML patients where low RBM25 levels are associated with high MYC activity and poor outcome. Thus, we demonstrate that RBM25 acts as a regulator of MYC activity and sensitizes cells to increased MYC levels.

| S-EPMC6329799 | biostudies-literature

Efficient, specific and combinatorial control of endogenous exon splicing with dCasRx-RBM25

Project description:Efficient targeted control of exon splicing is a major goal of functional genomic and therapeutic applications. Guide RNA-directed, deactivated (d)Cas CRISPR enzymes fused to splicing effectors represent a promising strategy due to the flexibility and presumed specificity of these systems. However, efficient, selective, and generalizable activation of targeted endogenous exons using this approach has not been reported. Here, we identify dCasRx-RBM25 as a potent activator of exons by screening over 300 dCasRx splicing factor fusions tethered to splicing reporters. dCasRx-RBM25 also strongly activates splicing of endogenous alternative exons, when recruited to downstream intron sequences using single guide RNAs. In transcriptome wide analyses we observe a high degree of specificity of dCasRx-RBM25 for endogenous exon targeting. We further leverage the guide array-processing activity of dCasRx to simultaneously target multiple endogenous exons for activation and repression by dCasRx-RBM25. Our results pave the way for versatile exon-resolution functional assays and splicing-directed therapeutic applications.

2024-09-19 | GSE243979 | GEO

RBM25 is a global splicing factor promoting inclusion of alternatively spliced exons

Project description:The goal of this study was to determine the role of RBM25 in pre-mRNA splicing and examine whether lysine 77 contributes to this function.

2016-10-26 | GSE89140 | GEO

Identification of Rbm25-binding RNAs in bone-marrow-derived macrophages by RIP-seq

Project description:To identify the potential mRNAs that bound by Rbm25, which might be the direct target of Rbm25 for alternative splicing in murine macrophages.

2024-11-06 | GSE240159 | GEO

An PWI- and RRM Motif-Containing Protein Is Critical for Pre-mRNA Splicing and ABA Responses in Arabidopsis

Project description:We used RNA-seq platform to determine role of a splicing factor RBM25 in regulation of gene expression and pre-mRNA splicing. We found that a loss-of-function allele of RBM25, rbm25-1, causes up- and down-regulation of a large number of genes. We further found that the rbm25-1 mutation results in defects in altenative splicing of transcripts of many genes including signal transduction components in stress responses. Examination of mRNA levels in bulked individual wild type and rbm25-1 mutant seedlings before and after ABA treatment.

2015-10-28 | E-GEOD-66737 | biostudies-arrayexpress

RBM25 affects the immune and inflammatory progress by binding to and modulating alternative splicing levels of associated genes in rat H9C2 cells [ABL2020-10020-ABF_H9C2_RBM25_iRIP]

Project description:Alternative splicing (AS) enables genes to be translated into a vast diversity of proteins while aberrant AS predisposes cells to abnormal biological processes. As is closely associated with AS, RNA binding proteins (RBPs) are gradually gaining attention. RBM 25 was reported to participate in the cardiac pathophysiological process via AS regulation. Nonetheless, gaps still existed in whether RBM 25 functions in heart failure by its splicing factor role. H9C2 cells with excessively expressed RBM25 were used to filtrate different expression genes (DEGs) and analyze for RBM25-regulated AS by RNA-seq. Next, iRIP-seq was performed to examine its binding targets. For genes screened, further RT-qPCR-based validation was conducted. RBM25 overexpression caused expressive alteration in 80 genes mainly involved in the inflammatory response and virus response. Notably, RBM25 partially modulated AS of differential genes enriched in the apoptotic process and bound to genes clustered at inflammation response. Further, qRT-PCR verified Slc38a9, IL-17RC, Csf1, and Coro6 as targets of RBM25 being bound to and AS-regulated.

2023-10-05 | GSE209941 | GEO

RBM25 affects the immune and inflammatory progress by binding to and modulating alternative splicing levels of associated genes in rat H9C2 cells [ABL2020-10020-ABF_RBM25_OE]

2023-10-05 | GSE209940 | GEO

An PWI- and RRM Motif-Containing Protein Is Critical for Pre-mRNA Splicing and ABA Responses in Arabidopsis

2015-10-28 | GSE66737 | GEO

Efficient, specific and combinatorial control of endogenous exon splicing with dCasRx-RBM25

Project description:Efficient, specific and combinatorial control of endogenous exon splicing with dCasRx-RBM25

| PRJNA1020835 | ENA