Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RBM25 depletion suppresses colon cancer progression through regulating alternative splicing of MNK2

ABSTRACT: RBM25 depletion suppresses colon cancer progression through regulating alternative splicing of MNK2

PROVIDER: PRJNA1027849 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR26384173_1.fastq.gz	Fastqsanger.gz
	SRR26384173_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 3 of 3

Similar Datasets

RBM25 depletion suppresses colon cancer progression through regulating alternative splicing of MNK2

Project description:To explore the molecular mechanism of RBM25 depletion in inhibiting colon cancer progression,we performed high-throughput mRNA sequencing (mRNA-seq) in HCT116 cells with RBM25 knockdown.

2025-06-21 | GSE245341 | 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

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]

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. Herein, our work demonstrated that by exerting its binding capability, RBM25 may serve as a regulator of related RNA expressive levels and AS process to confer negative impacts on cardiac inflammation in cardiomyocytes. Our study provided preliminary evidence regarding the understanding of RBM25 in heart failure complicated by inflammation.

2023-10-05 | GSE209940 | 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_H9C2_RBM25_iRIP]

2023-10-05 | GSE209941 | GEO

Talaromyces marneffei suppresses macrophage inflammation by regulating host alternative splicing

Project description:Talaromyces marneffei suppresses macrophage inflammation by regulating host alternative splicing

| PRJNA824858 | ENA

DIS3 dysfunction suppresses altered alternative splicing in cells with the depletion of U2 snRNP component

Project description:DIS3 dysfunction suppresses altered alternative splicing in cells with the depletion of U2 snRNP component

| PRJNA648742 | ENA

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

Kdm6a suppresses the alternative activation of macrophages

Project description:Kdm6a suppresses the alternative activation of macrophages

| PRJNA644806 | ENA

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

Exploring the binding sites of RBM25 by RIP-seq in the inner ear organoids.

Project description:Purpose: The goals of this study are to ecavate the binding sites of RNA-binding protein RBM25 during inner ear aging. Using the inn er organoids as model, RBM25 incubate with RNA from organois.Then transcriptome profiling (RNA-seq) was performed to analyze the binding genes and sites.

2025-06-02 | GSE273965 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data