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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]

ABSTRACT: 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.

ORGANISM(S): Rattus

PROVIDER: GSE209941 | GEO | 2023/10/05

REPOSITORIES: GEO

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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

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

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

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

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

2015-10-28 | GSE66737 | GEO

The splicing factor RBM25 controls MYC activity in Acute Myeloid Leukemia

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

| PRJNA454907 | ENA

RBM-5 modulates U2AF large subunit-dependent alternative splicing in C. elegans

Project description:A key step in pre-mRNA splicing is the recognition of 3’ splicing sites by the U2AF large and small subunits, a process regulated by numerous trans-acting splicing factors. How these trans-acting factors interact with U2AF in vivo is unclear. From a screen for suppressors of the temperature-sensitive (ts) lethality of the C. elegans U2AF large subunit gene uaf-1(n4588) mutants, we identified mutations in the RNA binding motif gene rbm-5, a homolog of the tumor suppressor RBM5. rbm-5 mutations can suppress uaf-1(n4588) ts-lethality by loss of function and neuronal expression of rbm-5 was sufficient to rescue the suppression. Transcriptome analyses indicate that uaf-1(n4588) affected the expression of numerous genes and rbm-5 mutations can partially reverse the abnormal gene expression to levels similar to that of wild type. Though rbm-5 mutations did not obviously affect alternative splicing per se, they can suppress or enhance, in a gene-specific manner, the altered splicing of genes in uaf-1(n4588) mutants. Specifically, the recognition of a weak 3’ splice site was more susceptible to the effect of rbm-5. Our findings provide novel in vivo evidence that RBM-5 can modulate UAF-1-dependent RNA splicing and suggest that RBM5 might interact with U2AF large subunit to affect tumor formation.

2018-06-13 | GSE115695 | GEO

Dysregulation of p53-RBM25-mediated circAMOTL1L biogenesis contributes to prostate cancer progression

Project description:Dysregulation of p53-RBM25-mediated circAMOTL1L biogenesis contributes to prostate cancer progression

| PRJNA450385 | ENA

RNA sequence in alveolar macrophage of mice treated with HDM or Combined with PR8

Project description:To research the different expressive genes in alveolar macrophage during asthma excerbation, we build asthma excerbation mice use HDM combined with PR8. we sepreated and collected the alveolar macrophages in BALF of mice then test the RNA expression. in this data, LysMCre Cul5fl/fl mice also challenaged with HDM combined with PR8 to compared the different expressive genes in alveolar macrophage.

2023-11-05 | GSE246601 | GEO

Gene expression profiling of pancreatic epithelial cells in response to tissue contextual changes

Project description:To understand the molecular process associated with tissue morphogenesis of pancreatic epithelial cells, we profiled the transcriptomes of normal or malignant pancreatic organoids formed in three-dimenstional reconsitututed basement membrance (rBM). Cell monolayers cultured on rBM-coated culture plastics were used as controls. HPDE (immortalized pancreatic epithelial cells) and PANC-1 cells (pancreatic cancer cells) were seeded on reconstituted basement membrane (rBM)-coated culture plastics or cultured on top of three-dimensional (3D) rBM gels. Total RNA samples were collected from cell monolayers or 3D cell clusters (formed at day 2), pancreatic tubules or tumor spheroids (formed at day 6) in the rBM culture, followed by global gene expression profiling.

2012-11-15 | E-GEOD-42270 | biostudies-arrayexpress

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