{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Erkelenz S"],"funding":["European Joint Project on Rare Diseases","funders had no role in study design, data collection and analysis"],"pagination":["1-13"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11575738"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(1)"],"pubmed_abstract":["<i>Rbm3</i> (RNA-binding motif protein 3) is a stress responsive gene, which maintains cellular homeostasis and promotes survival upon various harmful cellular stimuli. Rbm3 protein shows conserved structural and molecular similarities to heterogeneous nuclear ribonucleoproteins (hnRNPs), which regulate all steps of the mRNA metabolism. Growing evidence is pointing towards a broader role of Rbm3 in various steps of gene expression. Here, we demonstrate that Rbm3 deficiency is linked to transcriptome-wide pre-mRNA splicing alterations, which can be reversed through Rbm3 co-expression from a cDNA. Using an MS2 tethering assay, we show that Rbm3 regulates splice site selection similar to other hnRNP proteins when recruited between two competing 5 ' splice sites. Furthermore, we show that the "],"journal":["RNA biology"],"pubmed_title":["Rbm3 deficiency leads to transcriptome-wide splicing alterations."],"pmcid":["PMC11575738"],"funding_grant_id":["RD20-113","ID 73111208 – SFB 829"],"pubmed_authors":["Grzonka M","Gyenis A","Erkelenz S","Hoeijmakers JHJ","Schaal H","Papadakis A"],"additional_accession":[]},"is_claimable":false,"name":"Rbm3 deficiency leads to transcriptome-wide splicing alterations.","description":"<i>Rbm3</i> (RNA-binding motif protein 3) is a stress responsive gene, which maintains cellular homeostasis and promotes survival upon various harmful cellular stimuli. Rbm3 protein shows conserved structural and molecular similarities to heterogeneous nuclear ribonucleoproteins (hnRNPs), which regulate all steps of the mRNA metabolism. Growing evidence is pointing towards a broader role of Rbm3 in various steps of gene expression. Here, we demonstrate that Rbm3 deficiency is linked to transcriptome-wide pre-mRNA splicing alterations, which can be reversed through Rbm3 co-expression from a cDNA. Using an MS2 tethering assay, we show that Rbm3 regulates splice site selection similar to other hnRNP proteins when recruited between two competing 5 ' splice sites. Furthermore, we show that the ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jan","modification":"2026-06-01T15:24:34.433Z","creation":"2025-04-06T10:13:52.17Z"},"accession":"S-EPMC11575738","cross_references":{"pubmed":["39387568"],"doi":["10.1080/15476286.2024.2413820"]}}