| 2008 |
RBM25 binds directly to a CGGGCA sequence within exon 2 of BCL-x pre-mRNA and stimulates proapoptotic Bcl-xS 5' splice site selection in a dose-dependent manner; mutation of the CGGGCA element abolished Bcl-xS isoform promotion. RBM25 binding promotes recruitment of U1 snRNP to the weak 5' splice site and is not required when a strong consensus 5' ss is present. |
RNA binding assay, site-directed mutagenesis of exonic element, U1 snRNP recruitment assay, dose-dependent overexpression/depletion experiments |
Molecular and cellular biology |
High |
18663000
|
| 2008 |
RBM25 selectively associates with the human homolog of yeast U1 snRNP-associated factor hLuc7A, suggesting RBM25 stabilizes pre-mRNA-U1 snRNP interactions through hLuc7A to activate weak 5' splice site selection. |
Co-immunoprecipitation |
Molecular and cellular biology |
Medium |
18663000
|
| 2011 |
RBM25 (together with LUC7L3) mediates truncation of SCN5A (cardiac sodium channel) mRNA in Jurkat cells and human embryonic stem cell-derived cardiomyocytes; overexpression of either splicing factor increased truncated SCN5A mRNA and decreased full-length SCN5A transcript and Na+ channel current by ~91%. |
Gene array, overexpression in Jurkat cells and hESC-derived cardiomyocytes, mRNA/protein quantification, electrophysiology |
Circulation |
High |
21859973
|
| 2012 |
Angiotensin II and hypoxia (signals common to heart failure) increase LUC7L3 and RBM25 levels, resulting in increased RBM25 binding to SCN5A mRNA, increased SCN5A splice variants, and decreased full-length SCN5A mRNA, protein, and Na+ current. |
RIP (RNA immunoprecipitation), qPCR, Western blot, electrophysiology in cardiac cells treated with angiotensin II/hypoxia |
Trends in cardiovascular medicine |
Medium |
22939879
|
| 2013 |
Crystal structure of the RBM25 PWI domain and its flanking basic region revealed a conserved four-helix bundle; the flanking basic region forms two alpha-helices that associate with helix H4 of the PWI domain, enlarging the nucleic-acid-binding platform. Structure-guided mutagenesis identified a positively charged nucleic-acid-binding surface distinct from SRm160 PWI domain. The PWI domain is required in vivo for promotion of pro-apoptotic Bcl-xS isoform expression. |
X-ray crystallography, structure-guided mutagenesis, in vivo splicing reporter assay |
The Biochemical journal |
High |
23190262
|
| 2017 |
RBM25 is required for viability of multiple human cell lines and globally promotes inclusion of alternatively spliced exons across the human transcriptome. Proteomic analysis showed RBM25 interacts with components of the early spliceosome and regulators of alternative splicing. RBM25 is mono-methylated at lysine 77 (RBM25-K77me1); the region spanning K77 binds SRSF2 (crucial for exon definition) with high affinity only when K77 is unmethylated, providing a mechanism by which lysine methylation regulates RBM25 activity. |
shRNA knockdown viability assays, transcriptome-wide RNA-seq splicing analysis, quantitative mass spectrometry (proteomics), affinity binding assay for SRSF2 interaction with methylated vs. unmethylated peptides |
The Journal of biological chemistry |
High |
28655759
|
| 2019 |
RBM25 controls alternative splicing of BCL-X (promoting pro-apoptotic Bcl-xS) and BIN1 (MYC inhibitor) in AML cells; knockdown of RBM25 promotes proliferation, decreases apoptosis, and increases MYC activity. RBM25 acts as a tumor suppressor in AML and was identified via in vivo shRNA screen in a mouse model of CEBPA-mutant AML. |
In vivo shRNA screen, splicing analysis by RT-PCR, knockdown in multiple human leukemic cell lines with proliferation/apoptosis assays |
Nature communications |
High |
30635567
|
| 2018 |
RBM25 binds directly to circAMOTL1L RNA and induces its biogenesis; p53 activates RBM25 gene transcription, thereby regulating EMT via the circAMOTL1L-miR-193a-5p-Pcdha pathway in prostate cancer cells. |
RNA immunoprecipitation (RIP), p53 ChIP/reporter assay, circRNA overexpression/knockdown with EMT marker analysis, in vivo xenograft |
Oncogene |
Medium |
30531834
|
| 2023 |
RBM25 directly and specifically binds to GQ-2, an RNA G-quadruplex (rG4) of BCL-x pre-mRNA located near the alternative 5' splice site for Bcl-xS, through its RE (arginine-glutamate-rich) motif; this RBM25/rG4 interaction is required for Bcl-xS production. G4 ligands (PhenDC3, PhenDH8, PhenDH9) that enhance RBM25 binding to GQ-2 promote Bcl-xS isoform and apoptosis. |
RNA binding assays (EMSA/pull-down with rG4), domain mutagenesis (RE motif), splicing reporter assays, ligand screening with G4-stabilizing compounds |
Nucleic acids research |
High |
37811881
|
| 2023 |
RBM25 directly binds to ACLY pre-mRNA and mediates skipping of exon 14, generating two distinct Acly isoforms (Acly L and Acly S). In proinflammatory macrophages, Acly L (but not Acly S) undergoes protein lactylation at K918/K995, affecting metabolic substrate affinity. RBM25 deficiency shifts splicing toward Acly S, enhancing glycolysis and acetyl-CoA production for epigenetic remodeling and macrophage overactivation. Macrophage-specific RBM25 knockout leads to spontaneous arthritis in mice. |
RBM25 KO mice (conditional, macrophage-specific), multiomics (RNA-seq, proteomics, ChIP-seq), RIP, in vivo arthritis model, Acly inhibitor rescue |
Cellular & molecular immunology |
High |
39251781
|
| 2023 |
METTL3-mediated m6A methylation of RBM25 mRNA stabilizes RBM25 mRNA and maintains its expression in multiple myeloma cells; metformin reduces METTL3 activity, thereby decreasing m6A on RBM25 mRNA and reducing RBM25 mRNA stability and expression. RBM25 knockdown reverses METTL3-overexpression-driven MM cell malignancy. |
MeRIP (m6A immunoprecipitation), METTL3 knockdown/overexpression, mRNA stability assay, rescue experiments, in vivo xenograft |
Cell cycle |
Medium |
36762777
|
| 2023 |
RBM25 is localized to the nucleus in cardiomyocytes both in vitro and in vivo under hypoxia/ischemic conditions; ER stress stimulates RBM25 upregulation and promotes apoptosis via the CHOP signaling pathway. RBM25 knockdown blocks CHOP activation and reduces apoptosis, improving cardiac function. |
Immunofluorescence (nuclear localization), Western blot, ER-tracker, siRNA knockdown in OGD model and in vivo ischemic HF rat model, TUNEL, echocardiography |
Cell stress & chaperones |
Medium |
37736860
|
| 2023 |
RBM25 binds to a poly-G-rich region in exon 14a of MNK2 pre-mRNA (shown by iRIP-seq and validated by RT-PCR), inhibiting the proximal 3' splice site and producing the oncogenic short isoform MNK2b. RBM25 depletion shifts splicing to the MNK2a isoform; re-expression of MNK2b or ASO-blocking of the alternative splice site rescues the tumor suppression from RBM25 knockdown. |
iRIP-seq, RNA-seq, RT-PCR splicing assays, shRNA knockdown, ASO rescue, in vitro and in vivo tumor growth assays |
Science China. Life sciences |
High |
39110401
|
| 2023 |
RBM25 binds to Slc38a9, Csf1, and Coro6 mRNAs (identified by iRIP-seq) and regulates their alternative splicing in H9c2 cardiomyocytes, linking RBM25 to cardiac inflammatory responses. |
iRIP-seq, RNA-seq, RT-qPCR validation |
PeerJ |
Medium |
37953772
|
| 2024 |
dCasRx fused to RBM25 (dCasRx-RBM25) functions as a potent activator of exon inclusion; it efficiently activates ~90% of targeted endogenous alternative exons with high on-target specificity, identified through screening >300 dCasRx-splicing factor fusion proteins. |
CRISPR-dCasRx fusion protein screen with splicing reporters, endogenous alternative exon activation assays, gRNA array combinatorial targeting, RNA-seq specificity analysis |
Molecular cell |
High |
38917795
|
| 2025 |
RBM25 induces exon 16 skipping in MAP4K4 pre-mRNA (confirmed by qPCR), generating a truncated isoform predicted to enhance MAP3K1 binding and activate the p38 MAPK/ERK pathway; RBM25 overexpression exacerbates post-infarction heart failure via this MAP4K4 splicing-dependent MAPK activation, while RBM25 knockdown is cardioprotective. P38 MAPK inhibitor (SB203580) attenuated RBM25-mediated injury. |
Lentiviral OE/KD in rat LAD ligation model, qPCR, echocardiography, Western blot for MAPK phosphorylation, TUNEL, pharmacological rescue with SB203580 |
FASEB bioAdvances |
Medium |
41409803
|
| 2025 |
RBM25 promotes HBV replication by binding to cccDNA through its RE/RD and PWI domains, upregulating Yin Yang 1 (YY1) expression, which enhances acetylation of cccDNA-bound histones to promote HBV transcription. HBV core protein accumulation causes nuclear translocation of RBM25, while RBM25 overexpression promotes core protein degradation, establishing a reciprocal regulatory loop. |
ChIP on cccDNA, domain deletion/mutagenesis (RE/RD and PWI), RBM25 KD/OE in HBV-replicating and infected cell models and mouse hydrodynamic injection model, promoter activity assays, histone acetylation assays |
Virologica Sinica |
Medium |
40412480
|
| 2025 |
lnc-536 acts as a decoy for RBM25 in pulmonary artery smooth muscle cells; when lnc-536 is elevated, it sequesters RBM25 away from SFPQ (splicing factor proline/glutamine-rich), which in turn reduces SFPQ-HOXB13 mRNA interaction, decreasing HOXB13 expression and driving PASMC hyperproliferation. RBM25 knockdown increases SFPQ-HOXB13 mRNA interaction and attenuates PASMC proliferation. |
lncRNA pull-down, RNA immunoprecipitation (SFPQ antibody), RBM25 knockdown with proliferation assays, in vivo GapmeR antisense oligo in PAH rat models |
Arteriosclerosis, thrombosis, and vascular biology |
Medium |
40567228
|
| 2025 |
Rbm25 occupies promoters of pluripotency- and DNA methylation-related genes in embryonic stem cells and directly regulates their transcription; deletion or depletion of Rbm25 impairs ESC self-renewal and promotes transition to 2-cell-like cells (2CLCs) by altering the epigenetic state of ESCs, revealing a transcriptional (non-splicing) regulatory role. |
ChIP-seq (promoter occupancy), Rbm25 knockout/knockdown in ESCs, RNA-seq, 2CLC reporter assay |
Stem cell reports |
Medium |
41455468
|
| 2023 |
Rbm25 knockdown in vitro and in vivo accelerates clonal expansion of Tet2-knockout hematopoietic stem cells, placing Rbm25 as a downstream mediator of Tet2-loss-induced heterogeneous preleukemic clonal expansion. |
Genetic barcoding in conditional Tet2 KO mice, shRNA knockdown of Rbm25 in vitro and in vivo, hematopoietic colony assays |
Blood |
Medium |
36947858
|
| 2026 |
Conditional (homozygous) knockout of Rbm25 in mice causes collapse of multiple hematopoietic lineages including long-term hematopoietic stem cells, demonstrating that Rbm25 is essential for normal murine hematopoiesis. Mono-allelic deletion does not impair HSC self-renewal even under proliferative stress, showing Rbm25 is haplosufficient. |
Conditional knockout mouse model, bone marrow transplantation, flow cytometry of hematopoietic lineages |
Experimental cell research |
High |
41819468
|