Affinage

RBM25

RNA-binding protein 25 · UniProt P49756

Round 2 corrected
Length
843 aa
Mass
100.2 kDa
Annotated
2026-04-28
59 papers in source corpus 21 papers cited in narrative 21 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RBM25 is a nuclear RNA-binding protein that functions as an essential global splicing regulator, predominantly promoting exon inclusion and alternative 5′ splice site selection, while also acting as a direct transcriptional regulator at gene promoters in stem cells. It binds specific RNA elements—including a CGGGCA exonic motif, poly-G-rich sequences, and RNA G-quadruplexes—through its RRM, RE/RD, and PWI domains, recruiting U1 snRNP via hLuc7A to weak splice sites; its interaction with the exon-definition factor SRSF2 is regulated by mono-methylation at lysine 77, which abrogates binding (PMID:18663000, PMID:28655759, PMID:37811881). RBM25 controls alternative splicing of functionally critical transcripts including BCL-X (promoting pro-apoptotic Bcl-xS), BIN1, SCN5A, ACLY, MNK2, and MAP4K4, linking it to apoptosis, cardiac electrophysiology, macrophage inflammation, and cancer biology (PMID:30635567, PMID:21859973, PMID:39251781, PMID:39110401, PMID:41409803). Homozygous loss of Rbm25 causes collapse of hematopoiesis in mice and spontaneous multi-organ inflammation when deleted in macrophages, establishing it as essential for tissue homeostasis (PMID:41819468, PMID:39251781).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2008 High

    The question of how the weak pro-apoptotic Bcl-xS 5′ splice site is selected was answered by showing that RBM25 binds a CGGGCA exonic element in BCL-X pre-mRNA and recruits U1 snRNP via hLuc7A, establishing RBM25 as a splice-site-selector for apoptotic isoform choice.

    Evidence RNA binding assays, splice reporter mutagenesis, RNAi, and Co-IP with hLuc7A in human cells

    PMID:18663000

    Open questions at the time
    • Genome-wide target repertoire unknown
    • Structural basis of CGGGCA recognition unresolved
    • In vivo relevance not tested in animal models
  2. 2011 High

    Whether RBM25 splicing activity had pathophysiological relevance beyond apoptosis was addressed by demonstrating that RBM25 upregulation in human heart failure drives aberrant SCN5A truncation, reducing sodium channel current by ~91%, linking RBM25 to cardiac arrhythmogenic remodeling.

    Evidence Gene profiling of failing hearts, overexpression in ESC-derived cardiomyocytes and Jurkat cells, patch-clamp electrophysiology

    PMID:21859973 PMID:22939879

    Open questions at the time
    • No loss-of-function in cardiomyocytes to confirm necessity
    • Direct RBM25 binding site on SCN5A not mapped at nucleotide resolution
  3. 2013 High

    The structural basis for RBM25 nucleic acid engagement was resolved by crystallography of the PWI domain, revealing a four-helix bundle with a flanking basic region that creates an extended binding surface required for Bcl-xS splicing in vivo.

    Evidence X-ray crystallography of the PWI domain, structure-guided mutagenesis, functional splicing assay

    PMID:23190262

    Open questions at the time
    • Structure of RRM and RE/RD domains not determined
    • How PWI domain cooperates with other domains for target selectivity unknown
  4. 2017 High

    Whether RBM25 was a target-specific or genome-wide splicing factor was resolved by transcriptome-wide analysis showing it regulates hundreds of alternative exons (predominantly promoting inclusion) and is essential for cell viability; the discovery that K77 mono-methylation controls SRSF2 interaction revealed a post-translational regulatory switch for RBM25 activity.

    Evidence shRNA knockdown viability assays, RNA-seq, AP-MS proteomics, mass spectrometry for K77me1, in vitro SRSF2 binding assays

    PMID:28655759

    Open questions at the time
    • Identity of the K77 methyltransferase unknown
    • Whether K77me1 is dynamically regulated under physiological conditions untested
    • Structural basis of K77-SRSF2 interaction unresolved
  5. 2019 High

    The question of whether RBM25 functions as a tumor suppressor through splicing was answered in acute myeloid leukemia, where RBM25 controls pro-apoptotic BCL-X and BIN1 splicing to restrain MYC-driven proliferation.

    Evidence In vivo shRNA screen in mouse AML model, shRNA in human leukemic lines, RNA-seq splicing analysis

    PMID:30635567

    Open questions at the time
    • Whether RBM25 loss is a driver or passenger event in human AML not established
    • Mechanism of BIN1 splice regulation by RBM25 not dissected at the RNA element level
  6. 2023 High

    How RBM25 recognizes structured RNA was clarified by demonstrating that its RE motif directly and specifically binds an RNA G-quadruplex near the Bcl-xS splice site, defining a new rG4-binding modality that can be pharmacologically enhanced by G4-stabilizing ligands.

    Evidence EMSA, pull-down, RE motif mutagenesis, G4-ligand treatment, splicing reporter and apoptosis assays

    PMID:37811881

    Open questions at the time
    • Genome-wide prevalence of rG4-dependent RBM25 targets unknown
    • Whether the RE motif binds other RNA secondary structures not tested
  7. 2023 High

    A critical in vivo role for RBM25 in immune homeostasis was established: macrophage-specific deletion causes spontaneous arthritis via ACLY exon 14 mis-splicing, generating an isoform (Acly L) susceptible to protein lactylation that drives hyperacetylation and proinflammatory gene expression—a phenotype reversible by Acly inhibition.

    Evidence Conditional KO mice, RNA-seq/ATAC-seq/ChIP-seq, RIP for ACLY pre-mRNA binding, lactylation proteomics, pharmacological rescue

    PMID:39251781

    Open questions at the time
    • Whether this mechanism operates in human macrophages not demonstrated
    • How RBM25 selects ACLY exon 14 over other substrates in macrophages unknown
  8. 2023 Medium

    RBM25 downregulation was placed downstream of Tet2 loss in hematopoietic stem cells, showing that Rbm25 expression variability drives heterogeneous preleukemic clonal expansion, connecting epigenetic and splicing layers in clonal hematopoiesis.

    Evidence Genetic barcoding in inducible Tet2 KO mouse model, shRNA Rbm25 knockdown, in vivo HSC expansion assays

    PMID:36947858

    Open questions at the time
    • Direct mechanistic link between Tet2 and Rbm25 expression not delineated
    • Relevant RBM25 splicing targets in Tet2-null HSCs not identified
  9. 2024 High

    RBM25's exon-inclusion activity was shown to be context-independent and generalizable when dCasRx-RBM25 fusions efficiently activated ~90% of targeted endogenous alternative exons with high specificity, confirming RBM25 as a potent modular exon-inclusion effector.

    Evidence Large-scale CRISPR-dCasRx fusion screen (>300 constructs), RNA-seq specificity analysis, multiplexed gRNA arrays

    PMID:38917795

    Open questions at the time
    • Whether dCasRx-RBM25 activity requires co-factors or is fully autonomous not resolved
    • Off-target effects in primary cells or in vivo not assessed
  10. 2024 High

    Beyond exon inclusion, RBM25 was shown to inhibit a proximal 3′ splice site in MNK2 by binding a poly-G region in exon 14a, promoting the oncogenic MNK2b isoform in colon cancer—demonstrating that RBM25 can also act as an exon-skipping factor depending on target context.

    Evidence RNA-seq, RIP, ASO-mediated splice site blocking, rescue with MNK2b re-expression, xenograft model

    PMID:39110401

    Open questions at the time
    • Rules governing whether RBM25 promotes inclusion versus inhibition at a given target not established
    • Whether poly-G recognition uses the same domains as CGGGCA or rG4 binding unknown
  11. 2025 Medium

    A transcriptional role for RBM25 was discovered: Rbm25 directly occupies promoters of pluripotency and DNA methylation genes in embryonic stem cells, controlling ESC identity and preventing transition to totipotent-like 2-cell-like cells, expanding RBM25 function beyond splicing.

    Evidence Conditional KO in ESCs, ChIP-seq for promoter occupancy, RNA-seq, 2CLC reporter assays

    PMID:41455468

    Open questions at the time
    • Mechanism of transcriptional activation (co-factor recruitment, chromatin remodeling) not defined
    • Whether transcriptional and splicing functions are separable or coordinated unknown
    • Relevance to human ESCs not tested
  12. 2025 Medium

    RBM25 was shown to bind HBV cccDNA directly through RE/RD and PWI domains, upregulating YY1 to enhance histone acetylation on cccDNA and promote viral transcription, revealing a chromatin-level regulatory role in viral infection.

    Evidence ChIP for cccDNA binding, domain mutagenesis, HBV-replicating cell models, hydrodynamic injection mouse model

    PMID:40412480

    Open questions at the time
    • Whether cccDNA binding reflects a broader dsDNA-binding capacity of RBM25 not assessed
    • Single lab finding awaiting independent replication
  13. 2026 High

    The essential in vivo requirement for RBM25 was definitively demonstrated when conditional homozygous knockout caused complete hematopoietic collapse across multiple lineages including long-term HSCs, while haplosufficiency was confirmed by normal function with mono-allelic deletion.

    Evidence Conditional KO mice, bone marrow transplantation, flow cytometry, proliferative stress assays

    PMID:41819468

    Open questions at the time
    • Which specific splicing or transcriptional targets mediate hematopoietic collapse not identified
    • Whether collapse is cell-autonomous in all lineages or partly non-cell-autonomous unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the identity of the K77 methyltransferase regulating SRSF2 interaction, the structural basis for how RBM25 domains coordinate to select targets for inclusion versus skipping, and whether its transcriptional and splicing functions are mechanistically coupled or independent.
  • K77 methyltransferase identity unknown
  • No full-length RBM25 structure available
  • Rules governing inclusion vs. skipping outcome at different targets undefined
  • Relationship between transcriptional and splicing functions not delineated

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 6 GO:0140098 catalytic activity, acting on RNA 6 GO:0140110 transcription regulator activity 1
Localization
GO:0005634 nucleus 3 GO:0005654 nucleoplasm 2
Pathway
R-HSA-8953854 Metabolism of RNA 6 R-HSA-1643685 Disease 5 R-HSA-5357801 Programmed Cell Death 3 R-HSA-168256 Immune System 1 R-HSA-74160 Gene expression (Transcription) 1

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2008 RBM25 functions as a splicing factor that promotes pro-apoptotic Bcl-x(S) 5' splice site selection in a dose-dependent manner. RBM25 directly binds a CGGGCA exonic element in BCL-x pre-mRNA exon 2; mutation of this element abolishes Bcl-x(S) isoform production. RBM25 promotes recruitment of U1 snRNP to the weak Bcl-x(S) 5' splice site, and specifically associates with the U1 snRNP-associated factor hLuc7A. RNA binding assays, splice site reporter mutagenesis, RNAi depletion, Co-IP with hLuc7A, U1 snRNP recruitment assay Molecular and cellular biology High 18663000
2011 RBM25 and LUC7L3 are upregulated in human heart failure and together mediate aberrant truncation of SCN5A (cardiac sodium channel) mRNA. Overexpression of either factor in Jurkat cells and human embryonic stem cell-derived cardiomyocytes increases truncated SCN5A mRNA while decreasing full-length transcript, reducing Na+ channel current by ~91%. Gene array profiling, overexpression in cell lines and ESC-derived cardiomyocytes, RT-PCR for splice variants, patch-clamp electrophysiology Circulation High 21859973
2012 In heart failure, angiotensin II and hypoxia signals increase RBM25 expression, leading to increased binding of RBM25 to SCN5A mRNA, increased SCN5A splice variant production, decreased full-length SCN5A mRNA and protein, and decreased Na+ current, linking upstream HF signals to RBM25-mediated splicing dysregulation. RIP (RNA immunoprecipitation), RT-PCR, Western blot, patch clamp, cell treatment with angiotensin II and hypoxia Trends in cardiovascular medicine Medium 22939879
2013 Crystal structure of the human RBM25 PWI domain and its flanking basic region was determined. The PWI domain comprises a conserved four-helix bundle; the flanking basic region forms two α-helices that associate with helix H4 of the PWI domain, creating an enlarged nucleic-acid-binding platform. Structure-guided mutagenesis identified a positively charged nucleic-acid-binding surface distinct from that in SRm160. The PWI domain was shown to be required in vivo for RBM25-mediated promotion of pro-apoptotic Bcl-xS isoform expression. X-ray crystallography, structure-guided mutagenesis, functional splicing assay in cells The Biochemical journal High 23190262
2017 RBM25 is an essential global splicing factor required for viability of multiple human cell lines. Transcriptome-wide analysis showed RBM25 regulates a large fraction of alternatively spliced exons genome-wide, predominantly promoting exon inclusion. Proteomic analysis identified RBM25 interactions with components of the early spliceosome and alternative splicing regulators. RBM25 is mono-methylated at lysine 77 (K77me1), and the unmethylated K77-containing region binds with high affinity to SRSF2 (a key exon definition factor), whereas K77me1 abrogates this interaction, revealing a methylation-dependent regulatory mechanism. shRNA knockdown cell viability, RNA-seq (transcriptome-wide splicing analysis), AP-MS proteomics, quantitative mass spectrometry for K77me1, in vitro binding assays with SRSF2, mutagenesis The Journal of biological chemistry High 28655759
2018 p53 directly activates the RBM25 gene transcriptionally, and RBM25 protein binds directly to circAMOTL1L (a circular RNA derived from the AMOTL1 locus) and induces its biogenesis, thereby linking the p53/RBM25 axis to circRNA production and EMT regulation in prostate cancer. ChIP for p53 binding at RBM25 promoter, RBM25 knockdown/overexpression, RNA pull-down for RBM25-circAMOTL1L interaction, circRNA biogenesis assays Oncogene Medium 30531834
2019 In acute myeloid leukemia, RBM25 acts as a tumor suppressor by controlling splicing of BCL-X (promoting pro-apoptotic Bcl-xS) and BIN1 (a MYC inhibitor). RBM25 knockdown promotes proliferation and decreases apoptosis in multiple human leukemic cell lines, and low RBM25 levels are associated with high MYC activity. In vivo shRNA screen in mouse AML model, shRNA knockdown in human leukemic cell lines, RNA-seq splicing analysis, proliferation and apoptosis assays Nature communications High 30635567
2023 RBM25 directly and specifically binds GQ-2, an RNA G-quadruplex (rG4) located near the alternative Bcl-xS 5' splice site in BCL-x pre-mRNA. This interaction depends on the RE (arginine-glutamate-rich) motif of RBM25, defining a new rG4-interacting domain. The RBM25/rG4 interaction is required for Bcl-xS production, and G4 ligands that stabilize the rG4 enhance RBM25 binding and promote Bcl-xS isoform expression and apoptosis. In vitro binding assays (EMSA, pull-down), mutagenesis of RBM25 RE motif, G4-ligand treatment, splicing reporter assays, apoptosis assays Nucleic acids research High 37811881
2023 RBM25 deficiency in macrophages leads to increased proinflammatory gene expression coupled with histone acetylation changes (H3K9ac, H3K27ac) and HIF-1α activity. Mechanistically, RBM25 directly binds ACLY pre-mRNA and mediates skipping of exon 14, generating two distinct isoforms: Acly Long (Acly L) and Acly Short (Acly S). In proinflammatory macrophages, Acly L undergoes protein lactylation on K918/K995 whereas Acly S does not, affecting metabolic substrate affinity and acetyl-CoA production. Macrophage-specific RBM25 deletion causes spontaneous arthritis and multi-organ inflammation in mice, reversible by Acly inhibition. Conditional knockout mice, multiomics (RNA-seq, ATAC-seq, ChIP-seq), RIP for RBM25-ACLY pre-mRNA binding, splicing reporter assays, metabolic assays, lactylation proteomics Cellular & molecular immunology High 39251781
2023 METTL3-mediated m6A methylation stabilizes RBM25 mRNA; metformin reduces METTL3 activity, decreasing m6A on RBM25 mRNA and reducing RBM25 mRNA stability and expression in multiple myeloma cells, contributing to anti-proliferative effects. MeRIP (m6A RNA immunoprecipitation), METTL3 knockdown/overexpression, mRNA stability assays, rescue experiments, xenograft mouse model Cell cycle Medium 36762777
2023 RBM25 binds to and regulates alternative splicing of Slc38a9, Csf1, and Coro6 in H9c2 cardiomyoblasts, as identified by iRIP-seq; RBM25 overexpression upregulates genes involved in inflammatory response and mediates alternative splicing of apoptosis- and inflammation-related genes. RNA-seq, iRIP-seq, RT-qPCR validation, overexpression in H9c2 cells PeerJ Medium 37953772
2023 RBM25 is upregulated in ischemic heart failure and hypoxia-injured cardiomyocytes, localizes to the nucleus, and promotes cardiomyocyte apoptosis through upregulation of ER stress and the CHOP signaling pathway. Knockdown of RBM25 ameliorates apoptosis and improves cardiac function in a rat ischemic HF model. In vivo rat ischemic HF model, OGD in vitro model, Western blot, immunofluorescence, ER-tracker staining, echocardiography, RBM25 knockdown/overexpression Cell stress & chaperones Medium 37736860
2024 dCasRx fused to RBM25 (dCasRx-RBM25) acts as a potent, specific activator of endogenous alternative exon splicing when targeted by guide RNAs, efficiently activating ~90% of targeted endogenous alternative exons with high on-target specificity and enabling multiplexed combinatorial exon activation/repression. CRISPR-dCasRx fusion screen (>300 constructs), splicing reporter assays, endogenous gene targeting, gRNA array combinatorial experiments, RNA-seq specificity analysis Molecular cell High 38917795
2024 RBM25 regulates alternative splicing of MNK2 in colon cancer by binding a poly-G-rich region in exon 14a, inhibiting selection of the proximal 3' splice site and promoting production of the oncogenic short isoform MNK2b over the tumor-suppressive MNK2a. RBM25 depletion shifts the balance toward MNK2a and suppresses colon cancer cell growth in vitro and in vivo. Transcriptome-wide RNA-seq, RIP for RBM25-MNK2 pre-mRNA binding, ASO blocking of splice site, MNK2b re-expression rescue, xenograft mouse model Science China. Life sciences High 39110401
2025 RBM25 promotes HBV replication by binding to cccDNA through its RE/RD and PWI domains, upregulating Yin Yang 1 (YY1) expression, which enhances histone acetylation on cccDNA, thereby promoting HBV transcription. HBV core protein accumulation induces nuclear translocation of RBM25 and promotes its expression, while RBM25 overexpression promotes core protein degradation, revealing a reciprocal regulatory loop. RBM25 knockdown/overexpression in HBV-replicating cell models and hydrodynamic injection mouse model, ChIP for cccDNA binding, domain mutagenesis (RE/RD and PWI), YY1 expression analysis, histone acetylation assays Virologica Sinica Medium 40412480
2025 RBM25 induces exon 16 skipping in MAP4K4 pre-mRNA in a rat post-infarction heart failure model, generating a truncated MAP4K4 isoform that activates the p38 MAPK signaling pathway. RBM25 overexpression exacerbates myocardial injury and apoptosis, while knockdown is protective; p38 MAPK inhibition attenuates RBM25-mediated myocardial injury. LAD ligation rat HF model, lentiviral RBM25 OE/shRNA, qPCR for MAP4K4 splice variants, echocardiography, TUNEL, Western blot for MAPK pathway components, pharmacological p38 inhibition/activation rescue FASEB bioAdvances Medium 41409803
2025 In pulmonary artery smooth muscle cells, lncRNA-536 acts as a decoy for RBM25, sequestering it and preventing RBM25 from binding SFPQ (a transcriptional regulator). When RBM25 is free (lnc-536 low), it sequesters SFPQ, reducing SFPQ-HOXB13 mRNA interactions and leading to decreased HOXB13 expression and smooth muscle hyperproliferation. RBM25 knockdown reverses SFPQ-HOXB13 interactions and attenuates PASMC proliferation. RNA pull-down for lnc-536/RBM25 interaction, RNA-IP with SFPQ antibody showing direct RBM25-SFPQ interaction, knockdown/overexpression of lnc-536 and RBM25, in vivo GapmeR injection in pulmonary hypertension rat models Arteriosclerosis, thrombosis, and vascular biology Medium 40567228
2025 Rbm25 occupies promoters of pluripotency genes and DNA methylation-related genes in embryonic stem cells and directly regulates their transcription, thereby governing ESC identity and epigenetic state. Loss of Rbm25 impairs ESC self-renewal and differentiation while promoting transition toward totipotent-like 2-cell-like cells (2CLCs). Rbm25 conditional knockout/depletion in ESCs, ChIP-seq for Rbm25 promoter occupancy, RNA-seq, 2CLC reporter assays, differentiation assays Stem cell reports Medium 41455468
2026 Conditional homozygous knockout of Rbm25 in mice causes collapse of hematopoiesis affecting multiple lineages including long-term hematopoietic stem cells and embryonic stem cells, demonstrating that RBM25 is essential for normal hematopoietic maintenance. Mono-allelic deletion is haplosufficient and does not impair HSC self-renewal or differentiation under steady-state or proliferative stress. Conditional knock-out mouse model, bone marrow transplantation, flow cytometry of hematopoietic lineages, proliferative stress assays Experimental cell research High 41819468
2023 Rbm25 knockdown accelerates expansion of Tet2-knockout hematopoietic stem cells in vitro and in vivo, demonstrating that variability in Rbm25 expression downstream of Tet2 loss drives heterogeneous preleukemic clonal expansion. Genetic barcoding of HSCs in inducible Tet2 KO mouse model, shRNA knockdown of Rbm25, in vitro and in vivo HSC expansion assays Blood Medium 36947858
2025 RBM25 exhibits low inherent RNA-binding specificity compared to high-specificity RBPs such as HNRNPC. RNA binding domain swap CLIP experiments between RBM25 and HNRNPC demonstrated that sequence specificity can be transferred between protein contexts, and low-specificity RBPs like RBM25 can functionally enhance the specificity of high-specificity RBPs by occupying non-target sites. High-throughput sequencing of CLIP datasets, domain swap CLIP experiments, quantitative specificity metrics (inherent specificity and mutational sensitivity) bioRxivpreprint Low bio_10.1101_2025.03.28.646018

Source papers

Stage 0 corpus · 59 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1995 Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease. Nature 3346 7596406
2006 Global, in vivo, and site-specific phosphorylation dynamics in signaling networks. Cell 2861 17081983
2012 Insights into RNA biology from an atlas of mammalian mRNA-binding proteins. Cell 1718 22658674
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2006 A probability-based approach for high-throughput protein phosphorylation analysis and site localization. Nature biotechnology 1336 16964243
2004 Large-scale characterization of HeLa cell nuclear phosphoproteins. Proceedings of the National Academy of Sciences of the United States of America 1159 15302935
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
2012 The mRNA-bound proteome and its global occupancy profile on protein-coding transcripts. Molecular cell 973 22681889
2020 A reference map of the human binary protein interactome. Nature 849 32296183
2008 Global analysis of host-pathogen interactions that regulate early-stage HIV-1 replication. Cell 787 18854154
2003 Complete sequencing and characterization of 21,243 full-length human cDNAs. Nature genetics 754 14702039
2007 Large-scale mapping of human protein-protein interactions by mass spectrometry. Molecular systems biology 733 17353931
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2012 A census of human soluble protein complexes. Cell 689 22939629
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2018 High-Density Proximity Mapping Reveals the Subcellular Organization of mRNA-Associated Granules and Bodies. Molecular cell 580 29395067
2011 The Brd4 extraterminal domain confers transcription activation independent of pTEFb by recruiting multiple proteins, including NSD3. Molecular and cellular biology 437 21555454
2022 OpenCell: Endogenous tagging for the cartography of human cellular organization. Science (New York, N.Y.) 432 35271311
2015 Panorama of ancient metazoan macromolecular complexes. Nature 407 26344197
2021 A proximity-dependent biotinylation map of a human cell. Nature 339 34079125
2012 Dynamic protein-protein interaction wiring of the human spliceosome. Molecular cell 318 22365833
2016 Identification of Zika Virus and Dengue Virus Dependency Factors using Functional Genomics. Cell reports 306 27342126
2019 Intrinsically Disordered Protein TEX264 Mediates ER-phagy. Molecular cell 296 31006538
2018 Enhancer Activity Requires CBP/P300 Bromodomain-Dependent Histone H3K27 Acetylation. Cell reports 274 30110629
2018 Mapping the Genetic Landscape of Human Cells. Cell 225 30033366
2013 PRP19 transforms into a sensor of RPA-ssDNA after DNA damage and drives ATR activation via a ubiquitin-mediated circuitry. Molecular cell 204 24332808
2020 Systems analysis of RhoGEF and RhoGAP regulatory proteins reveals spatially organized RAC1 signalling from integrin adhesions. Nature cell biology 194 32203420
2013 The protein interaction landscape of the human CMGC kinase group. Cell reports 174 23602568
2018 Dysregulation of p53-RBM25-mediated circAMOTL1L biogenesis contributes to prostate cancer progression through the circAMOTL1L-miR-193a-5p-Pcdha pathway. Oncogene 153 30531834
2008 Novel splicing factor RBM25 modulates Bcl-x pre-mRNA 5' splice site selection. Molecular and cellular biology 116 18663000
2011 Role of RBM25/LUC7L3 in abnormal cardiac sodium channel splicing regulation in human heart failure. Circulation 77 21859973
2019 The splicing factor RBM25 controls MYC activity in acute myeloid leukemia. Nature communications 54 30635567
2017 RBM25 is a global splicing factor promoting inclusion of alternatively spliced exons and is itself regulated by lysine mono-methylation. The Journal of biological chemistry 50 28655759
2023 Indole-3-Lactic Acid, a Tryptophan Metabolite of Lactiplantibacillus plantarum DPUL-S164, Improved Intestinal Barrier Damage by Activating AhR and Nrf2 Signaling Pathways. Journal of agricultural and food chemistry 36 37996788
2008 The FF domains of yeast U1 snRNP protein Prp40 mediate interactions with Luc7 and Snu71. BMC biochemistry 33 19014439
2023 Metformin attenuates multiple myeloma cell proliferation and encourages apoptosis by suppressing METTL3-mediated m6A methylation of THRAP3, RBM25, and USP4. Cell cycle (Georgetown, Tex.) 31 36762777
2017 A Genetic Screen for Pre-mRNA Splicing Mutants of Arabidopsis thaliana Identifies Putative U1 snRNP Components RBM25 and PRP39a. Genetics 26 28971960
2012 RBM25/LUC7L3 function in cardiac sodium channel splicing regulation of human heart failure. Trends in cardiovascular medicine 25 22939879
2017 Cdc7-Dbf4-mediated phosphorylation of HSP90-S164 stabilizes HSP90-HCLK2-MRN complex to enhance ATR/ATM signaling that overcomes replication stress in cancer. Scientific reports 22 29209046
2024 Efficient, specific, and combinatorial control of endogenous exon splicing with dCasRx-RBM25. Molecular cell 20 38917795
2024 RBM25 is required to restrain inflammation via ACLY RNA splicing-dependent metabolism rewiring. Cellular & molecular immunology 20 39251781
2023 Alternative splicing of BCL-x is controlled by RBM25 binding to a G-quadruplex in BCL-x pre-mRNA. Nucleic acids research 20 37811881
2017 RBM25 Mediates Abiotic Responses in Plants. Frontiers in plant science 20 28344583
2023 RBM25 regulates hypoxic cardiomyocyte apoptosis through CHOP-associated endoplasmic reticulum stress. Cell stress & chaperones 15 37736860
2013 Crystal structure and functional characterization of the human RBM25 PWI domain and its flanking basic region. The Biochemical journal 14 23190262
2017 Human procaspase-2 phosphorylation at both S139 and S164 is required for 14-3-3 binding. Biochemical and biophysical research communications 13 28943433
2023 RBM25 induces trophoblast epithelial-mesenchymal transition and preeclampsia disorder by enhancing the positive feedback loop between Grhl2 and RBM25. Experimental biology and medicine (Maywood, N.J.) 9 37728157
2023 RBM25 binds to and regulates alternative splicing levels of Slc38a9, Csf1, and Coro6 to affect immune and inflammatory processes in H9c2 cells. PeerJ 5 37953772
2024 RBM25 depletion suppresses the growth of colon cancer cells through regulating alternative splicing of MNK2. Science China. Life sciences 4 39110401
2023 RNA splicing factor Rbm25 underlies heterogeneous preleukemic clonal expansion in mice. Blood 3 36947858
2024 ZC3H13 may participate in the ferroptosis process of sepsis-induced cardiomyopathy by regulating the expression of Pnn and Rbm25. Gene 2 39284557
2025 LncRNA-536 and RNA-Binding Protein RBM25 Interactions in Pulmonary Artery Smooth Muscle Cells: Implications in Pulmonary Hypertension. Arteriosclerosis, thrombosis, and vascular biology 1 40567228
2025 RBM25 Regulates p38 MAPK Pathway Activation via Exon 16 Skipping of MAP4K4 in a Rat Model of Post-Infarction Heart Failure. FASEB bioAdvances 1 41409803
2024 LncRNA-536 and RNA Binding Protein RBM25 Interactions in Pulmonary Arterial Hypertension. bioRxiv : the preprint server for biology 1 39253448
2026 Loss of splicing factor RBM25 promotes the collapse of murine hematopoiesis. Experimental cell research 0 41819468
2025 Host factor RBM25 promotes HBV replication through Yin Yang 1-mediated cccDNA transcription. Virologica Sinica 0 40412480
2025 Rbm25 governs embryonic stem cell identity and fate through transcriptional regulation of pluripotency and epigenetic programs. Stem cell reports 0 41455468