| 2014 |
RBM24 is sufficient to promote muscle-specific exon inclusion in nuclear extracts of non-muscle cells; binding of RBM24 to an intronic splicing enhancer (ISE) is essential and sufficient to overcome repression by an exonic splicing silencer (ESS) containing PTB and hnRNP A1/A2 binding sites. Introduction of ESS and ISE converted a constitutive exon into an RBM24-dependent alternative exon. |
In vitro splicing assays in nuclear extracts; recombinant protein; targeted inactivation in mice; exon reporter constructs |
Developmental Cell |
High |
25313962
|
| 2012 |
Rbm24 loss-of-function in zebrafish causes reduction in sarcomeric proteins, Z-disc abnormality, and diminished heart contractility, establishing a required role for Rbm24 in sarcomere assembly and cardiac function. |
Zebrafish loss-of-function; gene expression profiling; protein analysis |
Cardiovascular Research |
Medium |
22345307
|
| 2013 |
RBM24 binds to the 3'-UTR of p21 transcript via an AU/U-rich element and stabilizes p21 mRNA, increasing p21 half-life and protein levels. The RNA recognition motif (RRM) of RBM24 is required for this binding and p21 upregulation. |
mRNA stability assay; RBM24 overexpression/knockdown; RRM domain mutagenesis; RNA binding assay |
Journal of Biological Chemistry |
High |
24356969
|
| 2013 |
RBM24 binds to multiple regions in the p63 3'-UTR and destabilizes p63 transcript, decreasing p63 mRNA and protein levels. The 3'-UTR of p63 and the RNA-binding domain of RBM24 are both required for this regulatory interaction. |
RBM24 overexpression/knockdown; RNA binding assay; mRNA stability assay; domain deletion analysis |
Molecular Cancer Research |
Medium |
24375645
|
| 2018 |
Rbm24, a p53 target gene, regulates p53 mRNA translation by binding to p53 mRNA and interacting with translation initiation factor eIF4E, preventing eIF4E from binding to p53 mRNA and inhibiting assembly of the translation initiation complex. Rbm24-null mice die in utero with endocardial cushion defects partially rescued by p53 deficiency. |
Co-immunoprecipitation (RBM24–eIF4E interaction); RNA-binding assay; translation assay; Rbm24/p53 double-knockout mouse rescue |
Cell Death and Differentiation |
High |
29358667
|
| 2009 |
Rbm24 overexpression induces cell cycle arrest and promotes myogenic differentiation in C2C12 cells; knockdown delays differentiation and suppresses cell cycle arrest. Unlike Rbm38 (which binds p21 transcript), the p21-independent pathway of Rbm24 mediates this effect. |
RNA interference knockdown; overexpression in C2C12 cells; immunoprecipitation-RT-PCR |
Genes to Cells |
Medium |
19817877
|
| 2020 |
In zebrafish lens, Rbm24 binds broadly to lens-specific mRNAs via its RRM domain, interacts with cytoplasmic polyadenylation element-binding protein (Cpeb1b) and cytoplasmic poly(A)-binding protein (Pabpc1l) via its C-terminal region, and controls poly(A) tail length of crystallin mRNAs. Loss of Rbm24 shortens poly(A) tails of crystallin mRNAs and reduces their translation, impairing lens transparency. |
Zebrafish rbm24 loss-of-function; co-immunoprecipitation; poly(A) tail length assay; RRM domain functional analysis |
Proceedings of the National Academy of Sciences |
High |
32170011
|
| 2010 |
Xenopus Seb4/RBM24 expression is directly regulated by MyoD; a 0.65 kb RBM24 regulatory region containing E-boxes is activated by MyoD in reporter assays. Knockdown of Seb4 inhibits myogenic gene expression and myogenesis induced by MyoD. |
Hormone-inducible MyoD; RBM24 reporter construct injection; morpholino knockdown in Xenopus |
Mechanisms of Development |
Medium |
20338237
|
| 2014 |
Rbm24 protein expression is directly regulated by MyoD in vivo (ChIP assay in chick embryo); Rbm24 accumulates in MyoD-positive myoblasts and is required for somitic myogenic progenitor cells to differentiate into muscle cells. |
In vivo chromatin immunoprecipitation (ChIP); morpholino knockdown; immunofluorescence |
Mechanisms of Development |
Medium |
25217815
|
| 2016 |
Rbm24 regulates alternative splicing switch in ESC cardiac lineage differentiation; forced Rbm24 expression in ESCs dramatically induces cardiac specification and switches splicing of pluripotency genes including Tpm1, whose ESC/tissue-specific isoforms are functionally distinct and required for differentiation. |
Inducible mouse ESC line; genome-wide RNA-seq; forced expression; functional isoform comparison |
Stem Cells |
Medium |
26990106
|
| 2016 |
MicroRNA-222 targets Rbm24 mRNA; downregulation of Rbm24 by miR-222 results in defective exon inclusion in Coro6, Fxr1, and NACA muscle-specific transcripts. Reconstitution of Rbm24 in miR-222-overexpressing cells rescues muscle-specific splicing. |
RISC pulldown + RNA-seq; miR-222 overexpression; Rbm24 rescue experiment; splicing assays |
Cell Death & Disease |
Medium |
26844700
|
| 2016 |
RBM20 and RBM24 cooperatively promote expression of short ENH splice variants by binding the 5' intronic region of exon 11 of the enh gene, which contains an in-phase stop codon. |
Co-expression of RBM20 and RBM24; splicing reporter; RNA binding assay |
FEBS Letters |
Medium |
27289039
|
| 2017 |
Stk38 (serine/threonine kinase 38) is an endogenous binding partner of Rbm24 (identified by Co-IP/MS); Stk38 kinase activity-dependently regulates Rbm24 protein stability and phosphorylation in cardiomyocytes. Stk38 knockdown reduces Rbm24 protein levels and impairs sarcomere assembly. |
Co-immunoprecipitation coupled with mass spectrometry; kinase inhibitor/activator; Stk38 knockdown; sarcomere analysis |
Scientific Reports |
Medium |
28322254
|
| 2017 |
RBM24 functions as a cryptic intronic splicing enhancer by binding to an element (IVS20+13-29) downstream of the FD-associated 5' splice site mutation in IKBKAP and promotes U1 snRNP recognition specifically at the mutated (not wild-type) 5' splice site, explaining neuron-specific aberrant splicing in familial dysautonomia. |
Mammalian dual-color splicing reporter screen; RBP expression library screen; direct binding assay |
RNA |
Medium |
28592461
|
| 2018 |
RBM24 interacts with both the 5' and 3' terminal redundancy (TR) sequences of HBV 3.5-kb RNA via its RNA-binding domains. Interaction with 5' TR blocks 80S ribosome assembly on HBV pgRNA, inhibiting core protein translation; interaction with 3' TR enhances HBV RNA stability. |
RNA-binding domain interaction assays; 80S ribosome assembly assay; HBV transfection/infection cell model; RBM24 overexpression/knockdown |
Emerging Microbes & Infections |
Medium |
29760415
|
| 2019 |
RBM24 directly binds the lower bulge of the epsilon stem-loop of HBV pgRNA via RNP submotifs, and interacts with HBV polymerase (Pol) in an RNA-independent manner via its alanine-rich domain (ARD) and the Pol reverse transcriptase (RT) domain. RBM24 forms a Pol-RBM24-ε complex that mediates Pol-ε interaction and promotes pgRNA packaging. |
Co-immunoprecipitation; RNA binding assays; domain deletion mutants; pgRNA packaging efficiency assay |
Journal of Virology |
Medium |
30626666
|
| 2020 |
RBM24 protein binds Sox2 mRNA in mouse embryonic eye tissue (RNA immunoprecipitation) and directly binds the Sox2 mRNA 3'-UTR via AU-rich elements (EMSA). RBM24 elevates Sox2 mRNA half-life in an ARE-dependent manner. Loss of Rbm24 downregulates SOX2 and causes microphthalmia/anophthalmia. |
RNA immunoprecipitation (RIP) from mouse embryonic tissue; electrophoretic mobility shift assay (EMSA); mRNA half-life assay; CRISPR and morpholino knockdown in mouse and zebrafish |
Human Molecular Genetics |
High |
31814023
|
| 2018 |
Rbm24 displays cytoplasmic localization in lens, olfactory epithelium, and mechanosensory cells of auditory and vestibular systems during mouse development, consistent with cytoplasmic post-transcriptional regulatory activity in these tissues. |
Immunostaining and subcellular localization analysis in mouse embryo sections |
Developmental Dynamics |
Low |
30133047
|
| 2020 |
During C2C12 myoblast differentiation, Rbm24 undergoes cytoplasm-to-nucleus translocation. In regenerating adult muscle, Rbm24 accumulates in the myonucleus of nascent myofibers. Early in regeneration Rbm24 is required for myogenin expression; late in regeneration it regulates muscle-specific pre-mRNA alternative splicing. |
Subcellular fractionation/immunofluorescence during differentiation; satellite cell transplantation; injury-induced regeneration model |
Scientific Reports |
Medium |
33941806
|
| 2020 |
Rbm24 conditional knockout in skeletal muscle and satellite cells impairs myogenic fusion and differentiation, delays muscle regeneration after cardiotoxin injury, and dysregulates alternative splicing of Mef2d, Naca, Rock2, and Lrrfip1. |
Conditional knockout mice (skeletal muscle-specific and satellite cell-specific); CTX injury model; RNA-seq |
Theranostics |
Medium |
33042276
|
| 2021 |
RBM24 ablation in hESCs (CRISPR/Cas9) disrupts sarcomere assembly: core myofibrillogenesis proteins (ACTN2, TTN, MYH10) are misspliced, MYH6 cannot replace MYH10, and myofibrillogenesis arrests at the premyofibril stage. RBM24 promotes inclusion of ACTN2 exon 6 (actin-binding domain), and CRISPR deletion of exon 6 or forced expression of full-length ACTN2 in RBM24-/- hESCs confirms exon 6 inclusion is critical for sarcomere assembly. |
CRISPR/Cas9 KO in hESCs; transcriptomics; ACTN2 exon 6 CRISPR deletion; forced full-length ACTN2 rescue |
Circulation Research |
High |
34816743
|
| 2021 |
RBM24 directly binds the GT-rich region (positions 8101-8251) in the 3'-UTR of PTEN mRNA (RIP assay), prolongs PTEN mRNA half-life, and increases PTEN protein levels, suppressing PI3K-Akt signaling. Rbm24-knockout mice develop spontaneous colorectal adenomas with lower PTEN expression. |
RNA immunoprecipitation; mRNA stability assay; Rbm24 KO mouse model; APC-min mouse model |
Clinical and Translational Medicine |
Medium |
34709758
|
| 2021 |
RBM24 positively regulates Runx1t1 mRNA stability in bladder cancer cells by directly binding Runx1t1 mRNA; miR-625-5p directly targets and suppresses RBM24 expression; Runx1t1 promotes RBM24 expression via TCF4-mediated suppression of miR-625-5p, forming a positive feedback loop. |
RNA immunoprecipitation; luciferase reporter; mRNA stability assay; gain/loss-of-function |
Experimental & Molecular Medicine |
Medium |
34021255
|
| 2022 |
RBM24 ablation in mice and hESC-derived cardiomyocytes causes aberrant shift of CaMKIIδ splicing towards the δ-C isoform, leading to altered Ca2+ handling, prolongation of ventricular action potential and QT interval. CaMKIIδ inhibitor treatment attenuates these electrophysiological abnormalities. |
RBM24 knockout mice; hESC-derived cardiomyocyte KD; electrophysiology; CaMKIIδ inhibitor rescue |
Cellular and Molecular Life Sciences |
High |
36454480
|
| 2022 |
RBM24 recognizes and binds to the GUGUG element at stem-loop 4 (SL4) in the 5'-UTR of SARS-CoV-2 RNA via its RNP submotifs, prevents 80S ribosome assembly, and inhibits viral polyprotein translation and replication. |
RNA binding assay (RNP submotif mapping); 80S ribosome assembly assay; viral replication assay |
Antiviral Research |
Medium |
36464077
|
| 2022 |
RBM24 regulates mRNA stability of SLC7A11 (a ferroptosis inhibitor); overexpression of RBM24 protects cells from Erastin-induced ferroptosis while knockout sensitizes cells. RBM24 deficiency in mice leads to chronic inflammation and liver steatosis. |
RBM24 overexpression/knockout; Erastin-induced ferroptosis assay; SLC7A11 knockdown rescue; lipidomics; mouse model |
Frontiers in Cell and Developmental Biology |
Medium |
36478739
|
| 2016 |
RBM24 protein binds to MIR143HG RNA, destabilizes its transcript and facilitates its interaction with Ago2 to accelerate MIR143HG degradation. RBM24 also promotes biogenesis of miR-143 (evidenced by siRNA against DROSHA). MIR143HG in turn sponges miR-143 (which targets RBM24 mRNA), forming a negative feedback loop. |
RNA binding assay; mRNA stability assay; Ago2 co-immunoprecipitation; DROSHA siRNA; luciferase reporter |
Biochimica et Biophysica Acta |
Medium |
27565737
|
| 2017 |
Global RNA immunoprecipitation–microarray (RIP-Chip) profiling of Rbm24 in cardiomyocytes identifies its mRNA binding repertoire. Beyond splicing and mRNA stabilization, Rbm24 destabilizes Chrm2 mRNA via binding a coding-region element, and drives generation of isoforms with alternative transcriptional start sites. |
RNA immunoprecipitation coupled to microarray (RIP-Chip); mRNA stability assay; coding-region binding validation |
The International Journal of Biochemistry & Cell Biology |
Medium |
29104163
|
| 2016 |
NMR backbone and side-chain resonance assignments of the RRM domain of human RBM24 confirm the canonical RRM domain architecture by secondary chemical shift analysis and relaxation measurements. |
NMR spectroscopy (1H, 15N, 13C chemical shift assignments; secondary chemical shift analysis; relaxation measurements) |
Biomolecular NMR Assignments |
Medium |
27002326
|
| 2018 |
AAV9-mediated overexpression of Rbm24 in adult mouse heart induces cardiac fibrosis associated with increased TGFβ-signaling genes (TgfβR1, TgfβR2), periostin expression, and fibroblast activation; it also causes splicing changes in PDZ and Lim domain 5, Phospholamban, and Titin, but not in embryonic Rbm24 splicing targets (skNAC, αNAC, Coro6). |
AAV9 delivery in adult mice; high-resolution microarrays; histology; gene expression analysis |
Scientific Reports |
Medium |
30076363
|
| 2020 |
Rbm24 knockout in mice results in hearing loss and balance deficits; Rbm24 regulates inner-ear-specific alternative splicing including direct regulation of Cdh23 splicing (responsible for Usher syndrome 1D), and loss causes stereocilia integrity defects and hair cell death. |
Rbm24 conditional KO mice; auditory testing; RNA-seq splicing analysis; hair cell imaging |
RNA Biology |
Medium |
32887533
|
| 2020 |
RBM24 is recruited into stress granules under various stress conditions; RBM24 overexpression alone is sufficient to induce stress granule formation. However, knockdown of Rbm24 does not affect stress granule formation. |
Immunofluorescence under stress; RBM24 overexpression; Rbm24 knockdown |
Biochemical and Biophysical Research Communications |
Low |
35395551
|
| 2024 |
Psychological stress activates RBM24 S181 phosphorylation through eIF4E2-GSK3β signaling; S181 phosphorylation of RBM24 promotes APOE translation. Rbm24 S181A knock-in mice show cardiac contractile dysfunction, atrial fibrillation, dyslipidemia, and sudden death under stress; cardiomyocyte-specific APOE expression rescues cardiac electrophysiological and contractile defects via preventing ROS stress and mitochondrial dysfunction. |
Rbm24 S181A knock-in mice; eIF4E2-GSK3β signaling pathway analysis; APOE translation assay; cardiomyocyte-specific APOE rescue; electrophysiology; mitochondria/ROS assays |
Nature Communications |
High |
39580475
|
| 2024 |
POU4F3 directly binds three Rbm24 enhancers in cochlear hair cells (identified by transgenic reporter assays), and Rbm24 expression is completely absent in Pou4f3-null hair cells. GFI1 does not regulate Rbm24 expression. Ectopic Rbm24 alone cannot prevent Pou4f3-null hair cells from degenerating. |
In vivo transgenic reporter assay; Pou4f3 and Gfi1 KO mouse analysis; ectopic Rbm24 expression in Pou4f3-KO |
eLife |
Medium |
38483314
|
| 2024 |
RBM24 knockout in mouse brain impairs learning and memory; Rbm24 regulates alternative splicing of synapse-associated genes GluR2 and Prrt1. Rbm24 deletion disrupts excitatory synaptic function and plasticity in hippocampal slices. |
Conditional RBM24 KO mice; electrophysiology (hippocampal slices); RNA-seq splicing analysis; behavioral assays |
International Journal of Biological Macromolecules |
Medium |
39004256
|
| 2024 |
Rbm24 maintains Notch1 mRNA stability in adult neural stem/progenitor cells (NSPCs) in the SVZ; Rbm24 deletion impairs NSPC proliferation and neurogenesis in the olfactory bulb. Overexpression of Rbm24 rescues adult neurogenesis and olfactory dysfunction in PD mice, and this rescue is blocked by the Notch1 inhibitor DAPT. |
Rbm24 KO mice; Rbm24 overexpression in PD mouse model; DAPT pharmacological inhibition; RNA-seq; immunofluorescence; electrophysiology |
Theranostics |
Medium |
39113792
|
| 2025 |
RBM24 stabilizes JAK2 mRNA (via RNA immunoprecipitation and luciferase reporter assays) and promotes JAK2-STAT3-KLF4 signaling to drive VSMC phenotypic switching and vascular remodeling. VSMC-specific Rbm24 KO attenuates neointima formation; AAV-mediated RBM24 overexpression promotes it. |
VSMC-specific KO mice; AAV overexpression; mRNA stability assay; RNA immunoprecipitation; luciferase reporter; STAT3 inhibition (shRNA and nifuroxazide) |
Cardiovascular Research |
Medium |
41216933
|
| 2025 |
RBM24 directly binds pre-mRNA and facilitates exon inclusion to provide substrate for circ23679 production; RBM24-regulated circRNA production depends on its phosphorylation status. Circ23679 acts as a sponge for miR-15b-5p to inhibit cardiac apoptosis. |
circRNA profiling in Rbm24 KO mouse hearts; RBM24 pre-mRNA binding assay; phosphorylation manipulation; circ23679 overexpression in heart failure model |
International Journal of Biological Macromolecules |
Medium |
40250678
|
| 2026 |
Rbm24 exon 4 is alternatively spliced to produce a short isoform (RBM24-S) that, while sharing the same RRM, binds different mRNA targets affecting their splicing and/or stability compared to RBM24-L. Deletion of exon 4 (abolishing RBM24-S) causes severe hearing loss in both homozygous and heterozygous mice and stereocilia disorganization. Overexpression of RBM24-L in hair cells also causes stereocilia defects and profound hearing loss, demonstrating that proper balance of isoforms is critical. |
Exon 4 conditional deletion in mice; RBM24-L overexpression; hearing tests; hair cell imaging; RNA-seq target analysis (Strc) |
Proceedings of the National Academy of Sciences |
High |
41973913
|
| 2024 |
Rbm24 represses Insm1 expression in cochlear outer hair cells; in Rbm24-null OHCs, Insm1 remains aberrantly expressed and drives OHC death. Simultaneous inactivation of Rbm24 and Insm1 largely rescues OHC survival but only partially restores hair bundle morphology, demonstrating that Rbm24 promotes OHC survival via Insm1 repression independently of its role in hair bundle morphogenesis. |
Rbm24-/- mouse; Insm1 overexpression; Rbm24/Insm1 double KO; transcriptomic profiling of purified OHCs |
Development |
High |
41884985
|