| 2012 |
miR-383 targets RBMS1 by affecting its mRNA stability, thereby suppressing RBMS1 protein levels. Reduced RBMS1 subsequently lowers c-Myc levels (a downstream target of RBMS1), and forced expression of RBMS1 or c-Myc reverses miR-383-mediated promotion of estradiol release from granulosa cells. |
Overexpression and knockdown in mouse granulosa cells, luciferase reporter assay, mRNA stability assay, rescue experiments with forced RBMS1/c-Myc expression |
Molecular endocrinology (Baltimore, Md.) |
Medium |
22593182
|
| 2022 |
Rbms1 binds and stabilizes Efr3a mRNA in neuronal progenitors of the developing neocortex. Loss of Rbms1 delays the multipolar-to-bipolar transition and radial migration of neuronal progenitors, and ectopic Efr3a rescues the migration defect caused by Rbms1 knockdown both in vivo and in vitro. |
In utero electroporation knockdown, cross-linked RNA immunoprecipitation sequencing (CLIP-seq/RIP-seq), qRT-PCR, in vivo and in vitro migration assays, rescue by Efr3a overexpression |
Molecules and cells |
High |
35754370
|
| 2023 |
RBMS1 overexpression inhibits hepatocellular carcinoma cell growth by attenuating GPX4 expression and facilitating ferroptosis in vitro and in vivo. The circIDE/miR-19b-3p/RBMS1 axis regulates ferroptosis: circIDE sponges miR-19b-3p to elevate RBMS1 levels, and reduced RBMS1 (via miR-19b-3p targeting) suppresses ferroptosis. |
Overexpression and knockdown in HCC cells, in vitro and in vivo tumor models, circRNA sponge assays |
Epigenetics |
Medium |
36989117
|
| 2023 |
RBMS1 promotes ferroptosis resistance in colorectal cancer cells by inducing prion protein (PRNP) translation, thereby conferring resistance to oxaliplatin. Inhibiting RBMS1 reduces PRNP levels, restores ferroptosis sensitivity, and re-sensitizes cells to oxaliplatin. |
siRNA knockdown and overexpression in colorectal cancer cells, in vivo and in vitro models, western blot for PRNP, ferroptosis and drug sensitivity assays |
Molecular carcinogenesis |
Medium |
37861356
|
| 2025 |
RBMS1 promotes pulmonary fibrosis by binding the 3' UTR of Sumo2 mRNA and enhancing its stability, which elevates SUMO2 protein and promotes SUMOylation of Smad4 at lysine 158, thereby activating downstream fibrogenic signaling. Fibroblast-specific Rbms1 deletion reduces bleomycin-induced fibrosis in mice, and pharmacological inhibition by nortriptyline phenocopies this effect. |
RNA immunoprecipitation, RNA pull-down, mRNA stability assay, fibroblast-specific knockout mouse model, overexpression mouse model, bleomycin fibrosis model, site-directed mutagenesis (K158), siRNA knockdown |
The European respiratory journal |
High |
40473311
|
| 2026 |
RBMS1 drives cardiac fibrosis by binding to intron 19 of LMO7 pre-mRNA and splicing out exon 20, generating the LMO7-Δe20 isoform. LMO7-Δe20 activates the TGF-β1 pathway by upregulating activator protein 1, promoting fibroblast activation and heart failure. Fibroblast-specific RBMS1 ablation or pharmacological inhibition with nortriptyline or antisense oligonucleotides alleviates this fibrosis. |
RNA immunoprecipitation combined with RNA pull-down, unbiased RNA sequencing, fibroblast-specific knockout mice, LMO7-Δe20 overexpression model, TGF-β1 pathway inhibitor (SB431542), antisense oligonucleotides, human cardiac fibroblasts |
European heart journal |
High |
40471706
|
| 2026 |
RBMS1 directly binds the coding region of ANXA8 (Annexin A8) mRNA via its RRM2 domain, enhancing ANXA8 transcript stability. Elevated ANXA8 activates PI3K/AKT signaling to promote fibroblast activation and renal fibrosis. Fibroblast-specific RBMS1 knockout or nortriptyline treatment reduces renal fibrosis in UUO mice. |
RNA-seq, RNA immunoprecipitation (RIP), mRNA stability assay, domain-mapping (RRM2), siRNA knockdown, fibroblast-specific conditional knockout mice, UUO fibrosis model, ANXA8 overexpression/knockdown rescue experiments |
International journal of biological macromolecules |
High |
42184845
|
| 2025 |
RBMS1 promotes glioma cell proliferation by upregulating SSH1 through induction of c-Myc binding to SSH1 promoters. RBMS1 overexpression increases c-Myc activity, which transcriptionally activates SSH1, and this RBMS1–c-Myc–SSH1 axis drives tumor growth in xenograft models. |
Glioma cell lines, patient datasets, mouse xenograft models, chromatin immunoprecipitation (ChIP) for c-Myc binding to SSH1 promoter, overexpression and knockdown |
Biochemical and biophysical research communications |
Medium |
40120347
|
| 2023 |
RBMS1 knockdown in pre-adipocytes impairs differentiation and reduces expression of key adipogenic markers. Transcriptomic and proteomic analysis indicated that RBMS1 depletion affects genes involved in carbohydrate and lipid metabolism, implicating RBMS1 in adipocyte differentiation and metabolism. |
siRNA knockdown in 3T3-L1 pre-adipocytes, transcriptomics, proteomics, adipogenic differentiation assays |
International journal of molecular sciences |
Medium |
37511060
|
| 2026 |
YTHDC2 binds RBMS1 mRNA transcripts and promotes their degradation via its m6A-reader function. In ulcerative colitis, YTHDC2 is downregulated, leading to increased RBMS1 mRNA stability, elevated RBMS1 protein, and enhanced ferroptosis in colonic epithelial cells. YTHDC2 overexpression reduces RBMS1 levels and attenuates disease, whereas concurrent RBMS1 overexpression reverses these protective effects. |
RNA immunoprecipitation (RIP), mRNA stability assays, western blot, siRNA knockdown and overexpression in colonic epithelial cells, dextran sulfate sodium murine colitis model |
Inflammation |
Medium |
41811549
|
| 2026 |
The transcription factor ETV1 directly transcriptionally activates RBMS1 expression. RBMS1 knockdown abolishes the pro-tumorigenic effects of ETV1 overexpression in multiple myeloma cells and reverses ETV1-driven M2 polarization of tumor-associated macrophages. |
Luciferase reporter assay, chromatin immunoprecipitation (ChIP), gain-of-function/loss-of-function in MM cell lines, in vivo fluorescence imaging, flow cytometry |
Journal of translational medicine |
Medium |
41689098
|
| 2018 |
Linear CDKN2B-AS1 (ANRIL) transcripts directly bind RBMS1 mRNA by RNA immunoprecipitation and trans-regulate RBMS1 expression at the transcript and protein level, independent of cis-regulatory effects or the circular ANRIL isoforms. |
Inducible shRNA knockdown of CDKN2B-AS1, genome-wide mRNA expression, RNA immunoprecipitation (RIP), stable-transfected HeLa cells and HEK293 cells |
European journal of human genetics : EJHG |
Medium |
30108282
|
| 2024 |
RBMS1 is identified as a dynamically expressed regulator of RNA stabilization in growth cones of callosal projection neurons that is required for successful callosal circuit formation during neocortical development. |
Growth cone transcriptome profiling (localized transcriptomics), developmental stage comparisons; mechanistic detail limited in abstract |
bioRxivpreprint |
Low |
38328182
|