Affinage

RBM38

RNA-binding protein 38 · UniProt Q9H0Z9

Length
239 aa
Mass
25.5 kDa
Annotated
2026-04-28
66 papers in source corpus 32 papers cited in narrative 32 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RBM38 (RNPC1) is an RNA-binding protein that functions as a central post-transcriptional regulator of cell cycle, differentiation, and tumor suppression by controlling the mRNA stability, translation, and alternative splicing of key targets including p53, p21, p63, p73, MDM2, PTEN, HuR, HIF1α, c-Myc, and ferrochelatase (PMID:17050675, PMID:21764855, PMID:20457941, PMID:22508983, PMID:22710720, PMID:29052531, PMID:25622105, PMID:28399911, PMID:40961234). Its single RRM domain recognizes GU/AU/U-rich elements in target 3′ UTRs and 5′ UTRs, and its C-terminal domain physically interacts with eIF4E to block cap-dependent translation initiation; phosphorylation at Ser195 by GSK3β or CDK4 switches RBM38 from an eIF4E-sequestering translational repressor to an eIF4G-recruiting translational activator of p53, and also controls its association with the Ago2–miRNA machinery to modulate miRNA-mediated mRNA decay (PMID:24142875, PMID:30567739, PMID:33472892, PMID:41154395, PMID:25823026, PMID:31860021). RBM38 operates within autoregulatory feedback loops with p53, p63, p73, E2F1, and c-Myc, is targeted for K48-linked ubiquitin-dependent degradation by TRIM17, and its protein levels and phosphorylation status are reversed by PPM1D phosphatase (PMID:22798430, PMID:28399911, PMID:29520104, PMID:37219768, PMID:25823026). Rbm38-knockout mice develop accelerated aging, spontaneous tumors, hematopoietic defects, and microcytic hypochromic anemia with protoporphyrin IX accumulation resembling erythropoietic protoporphyria, rescued by enforced ferrochelatase expression (PMID:25512531, PMID:40961234).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2006 High

    The first mechanistic function of RBM38 was established: it directly binds AU-rich elements in the p21 3′ UTR and stabilizes p21 mRNA, thereby linking an RNA-binding protein to G1 cell-cycle arrest — an activity specific to the RNPC1a isoform.

    Evidence RNA immunoprecipitation, mRNA stability assays, isoform-specific functional assays in human cell lines

    PMID:17050675

    Open questions at the time
    • mechanism of isoform-specific functional difference unresolved
    • whether RBM38 binds p21 mRNA directly in a reconstituted system was not yet shown
  2. 2009 Medium

    RBM38 was shown to function beyond cancer cell lines: in myoblasts it binds p21 mRNA, induces cell-cycle arrest, and promotes myogenic differentiation in a p21-dependent manner, establishing a role in skeletal muscle lineage commitment.

    Evidence RIP, knockdown/overexpression in C2C12 cells, p21 rescue experiment

    PMID:19817877

    Open questions at the time
    • in vivo muscle phenotype not examined
    • whether other differentiation targets exist was unknown
  3. 2010 High

    The mechanism by which RBM38 stabilizes p21 mRNA was refined: RBM38 physically interacts with HuR via their respective RRM domains, enhancing HuR binding to p21 3′ UTR ARE, while RBM38 was simultaneously found to destabilize p63 mRNA through its own RRM-dependent binding — revealing target-specific opposing regulatory outcomes.

    Evidence Reciprocal co-IP, in vitro RNA EMSA, domain deletion mapping for HuR; mRNA stability and RIP assays for p63

    PMID:20064878 PMID:20457941

    Open questions at the time
    • structural basis for target-specific stabilization versus destabilization unknown
    • whether RBM38 recruits different effectors to different targets was not addressed
  4. 2011 High

    A fundamentally new regulatory mode was discovered: RBM38 represses p53 mRNA translation by blocking eIF4E binding to the mRNA cap, using its C-terminal domain for eIF4E interaction and its RRM for UTR binding — establishing RBM38 as a translational repressor, not only an mRNA stability factor.

    Evidence Polysome profiling, domain deletion mutants, eIF4E pulldown, reporter assays

    PMID:21764855

    Open questions at the time
    • whether this translation-repression mechanism applies to other targets was untested
    • structural details of the RBM38–eIF4E interface unresolved
  5. 2011 High

    RBM38 was found to selectively antagonize miRNA access to target mRNAs by binding uridine-rich regions near miRNA target sites, adding miRNA-mediated repression modulation as a third regulatory mechanism.

    Evidence Genetic screen, luciferase reporters, RIP, miRNA-target interaction assays

    PMID:22027593

    Open questions at the time
    • genome-wide scope of miRNA antagonism unclear
    • whether RBM38 directly competes with RISC or alters mRNA structure was not distinguished
  6. 2012 High

    The target repertoire expanded to include MDM2, HuR, p73, and E2F1: RBM38 destabilizes MDM2 and c-Myc transcripts, stabilizes HuR and p73 mRNAs, and is itself transcriptionally regulated by E2F1 — revealing multiple feedback loops placing RBM38 at a hub of p53-family and cell-cycle regulatory networks.

    Evidence mRNA stability assays, RIP, RNA-binding mutants, KO MEFs, ChIP of E2F1 on RBM38 promoter

    PMID:22371495 PMID:22508983 PMID:22710720 PMID:22798430

    Open questions at the time
    • hierarchy among feedback loops unresolved
    • whether HuR cooperation generalizes beyond p21 was not tested
  7. 2013 High

    The critical regulatory switch was identified: GSK3β phosphorylates RBM38 at Ser195, converting it from an eIF4E-binding translational repressor to an eIF4G-recruiting translational activator of p53, linking PI3K-Akt signaling to p53 expression control.

    Evidence In vitro kinase assay, phosphomimetic/non-phosphorylatable mutants, co-IP, PI3K inhibition

    PMID:24142875

    Open questions at the time
    • whether Ser195 phosphorylation affects all targets or is p53-specific was unknown
    • in vivo consequences of the phospho-switch were not yet tested
  8. 2013 High

    A splicing-regulatory function was established: RBM38 activates EPB41 exon 16 inclusion during erythroid differentiation, and SELEX-Seq defined a GU-rich binding motif — expanding its role to alternative splicing in hematopoiesis.

    Evidence Exon junction microarray, minigene, SELEX-Seq, tethering assay, erythroid differentiation model

    PMID:24250749

    Open questions at the time
    • full spectrum of splicing targets during erythropoiesis unknown
    • mechanism of splicing activation versus repression by RBM38 was not defined
  9. 2014 High

    Rbm38-knockout mice provided the first in vivo genetic validation: loss of Rbm38 causes accelerated aging, hematopoietic defects, and spontaneous tumors, while enhancing p53-dependent tumor suppression in p53-heterozygous mice — confirming the p53-RBM38 autoregulatory loop functions physiologically.

    Evidence Rbm38 KO mouse, ionizing radiation challenge, genetic epistasis with p53 alleles, tumor monitoring

    PMID:25512531

    Open questions at the time
    • tissue-specific contributions to aging phenotype unresolved
    • whether tumor phenotype is entirely p53-mediated was not determined
  10. 2015 High

    PPM1D was identified as the phosphatase that reverses GSK3-mediated Ser195 phosphorylation, restoring translational repression of p53, and RBM38 reciprocally promotes PPM1D mRNA translation — closing an additional feedback loop governing the phospho-switch.

    Evidence In vitro dephosphorylation, co-IP, RIP, reporter assays

    PMID:25823026

    Open questions at the time
    • whether other phosphatases act on Ser195 in specific tissues was untested
  11. 2018 High

    The Ser195 phospho-switch was shown to control RBM38's interaction with the Ago2–miRNA complex: phosphorylation disrupts Ago2 binding, preventing miR-203-mediated p63 mRNA degradation, while genetic epistasis in compound Rbm38/TAp63 knockout mice demonstrated that the RBM38-p63 feedback loop governs aging and tumorigenesis in vivo.

    Evidence S195A/S195D knock-in MEFs, co-IP with Ago2, compound KO mice, lifespan and tumor monitoring

    PMID:29520104 PMID:30567739

    Open questions at the time
    • whether phospho-dependent Ago2 modulation extends to miRNAs beyond miR-203 was not systematically tested
  12. 2018 High

    A synthetic peptide (Pep8) derived from 8 amino acids of RBM38 was shown to disrupt the RBM38–eIF4E complex and relieve p53 translational repression, suppressing tumor growth in xenografts in an RBM38- and p53-dependent manner — providing pharmacological validation of the translational control mechanism.

    Evidence Molecular simulation, peptide binding assay, co-IP, xenograft tumor model

    PMID:30591552

    Open questions at the time
    • peptide pharmacokinetics and clinical translatability not addressed
    • whether Pep8 also disrupts RBM38–Ago2 interaction was not initially clear
  13. 2020 High

    The crystal structure of the RBM38 RRM domain bound to RNA resolved the molecular basis of sequence specificity: two phenylalanines stack with RNA bases and hydrogen bonds specify G(U/C/A)GUG recognition — providing the first atomic-level understanding of target selection.

    Evidence X-ray crystallography with mutagenesis validation and RNA binding assays

    PMID:31860021

    Open questions at the time
    • structure of full-length RBM38 including C-terminal eIF4E-binding region unsolved
    • how RRM recognizes diverse AU-rich versus GU-rich elements structurally was not reconciled
  14. 2021 High

    The Pep8 peptide was shown to also block the RBM38–AGO2 interaction via the Ser195–Glu73/76 interface, and knock-in mice carrying RBM38-S193D or eIF4E-D202K mutations confirmed that fine-tuning of the RBM38–eIF4E interaction controls p53 levels, lifespan, and tumor susceptibility in vivo.

    Evidence Multiple knock-in mouse models, RIP of eIF4E, lifespan monitoring, Pep8 co-IP disruption

    PMID:33472892 PMID:33664057

    Open questions at the time
    • how phospho-RBM38 simultaneously coordinates eIF4G recruitment and Ago2 release on the same target is mechanistically unclear
  15. 2023 Medium

    CDK4 was identified as a second kinase phosphorylating RBM38 at Ser195, promoting mutant p53 translation via eIF4G; TRIM17 E3 ligase was shown to target RBM38 for K48-linked ubiquitin-dependent degradation, mediating cisplatin resistance — revealing additional layers of RBM38 regulation.

    Evidence In vitro kinase assay for CDK4, CDK4/6 inhibitor treatment; co-IP and K48-specific ubiquitination assays for TRIM17

    PMID:37219768 PMID:41154395

    Open questions at the time
    • whether CDK4 and GSK3β act redundantly or in different contexts is unresolved
    • TRIM17-mediated degradation confirmed in single lab only
    • other E3 ligases targeting RBM38 not systematically surveyed
  16. 2025 High

    RBM38 was established as an essential regulator of erythroid terminal differentiation by jointly controlling alternative splicing, mRNA decay, and translation of ferrochelatase (Fech); Rbm38-deficient mice develop microcytic hypochromic anemia with protoporphyrin IX accumulation resembling erythropoietic protoporphyria, rescued by enforced Fech expression.

    Evidence Conditional Rbm38 KO mice, RNA-seq splicing analysis, mRNA stability and translation assays, Fech rescue transplantation

    PMID:40961234

    Open questions at the time
    • whether RBM38 mutations cause erythropoietic protoporphyria in humans is unknown
    • full complement of erythroid splicing targets beyond EPB41 and Fech not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: the structural basis for how RBM38 switches between mRNA stabilization and destabilization on different targets; the full-length protein structure including the C-terminal eIF4E/eIF4G-binding and Ago2-interacting regions; tissue-specific hierarchies among the multiple feedback loops; and whether human RBM38 loss-of-function mutations cause hematologic disease.
  • no full-length RBM38 structure available
  • no human genetic disease association established
  • systematic transcriptome-wide identification of direct splicing versus stability versus translation targets not completed

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 10 GO:0098772 molecular function regulator activity 5 GO:0140098 catalytic activity, acting on RNA 3
Localization
GO:0005829 cytosol 3
Pathway
R-HSA-8953854 Metabolism of RNA 8 R-HSA-392499 Metabolism of proteins 5 R-HSA-1266738 Developmental Biology 4 R-HSA-1640170 Cell Cycle 3 R-HSA-5357801 Programmed Cell Death 2
Partners
AGO2EIF4EEIF4GGSK3BHURPPM1DRBM24TRIM17

Evidence

Reading pass · 32 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 RBM38 (RNPC1) directly binds to AU-rich elements in the 3' UTR of p21 mRNA and stabilizes the p21 transcript, maintaining basal and stress-induced p21 levels. The RNPC1a isoform, but not RNPC1b, stabilizes p21 mRNA and induces G1 cell cycle arrest, despite both isoforms binding the 3' UTR. RNA immunoprecipitation, mRNA stability assay, siRNA knockdown, isoform-specific functional assays Genes & Development High 17050675
2010 RBM38 physically interacts with HuR via its RRM domain (interacting with RRM3 of HuR), and this interaction enhances HuR's RNA-binding activity to p21 3'-UTR AU-rich elements; RBM38's ability to regulate p21 mRNA stability is dependent on HuR. Co-immunoprecipitation, RNA EMSA, in vitro and in vivo RNA binding assays, domain deletion mapping Nucleic Acids Research High 20064878
2010 RBM38 destabilizes p63 mRNA by binding to AU-/U-rich elements in p63 3' UTR via its RRM domain, leading to decreased p63 expression and promoting keratinocyte differentiation. mRNA stability assay, RNA immunoprecipitation, EMSA, RRM domain mutant, knockdown/overexpression PNAS High 20457941
2011 RBM38 represses p53 mRNA translation by preventing cap-binding protein eIF4E from binding to p53 mRNA; this requires the C-terminal domain of RBM38 for physical interaction with eIF4E, and the N-terminal RRM domain for binding p53 5' and 3' UTRs. Polysome profiling, RNA immunoprecipitation, pulldown, domain deletion mutants, reporter assays Genes & Development High 21764855
2011 RBM38 selectively inhibits miRNA access to target mRNAs by binding uridine-rich regions near miRNA target sequences, protecting p53 target mRNAs from miRNA-mediated repression while showing lower propensity to block miR-34a action on SIRT1. Genetic screen, luciferase reporter assay, RNA immunoprecipitation, functional miRNA-target interaction assays Nature Communications High 22027593
2012 RBM38 destabilizes MDM2 transcript by binding to multiple AU-/U-rich elements in MDM2 3' UTR, thereby decreasing MDM2 expression independently of p53; RNA-binding activity of RBM38 is required for this effect. mRNA stability assay, RNA immunoprecipitation, reporter assay, RNA-binding mutant, knockdown/knockout Oncogene High 22710720
2012 RBM38 post-transcriptionally stabilizes HuR mRNA by binding its 3' UTR; RNA-binding-deficient RBM38 mutant cannot stabilize HuR, and HuR mediates RBM38-induced growth suppression by repressing c-Myc. mRNA stability assay, RNA immunoprecipitation, RNA-binding mutant, knockdown/knockout Journal of Biological Chemistry High 22371495
2012 RBM38 expression is directly transcriptionally regulated by E2F1, and RBM38 in turn limits E2F1-induced cell-cycle progression, forming a negative feedback loop; endogenous E2F1 binds the RBM38 promoter. Chromatin immunoprecipitation, qRT-PCR, Western blot, E2F1 activation system, RBM38 knockdown + cell cycle analysis Molecular Cancer Research Medium 22798430
2012 RBM38 regulates p73 mRNA stability by binding a CU-rich element in the p73 3' UTR; loss of RNPC1 in p53-null MEFs reduces p73 expression and decreases cellular senescence. mRNA stability assay, RNA immunoprecipitation, EMSA, knockout MEFs, cellular senescence assay Molecular and Cellular Biology High 22508983
2013 RBM38 stabilizes MIC-1 mRNA by binding to an AU-rich element in the MIC-1 3' UTR, and MIC-1 is required for RBM38-induced cell growth suppression. mRNA stability assay, RNA immunoprecipitation, ARE-binding assay, knockdown Journal of Biological Chemistry Medium 23836903
2013 RBM38 is phosphorylated at Ser195 by GSK3, and this phosphorylation abolishes the RBM38-eIF4E interaction on p53 mRNA; phosphorylated RBM38 or phosphomimetic S195D instead interacts with eIF4G to promote assembly of the eIF4F complex and enhance p53 mRNA translation. Inhibition of PI3K-Akt activates GSK3, leading to increased RBM38 phosphorylation and elevated p53. In vitro kinase assay, phosphomimetic/non-phosphorylatable mutants, RNA immunoprecipitation, co-immunoprecipitation, reporter assay, PI3K pathway inhibition Genes & Development High 24142875
2013 RBM38 regulates alternative splicing during late erythroid differentiation, activating Protein 4.1R (EPB41) exon 16 inclusion. SELEX-Seq identified a GU-rich RBM38 binding motif, and tethering assays showed RBM38 can directly activate splicing when recruited downstream of an exon. Exon junction microarray, minigene splicing assay, SELEX-Seq, tethering assay, erythroid differentiation model PLoS ONE High 24250749
2014 Rbm38-null mice exhibit accelerated aging, hematopoietic defects, and spontaneous tumors; Rbm38 deficiency enhances p53 accumulation after ionizing radiation in vivo, and markedly decreases tumor penetrance in p53-heterozygous mice via enhanced p53 expression, providing genetic evidence that the p53-Rbm38 autoregulatory loop operates in vivo. Rbm38 knockout mouse model, ionizing radiation challenge, tumor monitoring, genetic epistasis with p53 alleles PNAS High 25512531
2015 PPM1D phosphatase directly interacts with and dephosphorylates RBM38 at Ser195, reversing GSK3-mediated phosphorylation; this dephosphorylation restores RBM38's ability to suppress p53 mRNA translation. RBM38 in turn promotes PPM1D mRNA translation by binding PPM1D 3' UTR. Co-immunoprecipitation, in vitro dephosphorylation assay, reporter assay, RNA immunoprecipitation Oncogene High 25823026
2015 RBM38 regulates HIF1α expression via mRNA translation: RBM38 binds HIF1α 5' and 3' UTRs and prevents eIF4E from binding HIF1α mRNA, reducing HIF1α protein synthesis under hypoxic conditions. Metabolic labeling (de novo protein synthesis), RNA immunoprecipitation, eIF4E-mRNA binding assay, reporter assay Oncotarget Medium 25622105
2017 RBM38 stabilizes PTEN mRNA by binding to multiple AU/U-rich elements in PTEN 3' UTR, increasing PTEN expression; RBM38-mediated growth suppression in breast cancer is partly dependent on PTEN. RNA immunoprecipitation, EMSA, luciferase reporter assay, siRNA, mRNA stability assay Journal of Experimental & Clinical Cancer Research Medium 29052531
2017 RBM38 stabilizes ZO-1 mRNA by binding to AU/U-rich elements in its 3' UTR; TGF-β-induced transcription repressor Snail directly suppresses RBM38 expression by binding E-box elements in the RBM38 promoter, thereby reducing ZO-1 and promoting EMT. Chromatin immunoprecipitation, luciferase reporter assay, RNA immunoprecipitation, EMSA, Transwell migration assay British Journal of Cancer Medium 28683467
2017 c-Myc directly represses RBM38 transcription by binding E-box motifs in the RBM38 promoter; RBM38 in turn destabilizes c-Myc mRNA by binding AU-rich elements in c-Myc 3' UTR, forming a mutually antagonistic feedback loop. Chromatin immunoprecipitation, luciferase reporter assay, RNA immunoprecipitation, mRNA stability assay Journal of Experimental & Clinical Cancer Research Medium 28399911
2018 Synthetic peptide Pep8 (8 amino acids from RBM38) disrupts the RBM38-eIF4E complex; Ser-6 of Pep8 forms a hydrogen bond with Asp-202 in eIF4E. Disruption of this complex relieves p53 mRNA translational repression and suppresses tumor growth in an RBM38- and p53-dependent manner. Molecular simulation, peptide binding assay, co-immunoprecipitation, colony formation, xenograft tumor model Cancer Research High 30591552
2018 Rbm38 stabilizes Pten mRNA through an AU-rich element in Pten 3' UTR; loss of Rbm38 in mutant p53 knock-in mice decreases Pten expression and promotes T-cell lymphomagenesis, demonstrating that Rbm38 jointly modulates mutant p53 and Pten in vivo. Rbm38 knockout mice crossed with mutant p53 knock-in, mRNA stability assay, luciferase reporter assay, tumor incidence monitoring Cancer Research High 29330147
2018 Ser195 phosphorylation of RBM38 by GSK3β disrupts its association with the Ago2-miR203 complex, thereby preventing miR203-mediated degradation of p63α mRNA and increasing p63 expression; non-phosphorylatable RBM38-S195A promotes Ago2-miR203-dependent p63 mRNA decay, whereas phosphomimetic S195D does not. Phosphomimetic/non-phosphorylatable knock-in MEFs, co-immunoprecipitation with Ago2, GSK3β activation, RT-qPCR Journal of Biological Chemistry High 30567739
2018 The Rbm38-p63 negative feedback loop controls aging and tumorigenesis in vivo: compound Rbm38-/-;TAp63+/- mice have extended lifespan and reduced tumor incidence compared to single mutants, and show reduced expression of inflammatory cytokines IL17D and Tnfsf15. Compound knockout mouse model, lifespan analysis, tumor incidence monitoring, cytokine expression analysis Oncogene High 29520104
2018 RBM38 facilitates HBV pgRNA packaging by directly binding the lower bulge of the epsilon (ε) stem-loop via its RNP submotifs, interacting with HBV Pol in an RNA-independent manner, forming heterogeneous oligomers with RBM24, and binding HBV core protein via its C-terminal ARD domain. RNA immunoprecipitation, co-immunoprecipitation, in vitro RNA binding assay, domain deletion analysis Antiviral Research Medium 35041910
2020 Crystal structure of the RRM domain of human RBM38 in complex with single-stranded RNA revealed that RBM38 recognizes G(U/C/A)GUG sequences; two phenylalanine residues stack with RNA bases and a series of hydrogen bonds determine sequence-specific recognition. X-ray crystallography, mutagenesis of key residues, RNA binding assays Biochemical Journal High 31860021
2021 RBM38 exerts opposing effects on survivin expression: it blocks let-7b-mediated survivin mRNA degradation (protecting survivin) while also interacting with AGO2 to facilitate miR-203a-mediated survivin mRNA degradation. Ser-195 in RBM38 interacts with Glu-73/-76 in AGO2; Pep8 blocks the RBM38-AGO2 interaction. RNA immunoprecipitation, co-immunoprecipitation, luciferase reporter assay, mutant analysis (S195-AGO2 interaction), Pep8 peptide treatment Cancer Research High 33472892
2021 Fine-tuning of RBM38-eIF4E interaction controls p53 expression in vivo: knock-in of RBM38-S195D enhances eIF4E binding to p53 mRNA and p53 expression, while knock-in of eIF4E-D202K weakens RBM38 interaction and enhances p53. S193D knock-in mice have shortened lifespan and are prone to spontaneous tumors and chronic inflammation. Multiple knock-in cell lines and mouse model (Rbm38-S193D KI), RNA immunoprecipitation of eIF4E, p53 expression analysis, lifespan monitoring Genes & Development High 33664057
2023 TRIM17 E3 ubiquitin ligase interacts with RBM38 and promotes K48-linked polyubiquitination and proteasomal degradation of RBM38, thereby mediating cisplatin resistance in NSCLC. Co-immunoprecipitation, ubiquitination assay (K48-linkage specific), knockdown/overexpression, in vitro and in vivo resistance assays Cellular Oncology Medium 37219768
2023 CDK4 phosphorylates RBM38 at Ser195, which enhances mutant p53 mRNA translation by promoting eIF4G interaction; CDK4/6 inhibitors reduce this phosphorylation and thereby suppress mutant p53 translation. In vitro kinase assay, phosphomimetic mutants, RNA immunoprecipitation, Western blot in CDK4/6 inhibitor-treated cells Cancers Medium 41154395
2023 CBX7 positively regulates RBM38 expression in cardiomyocytes via TARDBP in a TARDBP-dependent manner; overexpression of RBM38 inhibits proliferation of CBX7-depleted cardiomyocytes, placing RBM38 downstream of the CBX7-TARDBP axis in cell cycle exit. Co-immunoprecipitation, mass spectrometry, adenoviral overexpression, genetic KO mice (Tnnt2-Cre;Cbx7), neonatal cardiomyocyte proliferation assay Circulation Medium 37158107
2009 RBM38 binds to p21 transcript in vivo in myoblasts, and overexpression of RBM38 induces cell cycle arrest and promotes myogenic differentiation; knockdown of RBM38 suppresses cell cycle arrest and delays differentiation in C2C12 cells, and this effect is rescued by p21 overexpression. Immunoprecipitation-RT-PCR (RIP), RNA interference, overexpression, myogenic differentiation assay, p21 rescue experiment Genes to Cells Medium 19817877
2018 RBM38 binds to ISE2 (5'-UGUGUG-3') in parvovirus B19 pre-mRNA and promotes splicing at the D2 donor site required for 11-kDa protein expression; knockdown of RBM38 decreases D2-spliced mRNA encoding the 11-kDa protein but not VP2, thereby reducing viral DNA replication. In vitro RNA binding assay (EMSA), RBM38 knockdown, RT-PCR of splice isoforms, viral replication assay Journal of Virology Medium 29437973
2025 Rbm38 regulates erythroid terminal differentiation by controlling alternative splicing, mRNA decay, and translation of ferrochelatase (Fech); Rbm38-deficient mice develop microcytic hypochromic anemia, protoporphyrin IX accumulation resembling erythropoietic protoporphyria, and enforced Fech expression rescues erythroid defects. Whole-body and conditional Rbm38 knockout mice, RNA-seq splicing analysis, mRNA stability assay, translational assay, Fech rescue transplantation Blood High 40961234

Source papers

Stage 0 corpus · 66 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 RNPC1, an RNA-binding protein and a target of the p53 family, is required for maintaining the stability of the basal and stress-induced p21 transcript. Genes & development 124 17050675
2011 Translational repression of p53 by RNPC1, a p53 target overexpressed in lymphomas. Genes & development 117 21764855
2010 RNPC1 modulates the RNA-binding activity of, and cooperates with, HuR to regulate p21 mRNA stability. Nucleic acids research 101 20064878
2011 Selective inhibition of microRNA accessibility by RBM38 is required for p53 activity. Nature communications 84 22027593
2010 RNPC1, an RNA-binding protein and a target of the p53 family, regulates p63 expression through mRNA stability. Proceedings of the National Academy of Sciences of the United States of America 75 20457941
2014 Mice deficient in Rbm38, a target of the p53 family, are susceptible to accelerated aging and spontaneous tumors. Proceedings of the National Academy of Sciences of the United States of America 64 25512531
2009 RNA-binding proteins Rbm38 and Rbm24 regulate myogenic differentiation via p21-dependent and -independent regulatory pathways. Genes to cells : devoted to molecular & cellular mechanisms 60 19817877
2013 Glycogen synthase kinase 3 promotes p53 mRNA translation via phosphorylation of RNPC1. Genes & development 55 24142875
2012 p73 expression is regulated by RNPC1, a target of the p53 family, via mRNA stability. Molecular and cellular biology 51 22508983
2018 RBM38 plays a tumor-suppressor role via stabilizing the p53-mdm2 loop function in hepatocellular carcinoma. Journal of experimental & clinical cancer research : CR 48 30176896
2017 PTEN expression is upregulated by a RNA-binding protein RBM38 via enhancing its mRNA stability in breast cancer. Journal of experimental & clinical cancer research : CR 48 29052531
2013 The RNA binding protein RBM38 (RNPC1) regulates splicing during late erythroid differentiation. PloS one 44 24250749
2012 MDM2 expression is repressed by the RNA-binding protein RNPC1 via mRNA stability. Oncogene 43 22710720
2017 RBM38 is involved in TGF-β-induced epithelial-to-mesenchymal transition by stabilising zonula occludens-1 mRNA in breast cancer. British journal of cancer 42 28683467
2014 RNA-binding protein RNPC1: acting as a tumor suppressor in breast cancer. BMC cancer 41 24884756
2018 Disruption of the Rbm38-eIF4E Complex with a Synthetic Peptide Pep8 Increases p53 Expression. Cancer research 39 30591552
2018 RNA Binding Protein RNPC1 Inhibits Breast Cancer Cell Metastasis via Activating STARD13-Correlated ceRNA Network. Molecular pharmaceutics 36 29733656
2012 The RNA-binding protein RNPC1 stabilizes the mRNA encoding the RNA-binding protein HuR and cooperates with HuR to suppress cell proliferation. The Journal of biological chemistry 35 22371495
2017 The role of c-Myc-RBM38 loop in the growth suppression in breast cancer. Journal of experimental & clinical cancer research : CR 34 28399911
2012 RBM38 is a direct transcriptional target of E2F1 that limits E2F1-induced proliferation. Molecular cancer research : MCR 30 22798430
2015 The RNA binding proteins RBM38 and DND1 are repressed in AML and have a novel function in APL differentiation. Leukemia research 29 26740055
2018 Genetic Ablation of Rbm38 Promotes Lymphomagenesis in the Context of Mutant p53 by Downregulating PTEN. Cancer research 28 29330147
2013 RNPC1, an RNA-binding protein and a p53 target, regulates macrophage inhibitory cytokine-1 (MIC-1) expression through mRNA stability. The Journal of biological chemistry 28 23836903
2012 Radiation sensitivity of esophageal adenocarcinoma: the contribution of the RNA-binding protein RNPC1 and p21-mediated cell cycle arrest to radioresistance. Radiation research 27 22214381
2015 PPM1D phosphatase, a target of p53 and RBM38 RNA-binding protein, inhibits p53 mRNA translation via dephosphorylation of RBM38. Oncogene 25 25823026
2021 miR-125a-5p increases cellular DNA damage of aging males and perturbs stage-specific embryo development via Rbm38-p53 signaling. Aging cell 24 34751998
2015 Hypoxia-inducible factor 1 alpha is regulated by RBM38, a RNA-binding protein and a p53 family target, via mRNA translation. Oncotarget 23 25622105
2015 Estrogen receptor (ER) was regulated by RNPC1 stabilizing mRNA in ER positive breast cancer. Oncotarget 22 25881544
2020 RBM38 in cancer: role and mechanism. Cellular and molecular life sciences : CMLS 21 32642788
2017 The expression of RNA-binding protein RBM38 decreased in renal cell carcinoma and represses renal cancer cell proliferation, migration, and invasion. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 21 28459215
2018 RNA Binding Protein RBM38 Regulates Expression of the 11-Kilodalton Protein of Parvovirus B19, Which Facilitates Viral DNA Replication. Journal of virology 20 29437973
2021 RNA-binding protein RBM38 inhibits colorectal cancer progression by partly and competitively binding to PTEN 3'UTR with miR-92a-3p. Environmental toxicology 19 34453780
2018 The Rbm38-p63 feedback loop is critical for tumor suppression and longevity. Oncogene 19 29520104
2023 Polycomb Group Protein CBX7 Represses Cardiomyocyte Proliferation Through Modulation of the TARDBP/RBM38 Axis. Circulation 18 37158107
2017 RNPC1 enhances progesterone receptor functions by regulating its mRNA stability in breast cancer. Oncotarget 17 27634883
2017 RNPC1 inhibits non-small cell lung cancer progression via regulating miR-181a/CASC2 axis. Biotechnology letters 17 29288351
2023 TRIM17-mediated ubiquitination and degradation of RBM38 promotes cisplatin resistance in non-small cell lung cancer. Cellular oncology (Dordrecht, Netherlands) 15 37219768
2020 Alternative Splicing of Cdh23 Exon 68 Is Regulated by RBM24, RBM38, and PTBP1. Neural plasticity 14 32774357
2015 Integrative genomic analyses of the RNA-binding protein, RNPC1, and its potential role in cancer prediction. International journal of molecular medicine 14 26046131
2018 Serine 195 phosphorylation in the RNA-binding protein Rbm38 increases p63 expression by modulating Rbm38's interaction with the Ago2-miR203 complex. The Journal of biological chemistry 13 30567739
2017 The RNA-binding protein Rbm38 is dispensable during pressure overload-induced cardiac remodeling in mice. PloS one 13 28850611
2022 LncRNA CALML3-AS1 suppresses papillary thyroid cancer progression via sponging miR-20a-5p/RBM38 axis. BMC cancer 12 35351042
2017 TAp63γ and ΔNp63γ are regulated by RBM38 via mRNA stability and have an opposing function in growth suppression. Oncotarget 12 29108232
2020 Structural basis for mRNA recognition by human RBM38. The Biochemical journal 10 31860021
2019 Therapeutic modulation of RNA-binding protein Rbm38 facilitates re-endothelialization after arterial injury. Cardiovascular research 10 30843048
2022 RNA-Binding motif protein 38 (RBM38) mediates HBV pgRNA packaging into the nucleocapsid. Antiviral research 9 35041910
2021 Fine-tuning p53 activity by modulating the interaction between eukaryotic translation initiation factor eIF4E and RNA-binding protein RBM38. Genes & development 8 33664057
2020 RNA Binding Protein RNPC1 Suppresses the Stemness of Human Endometrial Cancer Cells via Stabilizing MST1/2 mRNA. Medical science monitor : international medical journal of experimental and clinical research 8 32088727
2023 Identification of a First-in-Class Small-Molecule Inhibitor of the EIF4E-RBM38 Complex That Enhances Wild-type TP53 Protein Translation for Tumor Growth Suppression. Molecular cancer therapeutics 7 36940176
2023 RBM38 Reverses Sorafenib Resistance in Hepatocellular Carcinoma Cells by Combining and Promoting lncRNA-GAS5. Cancers 7 37296859
2021 RBM38 is negatively regulated by miR-320b and enhances Adriamycin resistance in breast cancer cells. Oncology letters 7 34868364
2019 RBM38 induces SIRT1 expression during hypoxia in non-small cell lung cancer cells by suppressing MIR34A expression. Biotechnology letters 7 31760527
2017 RNA-binding protein RBM38 acts as a tumor suppressor in gastric cancer. International journal of clinical and experimental pathology 7 31966462
2021 Survivin Expression Is Differentially Regulated by a Selective Cross-talk between RBM38 and miRNAs let-7b or miR-203a. Cancer research 6 33472892
2020 Roles of ZEB2 and RBM38 in liver cancer stem cell proliferation. Journal of B.U.ON. : official journal of the Balkan Union of Oncology 6 32862581
2021 RNA-binding protein RNPC1 acts as an oncogene in gastric cancer by stabilizing aurora kinase B mRNA. Experimental cell research 5 34302858
2023 RNF26 Promotes Pancreatic Cancer Proliferation by Enhancing RBM38 Degradation. Pancreas 3 37099788
2022 Optimization of eIF4E-Binding Peptide Pep8 to Disrupt the RBM38-eIF4E Complex for Induction of p53 and Tumor Suppression. Frontiers in oncology 3 35574389
2021 Small Proline-Rich Protein 2A and 2D Are Regulated by the RBM38-p73 Axis and Associated with p73-Dependent Suppression of Chronic Inflammation. Cancers 3 34204113
2020 Rbm38 Reduces the Transcription Elongation Defect of the SMEK2 Gene Caused by Splicing Deficiency. International journal of molecular sciences 3 33233740
2016 [RNPC1 induces sensitivity of HER-2-positive breast cancer BT474 cells to trastuzumab through upregulation of HER2]. Zhonghua zhong liu za zhi [Chinese journal of oncology] 2 26988821
2025 Rbm38 deficiency impairs erythroid heme biosynthesis and induces porphyria via reduced ferrochelatase expression. Blood 1 40961234
2026 RNA-binding protein Rbm38 as a multifaceted post-transcriptional regulator in zebrafish pancreatic development. Journal of molecular cell biology 0 40796306
2025 EIF4A3-Mediated downregulation of circPTEN promotes hepatocellular carcinoma progression through the miR-1289/RBM38 Axis. Journal of molecular histology 0 40527976
2025 CDK4/6 Inhibitors Suppress RB-Null Triple-Negative Breast Cancer by Inhibiting Mutant P53 Expression via RBM38 RNA-Binding Protein. Cancers 0 41154395
2021 [RBM38 Mediates the Proliferation of Acute Myeloid Leukemia Cells HL-60 by Regulating FZD1 mRNA Stability]. Zhongguo shi yan xue ye xue za zhi 0 34893109