Affinage

RBM14

RNA-binding protein 14 · UniProt Q96PK6

Length
669 aa
Mass
69.5 kDa
Annotated
2026-06-10
35 papers in source corpus 26 papers cited in narrative 26 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RBM14 (CoAA) is a multifunctional nuclear RNA-binding protein with two N-terminal RNA recognition motifs and a C-terminal auxiliary/intrinsically disordered region that couples transcription, RNA processing, genome maintenance, and phase separation (PMID:11443112, PMID:14673176, PMID:31636951). As a transcriptional coactivator, it bridges TRBP and p300/CBP to potentiate hormone-receptor-dependent transcription, with its RRMs and auxiliary domain differentially engaged to drive promoter-preferential coactivation and alternative splicing (PMID:11443112, PMID:14673176); the same scaffolding underlies interactions with diverse transcription factors and partners including SYT, Runx2, and PEA3-group factors (PMID:16227627, PMID:19585539, PMID:21736557). RBM14 is recruited to DNA double-strand breaks in a PARP- and RNAPII-dependent manner, where it binds RNA:DNA hybrids and supports both non-homologous end joining—through control of XRCC4/XLF recruitment and KU release—and homologous recombination, by promoting CtIP-mediated end resection and subsequent RPA/RAD51 loading (PMID:32094185, PMID:28426349, PMID:37559455). Through its IDR, RBM14 phase-separates into ribonucleoprotein condensates that govern embryonic patterning and, in early embryos, concentrate maternal mRNAs at spindle poles where co-phase separation with the deadenylase PARN drives deadenylation and proper zygotic genome activation (PMID:31636951, PMID:36477743). RBM14 also suppresses ectopic centriole assembly via the STIL/CPAP pathway to preserve spindle integrity and genome stability (PMID:25385835). Post-translationally, O-GlcNAcylation at Ser521 governs its interaction with the E3 ligase TRIM33 to control OGA stability and cellular O-GlcNAc homeostasis, linking RBM14 to oncogenic transformation (PMID:38678556).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 2001 High

    Established RBM14's founding identity as a TRBP-interacting transcriptional coactivator, defining its domain architecture and link to hormone signaling.

    Evidence Yeast two-hybrid, in vitro binding, co-IP, and reporter assays identifying CoAA with two RRMs and a TRBP-interacting domain

    PMID:11443112

    Open questions at the time
    • Direct RNA targets not defined
    • Endogenous coactivator complex composition unresolved
  2. 2004 High

    Showed RBM14 couples transcription to alternative splicing in a promoter-preferential manner, defining how its two domains are differentially deployed.

    Evidence Transcription and splicing reporter assays with domain-swap mutants across promoter contexts

    PMID:14673176

    Open questions at the time
    • Mechanism of promoter-context sensing unknown
    • Endogenous splicing targets not mapped
  3. 2005 Medium

    Extended the coactivator scaffold to oncogenic SYT/SYT-SSX2 fusions, mapping the YQ hexapeptide-repeat domain as the interaction module.

    Evidence Co-IP, GST pulldown, domain mapping, and hormone-receptor reporter assays in human cells

    PMID:16227627

    Open questions at the time
    • Single-lab interaction data
    • Functional consequence in synovial sarcoma not tested in vivo
  4. 2006 Medium

    Connected RBM14 to cancer biology via 11q13 amplification, autoregulation, and transforming activity, establishing oncogenic potential.

    Evidence Amplicon mapping, autoregulation reporter assays, and soft-agar transformation assays

    PMID:16878147

    Open questions at the time
    • Driver vs passenger status of amplification unresolved
    • Mechanism of transformation not defined
  5. 2007 Medium

    Defined an alternative-splicing switch (CoAA to dominant-negative CoAM) regulated by p54nrb/PSF that controls RBM14 activity during differentiation.

    Evidence Minigene reporters, retinoic acid-induced P19 differentiation, and trans-factor perturbation

    PMID:17337438

    Open questions at the time
    • Physiological breadth of the isoform switch unknown
    • Single-lab assays
  6. 2009 Medium

    Broadened RBM14's transcription-factor repertoire to Runx factors and intergenic trans-splicing with RBM4, linking it to differentiation control.

    Evidence Co-IP, EMSA, reporter assays, and trans-spliced variant identification in neural differentiation models

    PMID:19416963 PMID:19585539

    Open questions at the time
    • In vivo relevance of trans-splicing unclear
    • Genome-wide Runx co-regulation not assessed
  7. 2011 Medium

    Identified RBM14 as a PEA3-group cofactor requiring both RRMs, tying its coactivation to cancer cell migration.

    Evidence Co-IP, domain-deletion mapping, reporter assays, and migration assays in MCF7 cells

    PMID:21736557

    Open questions at the time
    • Single readout system
    • Direct migration targets not defined
  8. 2014 Medium

    Established RBM14 as a regulator of NHEJ and a suppressor of ectopic centriole assembly, linking it to DNA repair and genome stability.

    Evidence siRNA knockdown with NHEJ reporters, xenograft irradiation, immunofluorescence, and STIL/CPAP epistasis

    PMID:24811242 PMID:25385835

    Open questions at the time
    • Molecular role in NHEJ not yet mechanistic
    • How RBM14 suppresses centriole assembly unknown
  9. 2015 Medium

    Linked RBM14 to paraspeckle-dependent RNA export, supporting HIV-1 Rev function via NEAT1 integrity.

    Evidence Complexome mining, Rev-dependent reporter, RNA quantification, and NEAT1 depletion epistasis

    PMID:25589658

    Open questions at the time
    • Direct RBM14-Rev contact not mapped
    • Generalizability beyond viral export unclear
  10. 2017 Medium

    Provided mechanistic detail for RBM14 in NHEJ, showing it controls XRCC4/XLF recruitment and KU release at damage sites.

    Evidence Chromatin fractionation, FRAP/immunofluorescence at damage sites, comet and γH2AX assays

    PMID:28426349

    Open questions at the time
    • Direct interactions with NHEJ factors not biochemically resolved
    • Single-lab data
  11. 2019 High

    Demonstrated that RBM14's IDR-driven phase separation is essential for embryonic patterning and that knockout causes DNA damage and altered DDR-gene splicing.

    Evidence In vitro droplet assays, zebrafish chimeric-IDR rescue, CRISPR knockout mouse, RNA-seq, IP-MS

    PMID:31636951 PMID:31794640

    Open questions at the time
    • Composition of physiological condensates incompletely defined
    • Causal link between splicing changes and lethality not fully established
  12. 2020 High

    Defined the recruitment logic and biochemical activity of RBM14 at DSBs: PARP/RNAPII-dependent recruitment and direct binding of RNA:DNA hybrids.

    Evidence Laser microirradiation kinetics, PARP/RNAPII inhibitors, S9.6 detection, RNA:DNA substrate pulldown

    PMID:32094185

    Open questions at the time
    • How hybrid binding promotes repair completion unresolved
    • Distinction between NHEJ and HR roles at hybrids not delineated
  13. 2021 Medium

    Implicated RBM14 in spindle-pole organization through α-tubulin interaction and modulation of tubulin acetylation in oocytes.

    Evidence Oocyte morpholino knockdown, immunofluorescence co-localization, co-IP with α-tubulin

    PMID:33604343

    Open questions at the time
    • Mechanism of acetylation control unknown
    • Relationship to nuclear functions unclear
  14. 2022 High

    Showed RBM14 condensates concentrate maternal mRNAs at spindle poles and recruit PARN to drive deadenylation, controlling zygotic genome activation.

    Evidence Live imaging, in vitro phase separation, m6A/m5C functional tests, PARN co-IP, zebrafish/mouse depletion, RNA-seq

    PMID:36477743

    Open questions at the time
    • RNA modification readers governing recruitment not identified
    • Asymmetric partitioning mechanism incompletely defined
  15. 2023 Medium

    Resolved RBM14's role in homologous recombination, showing it promotes CtIP-dependent resection and RPA/RAD51 loading by binding resected intermediates.

    Evidence RPA-coated ssDNA pulldown, CtIP co-IP, RPA/RAD51 recruitment, HR reporter and irradiation sensitivity

    PMID:37559455

    Open questions at the time
    • Choice between NHEJ and HR engagement not explained
    • Single-lab data
  16. 2024 High

    Identified Ser521 O-GlcNAcylation as a switch controlling RBM14-TRIM33 interaction, OGA stability, and oncogenicity, placing RBM14 in O-GlcNAc homeostasis.

    Evidence MS site mapping, S521A mutagenesis, co-IP, ubiquitination and proteasome assays, oncogenic assays

    PMID:38678556

    Open questions at the time
    • O-GlcNAc transferase responsible not defined here
    • Link to nuclear/splicing functions unexplored
  17. 2024 Medium

    Added antiviral and splicing-partner dimensions: RBM14 restricts PEDV via p62-autophagy and MAVS/TRAF3 interferon signaling, and competes with NONO to control DLG1 splicing.

    Evidence Co-IP, autophagy flux, IFN reporter, viral replication assays; IP/MS and splicing PSI quantification in cancer cells

    PMID:38341127 PMID:38411947

    Open questions at the time
    • Direct vs indirect MAVS engagement unclear
    • Generalizability of NONO competition across transcripts untested
  18. 2025 Medium

    Connected RBM14's RRM-mediated mRNA stabilization to cancer metabolism, stabilizing HK2 mRNA to drive glycolysis and H3K18 lactylation-dependent metastasis programs.

    Evidence RRM1/2 mutagenesis, RIP, mRNA stability and ECAR assays, H3K18la ChIP-seq, metastasis models

    PMID:42062247

    Open questions at the time
    • Breadth of stabilized mRNA targets unknown
    • Specificity of RRM binding not structurally defined
  19. 2025 Low

    Reported USP44-mediated deubiquitination as a stabilizing mechanism protecting RBM14 against radiation-induced damage.

    Evidence Co-IP, ubiquitination assay, knockdown and overexpression rescue with γH2AX and viability readouts

    PMID:41299552

    Open questions at the time
    • Deubiquitination inferred from co-IP and rescue, not directly reconstituted
    • Ubiquitination sites on RBM14 not mapped
    • Largely in vitro

Open questions

Synthesis pass · forward-looking unresolved questions
  • How RBM14's distinct activities—coactivation, splicing, DSB repair, phase-separated condensate formation, and O-GlcNAc homeostasis—are coordinated or partitioned within a single protein, and what determines context-specific engagement, remains unresolved.
  • No unifying structural model integrating RRM and IDR functions
  • Determinants of pathway selection at DSBs (NHEJ vs HR) unknown
  • Cross-talk between PTM control and condensate behavior unexplored

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 3 GO:0060090 molecular adaptor activity 3 GO:0140110 transcription regulator activity 3 GO:0003677 DNA binding 1
Localization
GO:0005815 microtubule organizing center 3 GO:0005634 nucleus 2 GO:0005654 nucleoplasm 1 GO:0005730 nucleolus 1 GO:0005829 cytosol 1
Pathway
R-HSA-73894 DNA Repair 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-8953854 Metabolism of RNA 3 R-HSA-1266738 Developmental Biology 2 R-HSA-168256 Immune System 2
Partners
CREBBPCTIPEP300NONOPARNTRBPTRIM33USP44
Complex memberships
paraspeckle

Evidence

Reading pass · 26 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 CoAA (RBM14) was identified as a TRBP-interacting protein via yeast two-hybrid screening; it contains two RNA recognition motifs (RRMs) and a TRBP-interacting domain. CoAA interacts with both TRBP and p300 in vitro, potently coactivates transcription mediated by multiple hormone-response elements synergistically with TRBP and CBP, and is associated with the DNA-dependent protein kinase–poly(ADP-ribose) polymerase complex. A splice variant, CoAM (lacking the TRBP-interacting domain), strongly represses TRBP and CBP action. Yeast two-hybrid screening, in vitro binding assay, co-immunoprecipitation, transfection-based transcriptional reporter assays The Journal of biological chemistry High 11443112
2004 CoAA (RBM14) mediates both transcriptional coactivation and alternative RNA splicing in a promoter-preferential manner downstream of steroid hormone signaling. Domain-swap experiments showed that the N-terminal RRMs and the C-terminal auxiliary domain are differentially engaged depending on the promoter context, and that this differential domain use underlies the promoter-preferential splicing effects. Transcriptional and splicing reporter assays with domain-swap mutants; promoter-specific functional comparisons Molecular and cellular biology High 14673176
2005 RBM14 (SIP/CoAA) specifically binds the QPGY domain of the proto-oncoprotein SYT and the SYT-SSX2 translocation fusion protein. The YQ domain (hexapeptide repeats) of RBM14 mediates interaction with SYT; the last 84 amino acids adjacent to YQ down-modulate YQ transactivation ~25-fold. SYT and SIP/CoAA cooperate to stimulate estrogen and glucocorticoid receptor-dependent transcriptional activation in a hormone- and hBRM/BRG1-dependent manner. Co-immunoprecipitation, GST pulldown, reporter gene transcriptional assays, deletion/domain mapping The Journal of biological chemistry Medium 16227627
2006 The CoAA (RBM14) gene is amplified at chromosome 11q13 in subsets of primary human cancers (non-small cell lung carcinoma, squamous cell skin carcinoma, lymphoma) with recurrent loss of upstream silencing sequences; CoAA protein is overexpressed in amplified tumors, positively autoregulates its own basal promoter, and displays transforming activity in soft agar assays. Genomic mapping of amplicons, Western blot, transfection reporter assays (autoregulation), soft agar colony assay Oncogene Medium 16878147
2007 CoAA (RBM14) alternative splicing is switched from CoAA to the dominant-negative variant CoAM during stem cell differentiation; this switch is regulated by a cis-regulatory sequence upstream of the CoAA basal promoter, and p54nrb and PSF induce CoAM production through this sequence. CoAM functionally inhibits CoAA; their switched expression upregulates the differentiation marker Sox6. CoAA minigene cassette reporter, retinoic acid-induced P19 differentiation model, overexpression/knockdown of p54nrb and PSF Nucleic acids research Medium 17337438
2009 CoAA (RBM14) was identified as a Runx2 binding protein; its carboxy-terminus is essential for binding the Runt domains of Runx1 and Runx2. CoAA represses Runx factor-dependent transcriptional activation and blocks Runx2-mediated repression of Axin2 in a histone deacetylase-independent manner. CoAA inhibits Runx2–DNA interactions as shown by EMSA. Co-immunoprecipitation, EMSA, reporter gene assays, siRNA knockdown, domain-deletion mapping Journal of cellular biochemistry Medium 19585539
2009 Trans-splicing between CoAA (RBM14) and downstream corepressor RBM4 transcripts generates intergenic splice variants (CoAZ and ncCoAZ) during stem/progenitor cell neural differentiation. CoAA and RBM4 counter-regulate alternative splicing of the target pre-mRNA Tau exon 10; stable expression of CoAA or RBM4 blocks the trans-splicing switch and disrupts embryoid body formation. RT-PCR identification of trans-spliced variants, stable expression and knockdown in neural differentiation model, minigene splicing assays The Journal of biological chemistry Medium 19416963
2011 CoAA (RBM14) interacts with PEA3 group members (ERM, ER81, PEA3) via its YQ domain (tyrosine/glutamine hexapeptide repeats); the two N-terminal RRMs are required for transcriptional enhancement. CoAA is involved in the migration-enhancing action of PEA3 on MCF7 cells. Co-immunoprecipitation, domain-deletion mapping, reporter gene transcriptional assays, cell migration assay The Biochemical journal Medium 21736557
2014 RBM14 controls DNA repair pathways (specifically DNA-PK-dependent non-homologous end joining, NHEJ) and prevents cell differentiation in GBM tumor-initiating cells. Knockdown of RBM14 sensitizes GBM cells to radiation and blocks tumor regrowth after irradiation in vivo. siRNA knockdown, NHEJ reporter assay, in vivo xenograft irradiation model, sphere-formation assay Oncotarget Medium 24811242
2014 RBM14 depletion in human cells induces ectopic formation of centriolar protein complexes through function of the STIL/CPAP complex, which can recruit pericentriolar material, nucleate microtubules, and incorporate HsSAS-6 to form aberrant centriole-like structures, causing multipolar spindle formation and genome instability. siRNA knockdown in human cells, immunofluorescence microscopy, co-localization analysis, spindle assembly assays The EMBO journal Medium 25385835
2015 RBM14 associates with XPO1 (CRM1) and HIV-1 Rev in the nuclear complexome. RBM14 depletion decreases Rev activity and Rev-mediated nuclear export of unspliced viral transcripts; this function depends on paraspeckle integrity (NEAT1 RNA). Overexpressed RBM14 enhancement of Rev function is abolished by NEAT1 depletion. Nuclear complexome mining, siRNA knockdown, Rev-dependent p24 reporter assay, cytoplasmic RNA quantification, NEAT1 depletion Journal of virology Medium 25589658
2017 RBM14 is required for efficient recruitment of XRCC4 and XLF to chromatin and for the release of KU proteins from chromatin upon DNA damage; failure leads to accumulation of double-strand breaks. This places RBM14 as a regulator of NHEJ factor dynamics at damage sites. siRNA knockdown, chromatin fractionation, immunofluorescence/FRAP at damage sites, comet assay, γH2AX quantification Cell cycle (Georgetown, Tex.) Medium 28426349
2017 The lincRNA Paral1 promotes adipogenesis and coactivates PPARγ through physical interaction with RBM14 (NCoAA/RBM14), identifying RBM14 as a mediator of Paral1-dependent transcriptional coactivation of PPARγ. RNA immunoprecipitation (RIP), knockdown and overexpression in adipocyte differentiation model, reporter gene assays Scientific reports Low 29075020
2018 RBM14 localizes to nuclear paraspeckles; upon influenza A virus (IAV) infection, RBM14 relocalizes to the nucleolus. This relocalization is necessary and sufficient through the IAV NS1 protein and requires the double-stranded RNA-binding capacity of NS1. RBM14 was validated as a required host factor for IAV replication. siRNA knockdown (two IAV subtypes, primary and transformed cells), immunofluorescence localization, NS1 overexpression/mutants, viral replication assay mSphere Medium 30429226
2019 Zebrafish Rbm14 regulates embryonic dorsoventral patterning through phase separation mediated by its intrinsically disordered region (IDR). Rbm14 IDR forms liquid droplets in vitro; phase-separation mutants or isolated IDR fail to rescue dorsalized morphant phenotypes, but chimeric proteins with heterologous IDRs from other phase-separating proteins are effective. Rbm14 complexes with proteins involved in RNA metabolism and phase separates into cellular ribonucleoprotein compartments. Zebrafish morpholino knockdown, in vitro phase-separation assays, chimeric protein rescue experiments, RNA-seq (alternative splicing analysis), co-immunoprecipitation Cell discovery High 31636951
2019 Rbm14 knockout in mice causes embryonic lethality due to gastrulation disruption; Rbm14-null ESCs accumulate DNA damage (γH2AX, comet assay) and show altered splicing of DNA damage response genes. IP-MS confirmed RBM14 interaction with alternative splicing-related proteins. CRISPR/Cas9 knockout mouse, histological analysis, γH2AX staining, comet assay, RNA-seq, IP-MS, co-IP Cell proliferation Medium 31794640
2020 RBM14 is recruited to DNA damage sites in a PARP- and RNA polymerase II (RNAPII)-dependent manner. Both KU and RBM14 are required for RNAPII-dependent generation of RNA:DNA hybrids (R-loops) at double-strand break sites; RBM14 directly binds RNA:DNA hybrids. RNA:DNA hybrids and RNAPII are detected at gene-coding and intergenic areas upon DSB induction. Laser microirradiation/live-cell imaging for recruitment kinetics, PARP and RNAPII inhibitor experiments, S9.6 antibody-based RNA:DNA hybrid detection, RBM14 pulldown with RNA:DNA substrates Proceedings of the National Academy of Sciences of the United States of America High 32094185
2021 RBM14 co-localizes with α-tubulin at spindle poles during mouse oocyte meiosis; RBM14 knockdown causes spindle defects, chromosome abnormalities, and α-tubulin hyperacetylation. Co-immunoprecipitation demonstrates RBM14 interaction with endogenous α-tubulin in mammalian cells, suggesting RBM14 modulates tubulin acetylation to regulate spindle morphology. Morpholino knockdown in oocytes, immunofluorescence co-localization, co-immunoprecipitation, spindle perturbation assays Frontiers in cell and developmental biology Medium 33604343
2022 Nuclear RBM14 and maternal mRNAs co-phase separate into cytoplasmic condensates in zebrafish blastomeres. These condensates concentrate at spindle poles by associating with centrosomal γ-tubulin, undergo preferentially asymmetric divisions, and are stimulated by m6A modification but repressed by m5C modification of maternal mRNA. Deadenylase PARN co-phase separates with these condensates, which is required for deadenylation of maternal mRNAs. Rbm14 depletion impairs zygotic genome activation and causes developmental arrest. Live-cell imaging, in vitro phase-separation assay, m6A/m5C modification functional tests, co-IP for PARN interaction, zebrafish and mouse morpholino/knockout, RNA-seq The EMBO journal High 36477743
2022 METTL3-mediated m6A methylation of RBM14 mRNA promotes its expression via YTHDF1 binding. METTL3 knockdown in Kupffer cells suppresses RBM14 expression by decreasing m6A methylation; overexpression of RBM14 rescues the anti-tumor effects of METTL3 depletion, placing RBM14 downstream of the METTL3-YTHDF1 m6A axis. m6A-seq/meRIP, siRNA/shRNA knockdown and overexpression, in vitro and in vivo functional rescue assays Human cell Medium 36087219
2023 RBM14 promotes DNA end resection during homologous recombination (HR) repair by interacting with the HR factor CtIP; RBM14 is required for CtIP recruitment to DSB sites and for subsequent RPA coating and RAD51 replacement. RBM14 was identified as a binding partner of RPA-coated resected DNA intermediates by pulldown assay. ssDNA/dsDNA-RPA pulldown assay, co-immunoprecipitation with CtIP, chromatin recruitment assays (RPA, RAD51), HR reporter assay, irradiation sensitivity assay Acta biochimica et biophysica Sinica Medium 37559455
2024 RBM14 is O-GlcNAcylated at serine 521; this modification regulates its interaction with the E3 ubiquitin ligase TRIM33, which affects OGA (O-GlcNAcase) protein stability through ubiquitin-dependent proteasomal degradation. Mutation S521A abrogates RBM14–TRIM33 interaction, restores OGA levels, and abolishes the oncogenic properties of RBM14. RBM14 thus acts as a regulator of cellular O-GlcNAcylation homeostasis. O-GlcNAc site mapping (mass spectrometry), site-directed mutagenesis (S521A), co-immunoprecipitation, ubiquitination assay, proteasome inhibitor experiments, in vitro and in vivo oncogenic assays Cell reports High 38678556
2024 RBM14 inhibits PEDV replication by (1) recruiting cargo receptor p62 to degrade the viral nucleocapsid (N) protein via the autophagy pathway (RBM14-p62-autophagosome axis), and (2) interacting with mitochondrial antiviral signaling protein (MAVS) and TRAF3 to activate interferon signaling. Co-immunoprecipitation, autophagy flux assay (autophagosome formation), interferon reporter assay, viral replication assay, knockdown/overexpression Journal of virology Medium 38411947
2024 RBM14 binds to NONO and interferes with NONO-mediated DLG1 exon6 skipping in gallbladder cancer cells. IP/MS identified RBM14 as NONO-bound; IGF2BP3 disrupts the RBM14-NONO interaction to promote exon skipping. IP/MS, co-immunoprecipitation, mRNA-seq/RIP-seq, alternative splicing quantification (PSI) Cancer letters Medium 38341127
2025 RBM14 stabilizes HK2 mRNA via its RRM1/2 domains, enhancing HK2 expression and glycolytic capacity in prostate cancer cells; increased glycolysis elevates H3K18 lactylation at promoters of metastasis-related genes, driving their transcriptional upregulation. RNA-binding domain mutagenesis (RRM1/2), RNA immunoprecipitation (RIP), mRNA stability assay, glycolysis assay (ECAR), ChIP-seq for H3K18la, in vitro and in vivo metastasis assays Cell death discovery Medium 42062247
2025 RBM14 deubiquitination by USP44 stabilizes RBM14 protein; stabilization of RBM14 by USP44 (delivered via mesenchymal stem cell-derived extracellular vesicles) counteracts radiation-induced DNA damage, apoptosis, and cell cycle disruption. RBM14 overexpression partially restores cell survival when USP44 is silenced. Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, RBM14 overexpression rescue, DNA damage markers (γH2AX), cell viability assay Stem cell research & therapy Low 41299552

Source papers

Stage 0 corpus · 35 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 CoAA, a nuclear receptor coactivator protein at the interface of transcriptional coactivation and RNA splicing. Molecular and cellular biology 141 14673176
2001 Identification and characterization of RRM-containing coactivator activator (CoAA) as TRBP-interacting protein, and its splice variant as a coactivator modulator (CoAM). The Journal of biological chemistry 116 11443112
1992 Cloning, sequencing, and expression of the pantothenate kinase (coaA) gene of Escherichia coli. Journal of bacteriology 72 1328157
2003 Role of feedback regulation of pantothenate kinase (CoaA) in control of coenzyme A levels in Escherichia coli. Journal of bacteriology 70 12754240
2014 RNA binding protein RBM14 promotes radio-resistance in glioblastoma by regulating DNA repair and cell differentiation. Oncotarget 53 24811242
2020 Intrinsically disordered protein RBM14 plays a role in generation of RNA:DNA hybrids at double-strand break sites. Proceedings of the National Academy of Sciences of the United States of America 36 32094185
2017 RNA-binding protein RBM14 regulates dissociation and association of non-homologous end joining proteins. Cell cycle (Georgetown, Tex.) 36 28426349
2017 The RBM14/CoAA-interacting, long intergenic non-coding RNA Paral1 regulates adipogenesis and coactivates the nuclear receptor PPARγ. Scientific reports 36 29075020
2005 The proto-oncoprotein SYT interacts with SYT-interacting protein/co-activator activator (SIP/CoAA), a human nuclear receptor co-activator with similarity to EWS and TLS/FUS family of proteins. The Journal of biological chemistry 36 16227627
1987 Isolation and characterization of temperature-sensitive pantothenate kinase (coaA) mutants of Escherichia coli. Journal of bacteriology 36 2824448
2014 RBM14 prevents assembly of centriolar protein complexes and maintains mitotic spindle integrity. The EMBO journal 33 25385835
2009 Functional pre- mRNA trans-splicing of coactivator CoAA and corepressor RBM4 during stem/progenitor cell differentiation. The Journal of biological chemistry 32 19416963
2015 Mining the human complexome database identifies RBM14 as an XPO1-associated protein involved in HIV-1 Rev function. Journal of virology 30 25589658
2006 Gene amplification and associated loss of 5' regulatory sequences of CoAA in human cancers. Oncogene 28 16878147
2007 Switched alternative splicing of oncogene CoAA during embryonal carcinoma stem cell differentiation. Nucleic acids research 26 17337438
2022 METTL3 promotes m6A hypermethylation of RBM14 via YTHDF1 leading to the progression of hepatocellular carcinoma. Human cell 23 36087219
2011 Screening, identification, and characterization of mechanistically diverse inhibitors of the Mycobacterium tuberculosis enzyme, pantothenate kinase (CoaA). Journal of biomolecular screening 18 22086722
2009 Co-activator activator (CoAA) prevents the transcriptional activity of Runt domain transcription factors. Journal of cellular biochemistry 18 19585539
2019 Regulation of zebrafish dorsoventral patterning by phase separation of RNA-binding protein Rbm14. Cell discovery 16 31636951
2019 Rbm14 maintains the integrity of genomic DNA during early mouse embryogenesis via mediating alternative splicing. Cell proliferation 15 31794640
2024 O-GlcNAcylation of RBM14 contributes to elevated cellular O-GlcNAc through regulation of OGA protein stability. Cell reports 13 38678556
2022 Maternal mRNA deadenylation and allocation via Rbm14 condensates facilitate vertebrate blastula development. The EMBO journal 13 36477743
2023 RBM14 as a novel epigenetic-activated tumor oncogene is implicated in the reprogramming of glycolysis in lung cancer. World journal of surgical oncology 12 37060064
2024 NONO promotes gallbladder cancer cell proliferation by enhancing oncogenic RNA splicing of DLG1 through interaction with IGF2BP3/RBM14. Cancer letters 11 38341127
2024 RBM14 inhibits the replication of porcine epidemic diarrhea virus by recruiting p62 to degrade nucleocapsid protein through the activation of autophagy and interferon pathway. Journal of virology 11 38411947
2018 RBM14 is indispensable for pluripotency maintenance and mesoderm development of mouse embryonic stem cells. Biochemical and biophysical research communications 10 29729270
2018 Nucleolar Relocalization of RBM14 by Influenza A Virus NS1 Protein. mSphere 10 30429226
1979 Isolation of temperature-sensitive pantothenate kinase mutants of Salmonella typhimurium and mapping of the coaA gene. Journal of bacteriology 10 230178
2021 RBM14 Modulates Tubulin Acetylation and Regulates Spindle Morphology During Meiotic Maturation in Mouse Oocytes. Frontiers in cell and developmental biology 9 33604343
2011 The coactivator activator CoAA regulates PEA3 group member transcriptional activity. The Biochemical journal 8 21736557
2023 RBM14 promotes DNA end resection during homologous recombination repair. Acta biochimica et biophysica Sinica 6 37559455
2025 RBM14 enhances transcriptional activity of p23 regulating CXCL1 expression to induce lung cancer metastasis. Acta pharmaceutica Sinica. B 3 40654360
2026 RBM14 drives prostate cancer metastasis via stabilizing HK2 mRNA to activate glycolysis and H3K18 lactylation. Cell death discovery 0 42062247
2025 Protective effects of mouse bone marrow mesenchymal stem cell-derived extracellular vesicles on radiation-induced epididymal cells damage via USP44/RBM14 axis. Stem cell research & therapy 0 41299552
2024 Molecular mechanism of RBM14-mediated promotion of proliferation, migration, and invasion in osteosarcoma. Translational cancer research 0 38881928

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