Affinage

SRSF9

Serine/arginine-rich splicing factor 9 · UniProt Q13242

Length
221 aa
Mass
25.5 kDa
Annotated
2026-06-10
33 papers in source corpus 29 papers cited in narrative 29 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SRSF9 (SRp30c) is a multifunctional SR-family RNA-binding protein that governs alternative pre-mRNA splicing as both an activator and a repressor depending on its binding context (PMID:12024014, PMID:18534987). As an activator it promotes inclusion of specific exons by engaging exonic splicing enhancers—often indirectly, through a direct protein-protein interaction with hTra2β1 rather than direct RNA contact, as shown for SMN exon 7 (PMID:11875052). As a repressor it binds intronic and exonic silencer elements: it recognizes the intronic CE9 element in hnRNP A1 pre-mRNA to repress 3' splice-site use (PMID:12024014), and it forms an inhibitory heterodimer with SRp55 on tau exons 2 and 10 (PMID:15695522); this repressor activity is antagonized in trans by PTB, which displaces SRSF9 from CE9 (PMID:17548433). Across many transcripts SRSF9 binds short defined sequence elements to direct isoform choice, including AAGAC in CD44 exon v10 (PMID:33143085), AGGAG in Caspase-2 exon 10 (PMID:33808656), and elements in AXIN1 and BNIP3 exons (PMID:38748384, PMID:40675219). Beyond splicing, SRSF9 acts as an mRNA-stabilizing factor, functioning as an m6A reader that binds m6A-modified DSN1 mRNA to stabilize it in a METTL3-dependent manner (PMID:35509101) and stabilizing other targets such as EEF1D, GPX4, and USP22 through 3'UTR or transcript binding (PMID:34336668, PMID:38771720, PMID:39530604), and it enhances β-catenin mRNA translation in an mTOR-dependent manner (PMID:23592547). It also represses ADAR2-mediated A-to-I editing by interacting with ADAR2 through its RRM2 domain to disrupt ADAR2 dimerization (PMID:29992293, PMID:29733375). SRSF9 activity is controlled by post-translational and condensate-level regulation: PRMT1-mediated arginine methylation determines its subnuclear localization (PMID:19557313), and RS-domain-driven liquid-liquid phase separation in the nucleus is required for its splicing function (PMID:40064440, PMID:40773673). Its own expression is set upstream by Mettl1-mediated m7G modification of SRSF9 mRNA and by miR-1/miR-206 targeting of its 3'UTR (PMID:38810124, PMID:31791406).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1999 Medium

    The first SRSF9-interacting partner question—does SRp30c contact other nuclear proteins through a defined domain to influence splicing—was addressed by identifying Nop30 as an RS-domain partner that alters alternative exon usage.

    Evidence Yeast two-hybrid with SRp30c bait, in vitro pulldown, Co-IP, and minigene reporters

    PMID:10196175

    Open questions at the time
    • No direct RNA target of the SRp30c-Nop30 complex defined
    • Physiological splicing substrates not mapped genome-wide
  2. 2002 High

    Whether SRSF9 acts as a splicing activator or repressor was resolved by showing it can do both: it stimulates SMN exon 7 inclusion through hTra2β1 (without direct RNA binding) yet directly binds the intronic CE9 element to repress 3' splice-site use.

    Evidence Co-IP and minigene assays for SMN; RNA affinity chromatography, UV cross-linking, and in vitro splicing with recombinant protein for CE9

    PMID:11875052 PMID:12024014

    Open questions at the time
    • Determinants selecting activator versus repressor mode not defined
    • CE9 repression mechanism on spliceosome assembly not resolved
  3. 2003 Medium

    How SRSF9 partners and localization are coordinated was probed by showing an RNA-independent interaction with YB-1 that controls nuclear co-localization and shifts E1A splice-site choice, linking SRSF9 partnering to subcellular distribution.

    Evidence Yeast two-hybrid, Co-IP, fluorescence localization with heat-shock perturbation, E1A minigene

    PMID:12604611

    Open questions at the time
    • Functional consequence of Sam68-body sequestration not defined
    • Direct RNA targets of the SRSF9-YB-1 complex unknown
  4. 2005 Medium

    The combinatorial logic of SRSF9 with other SR proteins was established by showing it forms an inhibitory SRp55 heterodimer on tau exons and cooperates with Tra2α/9G8 on GnRH pre-mRNA, demonstrating context-dependent partner-driven outcomes.

    Evidence Deletion/binding assays and splicing reporters for tau; RNA binding, Co-IP, and knockdown/overexpression for GnRH

    PMID:15695522 PMID:16249178

    Open questions at the time
    • Structural basis of the SRp55 heterodimer not solved
    • Stoichiometry and assembly order on enhancer/silencer elements unknown
  5. 2007 High

    How SRSF9 repressor activity is counteracted in trans was answered by showing PTB displaces SRSF9 from CE9 and relieves repression, defining an antagonistic regulatory layer.

    Evidence RNA affinity chromatography, SELEX, binding competition, in vitro and in vivo splicing reporters

    PMID:17548433

    Open questions at the time
    • Whether PTB antagonism generalizes beyond CE9 targets untested
    • Cellular signals controlling the PTB/SRSF9 balance unknown
  6. 2008 High

    The role of SRSF9 in apoptotic isoform choice was addressed by showing it binds the B3 region of Bcl-x to favor the anti-apoptotic Bcl-xL isoform, extending its splicing control to cell-fate transcripts.

    Evidence In vitro and in vivo minigene splicing with ML2/AM2 element mutagenesis and RNA-protein binding

    PMID:18534987

    Open questions at the time
    • Upstream regulators directing SRSF9 to Bcl-x in vivo unknown
    • Contribution to apoptosis resistance in disease contexts not tested here
  7. 2009 Medium

    How SRSF9 localization is regulated post-translationally was answered by identifying it as a PRMT1 arginine-methylation substrate whose methylation status governs nucleolar versus nucleoplasmic distribution.

    Evidence In vitro methylation assay, methylarginine-antibody IP, and confocal imaging with methylation inhibitor Adox

    PMID:19557313

    Open questions at the time
    • Specific methylated residues not mapped
    • Functional impact of methylation on splicing activity not measured
  8. 2013 Medium

    Whether SRSF9 acts beyond splicing on protein output was addressed by showing it recruits β-catenin mRNA and enhances its translation via mTOR, linking SRSF9 to Wnt-driven tumorigenesis.

    Evidence Overexpression, mRNA recruitment and mTOR-dependent translation assays, cell-based functional readouts

    PMID:23592547

    Open questions at the time
    • Direct binding element on β-catenin mRNA not mapped
    • Mechanistic link between SRSF9 and mTOR not defined
  9. 2018 High

    The non-splicing role of SRSF9 in RNA editing was established by showing it represses ADAR2-mediated A-to-I editing at brain-specific sites via an RRM2-dependent interaction that disrupts ADAR2 dimerization, with a substrate-RNA-dependent contribution at CaV1.3.

    Evidence Co-IP, RRM2 domain mapping, transcriptome-wide CLIP/RNA-seq, and minigene/RNA-interaction analysis

    PMID:29733375 PMID:29992293

    Open questions at the time
    • Structural basis of ADAR2 dimer disruption not solved
    • Why SRSF9 selects brain-specific editing sites unclear
  10. 2019 Medium

    How SRSF9 abundance is set in a developmental context was answered by showing miR-1/miR-206 target its 3'UTR to clear SRSF9 during myogenesis, with persistent expression blocking myotube formation.

    Evidence Luciferase reporters, miRNA-resistant 3'UTR rescue, and C2C12 differentiation time course

    PMID:31791406

    Open questions at the time
    • Direct splicing/stability targets driving the myogenic block not identified
    • Generalizability beyond C2C12 unknown
  11. 2022 Medium

    How SRSF9 stabilizes target mRNAs was clarified by showing it functions as an m6A reader binding m6A-modified DSN1 mRNA in a METTL3-dependent manner, defining a reader-mediated stabilization mechanism distinct from splicing.

    Evidence Methylated ssRNA affinity assay, gene-specific m6A qPCR, RNA stability and reporter assays, RIP, METTL3 knockdown

    PMID:35509101

    Open questions at the time
    • Reader domain on SRSF9 mediating m6A recognition not mapped
    • Breadth of the m6A-dependent stabilization program unknown
  12. 2024 Medium

    Upstream control of SRSF9 expression by RNA modification was established by showing Mettl1-mediated m7G of SRSF9 mRNA raises SRSF9 levels, which then drive NFATc4 splicing/stabilization and cardiac hypertrophy, embedding SRSF9 in an epitranscriptomic regulatory axis.

    Evidence m7G modification assays, cardiac-specific mouse overexpression/knockout, TAC/Ang II models, knockdown

    PMID:38810124

    Open questions at the time
    • Direct NFATc4 binding elements not fully mapped
    • Whether m7G control of SRSF9 operates outside heart unknown
  13. 2025 Medium

    The biophysical requirement underlying SRSF9 splicing activity was answered by showing its RS domain drives nuclear liquid-liquid phase separation that is indispensable for splicing regulation, with m6A competing at target transcripts such as NUMB.

    Evidence FRAP, live-cell imaging, LLPS inhibitors, RS-domain mutagenesis, minigene reporters, and m6A competition assays

    PMID:40064440 PMID:40773673

    Open questions at the time
    • Composition and partners of SRSF9 condensates not defined
    • How m6A excludes SRSF9 from target RNA at the molecular level unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • What determines, on a given transcript, whether SRSF9 acts as splicing activator, splicing repressor, mRNA stabilizer, translation enhancer, or editing repressor remains unresolved.
  • No unified rule linking binding-element context, post-translational state, and condensate behavior to functional outcome
  • No high-resolution structure of SRSF9 bound to RNA or partner proteins

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 8 GO:0140110 transcription regulator activity 3 GO:0045182 translation regulator activity 1 GO:0048018 receptor ligand activity 1 GO:0140098 catalytic activity, acting on RNA 1
Localization
GO:0005634 nucleus 4 GO:0005730 nucleolus 1
Pathway
R-HSA-8953854 Metabolism of RNA 4 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-162582 Signal Transduction 2
Partners
ADAR2NOP30PTBP1SRSF6TRA2BYBX1

Evidence

Reading pass · 29 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 SRp30c (SRSF9) stimulates SMN exon 7 inclusion in SMN2-derived transcripts, but does not directly bind SMN exon 7; instead, its association with the AG-rich exonic splice enhancer is mediated by a direct protein-protein interaction with hTra2β1, requiring the hTra2β1 binding site on exon 7. Transient expression, co-immunoprecipitation, minigene splicing assays Human molecular genetics Medium 11875052
2002 SRp30c (SRSF9) functions as a repressor of 3' splice site utilization: it binds specifically to the intronic CE9 element (with the first 7 nucleotides sufficient) in hnRNP A1 pre-mRNA via RNA affinity chromatography, and recombinant SRp30c promotes splicing repression in vitro in a CE9-dependent manner. The closest homologue ASF/SF2 does not bind CE9 and does not repress splicing. RNA affinity chromatography, UV cross-linking, in vitro splicing assays, recombinant protein binding, mutagenesis Molecular and cellular biology High 12024014
2003 SRp30c (SRSF9) directly interacts with the multifunctional RNA/DNA-binding protein YB-1 via two independent protein domains of YB-1 (high-affinity interaction through YB-1 N-terminal region), in the absence of RNA. This interaction is RNA-independent and controls subcellular localization: overexpression of both proteins leads to co-localization in the nucleus, and heat shock, which sequesters SRp30c to Sam68 nuclear bodies, causes YB-1 to shuttle back to the cytoplasm. The YB-1/SRp30c interaction functionally shifts E1A minigene splice site selection toward the 12S isoform. Yeast two-hybrid screen, co-immunoprecipitation, subcellular localization by fluorescence microscopy, E1A minigene splicing assay The Journal of biological chemistry Medium 12604611
1999 SRp30c (SRSF9) interacts with the nuclear protein Nop30 via the RS domain of SRp30c; Nop30 was identified by yeast two-hybrid screen using SRp30c as bait, and confirmed by in vitro protein interaction assays and co-immunoprecipitation. Overexpression of Nop30 alters alternative exon usage in preprotachykinin and SRp20 reporter genes. Yeast two-hybrid screen, in vitro protein interaction assay, co-immunoprecipitation, minigene reporter splicing assay The Journal of biological chemistry Medium 10196175
2005 SRp30c (SRSF9) and SRp55 form a heterodimer that binds to splicing silencers at the 5' end of tau exons 2 and 10, inhibiting inclusion of both exons. In tau exon 2, hTra2β1 binds the inhibitory heterodimer through its RS1 domain but not directly to exon 2. In tau exon 10, the SRp30c/SRp55 heterodimer may sterically interfere with hTra2β1 binding to a purine-rich enhancer. FTDP-17 mutation N279K in exon 10 abolishes SRp30c binding. Deletion analysis, in vitro binding assays, splicing reporter assays, mutagenesis The Journal of biological chemistry Medium 15695522
2004 SRp30c (SRSF9) enhances splicing of tau exon 10 in vitro through interaction with an exonic splicing enhancer (ESE) in tau exon 10 (nucleotides 12-45). SRp30c associated with the ESE indirectly (via nuclear extract components), as determined by binding assay. Exon trapping, in vitro splicing assay, binding assay with nuclear extracts Genes to cells Low 15009090
2007 hnRNP I/PTB antagonizes the splicing repressor activity of SRp30c (SRSF9): PTB reduces SRp30c binding to the CE9 element, stimulates splicing to a downstream 3' splice site, and relieves CE9-mediated splicing repression in vitro. Elevated PTB in vivo also alleviates CE9-imposed repression, establishing PTB as an anti-repressor counteracting SRp30c. RNA affinity chromatography, SELEX, in vitro splicing assay, in vivo splicing reporter, His-tagged protein binding competition RNA High 17548433
2007 Bombesin induces expression of SRp30c (SRSF9) in prostate cancer PC-3 cells, and siRNA-mediated knockdown of SRp30c specifically antagonizes bombesin's effect on glucocorticoid-mediated inhibition, indicating that SRp30c regulates GR pre-mRNA alternative splicing to produce the GRβ isoform in response to bombesin. Western blotting, real-time PCR, siRNA knockdown, functional cell assay Biochimica et biophysica acta Low 17540466
2008 SRp30c (SRSF9) binds to two exonic elements (ML2 and AM2) within the 86-nucleotide B3 region immediately upstream of the Bcl-xL 5' splice site, and shifts alternative splicing toward the Bcl-xL (anti-apoptotic) isoform in an ML2/AM2-dependent manner both in vitro and in vivo. This activity antagonizes upstream cryptic U1 snRNP binding sites that repress Bcl-xL usage. In vitro splicing assay, in vivo minigene reporter, mutagenesis of ML2/AM2 elements, RNA-protein binding analysis The Journal of biological chemistry High 18534987
2009 SRSF9 (SFRS9) is a substrate for PRMT1-mediated arginine methylation in vitro, is immunoprecipitated from HEK-293 lysates by antibodies recognizing mono- and dimethylated arginines, and arginine methylation controls its subnuclear localization: inhibition of methylation by Adox causes EGFP-SFRS9 to relocalize to nucleolar dot-like structures. In vitro methylation assay, immunoprecipitation with methylarginine antibodies, confocal microscopy with EGFP-SFRS9 and methylation inhibitor Adox Cellular & molecular biology letters Medium 19557313
2005 SRp30c (SRSF9) cooperates with Tra2α and 9G8 in GnRH pre-mRNA splicing: SRp30c specifically binds both ESE3 and ESE4 in GnRH exons, and Tra2α can interact with SRp30c (but no interaction between 9G8 and SRp30c was detected). Overexpression and knockdown studies in cultured cells confirm that all three SR proteins are required for intron A excision. RNA-protein binding assay, co-immunoprecipitation for protein-protein interaction, overexpression and knockdown in cells, minigene splicing reporter The Journal of biological chemistry Medium 16249178
2013 SRSF9 promotes β-catenin accumulation by recruiting β-catenin mRNA and enhancing its translation in an mTOR-dependent manner, thereby promoting Wnt signaling-mediated tumorigenesis. Overexpression, mRNA recruitment assay, mTOR-dependent translation assay, cell-based functional assays EMBO molecular medicine Medium 23592547
2018 SRSF9 selectively represses ADAR2-mediated A-to-I RNA editing at many brain-specific sites. Mechanistically, SRSF9 biochemically interacts with ADAR2 in the nucleus via its RRM2 domain, in an RNA substrate-dependent manner, and this interaction disrupts ADAR2 dimer formation. Transcriptome-wide CLIP identified 1328 editing sites directly controlled by SRSF9, enriched for brain-specific sites. Co-immunoprecipitation, domain mapping (RRM2), transcriptome-wide CLIP/RNA-seq, gene perturbation experiments, minigene analysis Nucleic acids research High 29992293
2018 SRSF9 inhibits ADAR2-mediated A-to-I editing of CaV1.3 mRNA in a direct RNA interaction-dependent manner (not requiring protein-protein contact alone). Selective downregulation of SRSF9 in neurons provides the mechanistic basis for neuron-specific editing of CaV1.3 transcripts. The editing requires a 40 bp RNA duplex between exon 41 and an intronic ECS. Minigene reporter assay, SRSF9 heterologous expression, RNA interaction analysis, neuronal expression profiling Nucleic acids research Medium 29733375
2019 miR-1 and miR-206 directly target the 3'UTR of Srsf9 mRNA to reduce its expression during myoblast differentiation; persistent Srsf9 expression impairs myotube formation and blunts induction of myogenin (early) and Myh8 (late) differentiation markers, establishing miRNA-mediated clearance of Srsf9 as a key myogenic event. Reporter gene assays (luciferase), stable cDNA expression with heterologous miRNA-resistant 3'UTR, C2C12 differentiation time course, fusion index and myogenic marker measurement Skeletal muscle Medium 31791406
2020 SRSF9 inhibits CD44 exon v10 inclusion, acting antagonistically to Tra2β which promotes inclusion. SRSF9 binds the AAGAC sequence in the v10 exon, whereas Tra2β binds GAAGAAG. Both proteins target the v10 exon directly. Overexpression/knockdown splicing assays, mutagenesis of binding sites, in vitro RNA binding Cancers Medium 33143085
2021 SRSF9 regulates alternative splicing of Caspase-2 cassette exon 9 by binding the AGGAG sequence in exon 10 downstream of the cassette exon; knockdown increases exon 9 inclusion (pro-apoptotic isoform) while overexpression decreases it. Deletion and substitution mutagenesis showed exon 9, intron 9, and exon 8 are not required, but the AGGAG element in exon 10 is essential. RNA pulldown confirmed direct SRSF9-exon 10 binding. Knockdown/overexpression, deletion mutagenesis, substitution mutagenesis, RNA pulldown with immunoblotting, RNA-seq Cells Medium 33808656
2021 SRSF9 knockdown in colorectal cancer cells reduces GPX4 protein expression, promoting ferroptosis sensitivity to erastin. SRSF9 overexpression upregulates GPX4 and confers erastin resistance. RNA immunoprecipitation confirmed SRSF9 binds GPX4 mRNA directly. shRNA knockdown, overexpression, RNA immunoprecipitation (RIP), Western blot, in vivo xenograft Frontiers in oncology Medium 34336668
2022 SRSF9 functions as an m6A-binding protein ('reader') that binds to m6A-modified DSN1 mRNA in CRC cells in an m6A motif- and dose-dependent manner, thereby stabilizing DSN1 mRNA. This stabilization is impaired upon METTL3 knockdown. Two m6A modification sites in the SRSF9-binding region of DSN1 mRNA were identified. Methylated ssRNA affinity assay, gene-specific m6A qPCR, RNA stability assay, dual-luciferase reporter, RIP, METTL3 knockdown Journal of translational medicine Medium 35509101
2022 SRSF9 overexpression inhibits HIV-1 production and infectivity in HEK293T and MT-4 cells by inducing imbalanced viral mRNA splicing (increasing multiply-spliced forms such as Vpr mRNA). Deletion analysis of SRSF9 showed the RRM domain is required for the anti-HIV-1 effects. Overexpression in cell lines, deletion analysis, viral production and infectivity assays, RT-PCR for viral mRNA isoforms BMB reports Low 36330710
2024 Mettl1 increases SRSF9 expression by inducing m7G modification of SRSF9 mRNA. SRSF9 in turn promotes alternative splicing and stabilization of NFATc4, driving cardiac hypertrophy. SRSF9 knockdown protects against TAC- or Mettl1-induced cardiac hypertrophic phenotypes in vivo and in vitro. m7G RNA modification assay, cardiac-specific overexpression and knockout mouse models, TAC/Ang II models, knockdown experiments, in vivo/in vitro cardiac hypertrophy readouts Advanced science Medium 38810124
2024 SRSF9 promotes production of the truncated AXIN1-S isoform (exon 9 skipping) by interacting with sequences in exons 8 and 10 of AXIN1 pre-mRNA, as confirmed by UV crosslink RIP, RNA pulldown, and RIP assays. AXIN1-S activates Wnt/β-catenin signaling and promotes HCC metastasis. UV crosslink RNA immunoprecipitation, RNA pulldown, RIP, wound healing and Transwell assays, in vivo nude mouse metastasis model Molecular and cellular biochemistry Medium 38748384
2024 CLK2 regulates SRSF9 expression/activity, and SRSF9 binds to and promotes inclusion of the cryptic exon 3 of ARV7 at the alternative C allele of SNP rs5918762, increasing ARV7 expression. CLK family inhibitors reduce ARV7 expression through this CLK2/SRSF9 axis. RNA binding assay, splicing reporter assay, SNP allele-specific analysis in cell models and patient specimens, CLK inhibitor treatment Molecular oncology Medium 39258426
2024 SRSF9 binds to the 3'UTR of EEF1D mRNA, stabilizing it and upregulating EEF1D expression in colorectal cancer, as confirmed by RNA immunoprecipitation and RNA pull-down assay. EEF1D knockdown reverses the malignant phenotype induced by SRSF9 overexpression. RNA immunoprecipitation, RNA pull-down, Western blot, functional cell assays, in vivo xenograft International journal of cancer Medium 38771720
2024 SRSF9 binds USP22 mRNA, increasing its stability, thereby promoting USP22 expression. USP22 in turn mediates deubiquitination of ZEB1, and ZEB1 transcriptionally activates SRSF9, forming a positive feedback loop that drives ovarian cancer progression. RNA pull-down, RIP, actinomycin D mRNA stability assay, Co-IP for USP22-ZEB1, ChIP, dual-luciferase reporter assay Cancer biology & therapy Medium 39530604
2025 SRSF9 undergoes liquid-liquid phase separation (LLPS) driven by its arginine-serine-rich (RS) domain in the nucleus. LLPS is required for SRSF9's regulatory role in alternative splicing of SLC37A4 exon 7; disruption of LLPS by inhibitors or RS-domain mutants prevents SRSF9-mediated splicing regulation. FRAP, live-cell immunofluorescence, LLPS inhibitors, RS-domain mutagenesis, minigene reporter, in vivo/in vitro cancer assays Journal of advanced research Medium 40064440
2025 SRSF9 recognizes non-m6A-modified NUMB mRNA and drives an oncogenic isoform switch in ovarian cancer; NUMB mRNA m6A modification antagonizes SRSF9-mediated alternative splicing. SRSF9 forms phase-separated condensates in the nucleus that are indispensable for its splicing function. Phase separation assays, m6A modification analysis, minigene splicing reporter, gain/loss of function, in vivo tumor assays, antisense oligonucleotide isoform switch Cancer research Medium 40773673
2025 SRSF9 directly controls alternative splicing of BNIP3 by binding to its third exon, generating two isoforms: BNIP3-FL promotes canonical autophagy by interacting with the BCL-2-BECN1 complex, while BNIP3-Δ3 (lacking exon 3) instead promotes the Warburg effect and confers chemoresistance to paclitaxel. SRSF9 expression is reduced under hypoxia, which tips the balance toward BNIP3-Δ3. Pooled shRNA screen, direct binding assay (SRSF9 to BNIP3 exon 3), BNIP3 isoform splicing assays, BCL-2-BECN1 interaction assay, metabolic assays, in vitro and in vivo functional assays The Journal of biological chemistry Medium 40675219
2025 SRSF9 promotes exon 2 inclusion in Mecp2 pre-mRNA alternative splicing via an exonic splicing enhancer (ESE) in exon 2, likely through exon recognition mediated by strong adjacent splice sites. Minigene splicing reporter assay, ESE deletion/mutagenesis analysis International journal of molecular sciences Low 40244165

Source papers

Stage 0 corpus · 33 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 SRp30c-dependent stimulation of survival motor neuron (SMN) exon 7 inclusion is facilitated by a direct interaction with hTra2 beta 1. Human molecular genetics 121 11875052
2003 Splicing factor SRp30c interaction with Y-box protein-1 confers nuclear YB-1 shuttling and alternative splice site selection. The Journal of biological chemistry 104 12604611
2013 SRSF1 and SRSF9 RNA binding proteins promote Wnt signalling-mediated tumorigenesis by enhancing β-catenin biosynthesis. EMBO molecular medicine 101 23592547
2011 Tumor suppressive microRNA-1 mediated novel apoptosis pathways through direct inhibition of splicing factor serine/arginine-rich 9 (SRSF9/SRp30c) in bladder cancer. Biochemical and biophysical research communications 74 22178073
2008 Antagonistic effects of the SRp30c protein and cryptic 5' splice sites on the alternative splicing of the apoptotic regulator Bcl-x. The Journal of biological chemistry 63 18534987
2005 Tau exons 2 and 10, which are misregulated in neurodegenerative diseases, are partly regulated by silencers which bind a SRp30c.SRp55 complex that either recruits or antagonizes htra2beta1. The Journal of biological chemistry 62 15695522
2004 Tra2 beta, SF2/ASF and SRp30c modulate the function of an exonic splicing enhancer in exon 10 of tau pre-mRNA. Genes to cells : devoted to molecular & cellular mechanisms 57 15009090
2002 SRp30c is a repressor of 3' splice site utilization. Molecular and cellular biology 54 12024014
2024 The m7G Methyltransferase Mettl1 Drives Cardiac Hypertrophy by Regulating SRSF9-Mediated Splicing of NFATc4. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 41 38810124
2007 hnRNP I/PTB can antagonize the splicing repressor activity of SRp30c. RNA (New York, N.Y.) 41 17548433
2021 Inhibition of SRSF9 enhances the sensitivity of colorectal cancer to erastin-induced ferroptosis by reducing glutathione peroxidase 4 expression. The international journal of biochemistry & cell biology 38 33609745
2022 SRSF9 promotes colorectal cancer progression via stabilizing DSN1 mRNA in an m6A-related manner. Journal of translational medicine 37 35509101
2007 Bombesin attenuates pre-mRNA splicing of glucocorticoid receptor by regulating the expression of serine-arginine protein p30c (SRp30c) in prostate cancer cells. Biochimica et biophysica acta 35 17540466
1999 Alternative splicing determines the intracellular localization of the novel nuclear protein Nop30 and its interaction with the splicing factor SRp30c. The Journal of biological chemistry 35 10196175
2021 Knockdown of SFRS9 Inhibits Progression of Colorectal Cancer Through Triggering Ferroptosis Mediated by GPX4 Reduction. Frontiers in oncology 34 34336668
2018 SRSF9 selectively represses ADAR2-mediated editing of brain-specific sites in primates. Nucleic acids research 27 29992293
2018 Tissue-selective restriction of RNA editing of CaV1.3 by splicing factor SRSF9. Nucleic acids research 24 29733375
2009 Arginine methylation analysis of the splicing-associated SR protein SFRS9/SRP30C. Cellular & molecular biology letters 18 19557313
2023 Cisplatin-induced PANDAR-Chemo-EVs contribute to a more aggressive and chemoresistant ovarian cancer phenotype through the SRSF9-SIRT4/SIRT6 axis. Journal of gynecologic oncology 17 37921598
2019 miR-1/206 downregulates splicing factor Srsf9 to promote C2C12 differentiation. Skeletal muscle 14 31791406
2021 SRSF9 Regulates Cassette Exon Splicing of Caspase-2 by Interacting with Its Downstream Exon. Cells 13 33808656
2005 Cooperative actions of Tra2alpha with 9G8 and SRp30c in the RNA splicing of the gonadotropin-releasing hormone gene transcript. The Journal of biological chemistry 11 16249178
2020 Opposite Roles of Tra2β and SRSF9 in the v10 Exon Splicing of CD44. Cancers 9 33143085
2025 SRSF9 mediates oncogenic RNA splicing of SLC37A4 via liquid-liquid phase separation to promote oral cancer progression. Journal of advanced research 7 40064440
2024 The truncated AXIN1 isoform promotes hepatocellular carcinoma metastasis through SRSF9-mediated exon 9 skipping. Molecular and cellular biochemistry 6 38748384
2024 SRSF9 promotes cell proliferation and migration of glioblastoma through enhancing CDK1 expression. Journal of cancer research and clinical oncology 5 38842611
2024 Targeting the CLK2/SRSF9 splicing axis in prostate cancer leads to decreased ARV7 expression. Molecular oncology 5 39258426
2024 EEF1D stabilized by SRSF9 promotes colorectal cancer via enhancing the proliferation and metastasis. International journal of cancer 4 38771720
2022 Investigation of the effect of SRSF9 overexpression on HIV-1 production. BMB reports 3 36330710
2025 Identification of SRSF9 through pooled shRNA screening links BNIP3 splicing to autophagy and metabolic reprogramming in breast cancer. The Journal of biological chemistry 2 40675219
2024 A positive feedback loop of SRSF9/USP22/ZEB1 promotes the progression of ovarian cancer. Cancer biology & therapy 2 39530604
2025 SRSF9 Forms Phase-Separated Condensates to Promote Ovarian Cancer Progression by Inducing RNA Alternative Splicing That Is Inhibited by m6A Modification. Cancer research 1 40773673
2025 SRSF9-Mediated Exon Recognition Promotes Exon 2 Inclusion in Mecp2 Pre-mRNA Alternative Splicing. International journal of molecular sciences 0 40244165

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