Affinage

CSTF2

Cleavage stimulation factor subunit 2 · UniProt P33240

Length
577 aa
Mass
61.0 kDa
Annotated
2026-04-28
39 papers in source corpus 24 papers cited in narrative 24 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CSTF2 (CstF-64) is the RNA-binding subunit of the cleavage stimulation factor (CstF) complex and a central regulator of pre-mRNA 3′-end processing, alternative polyadenylation (APA), and replication-dependent histone mRNA 3′ maturation. Its N-terminal RRM domain recognizes GU/U-rich downstream sequence elements through an electrostatically driven, multistep binding mechanism in which the C-terminal α-helix of the RRM unfolds upon RNA engagement, propagating a conformational change into the hinge domain that nucleates polyadenylation complex assembly (PMID:12773396, PMID:35090899, PMID:39305233). The hinge domain mediates mutually exclusive interactions with CstF-77 — required for nuclear import and canonical cleavage/polyadenylation — and with symplekin, which is essential for histone RNA 3′ processing; CstF-64 protein levels are rate-limiting for CstF complex formation, and altering its concentration directly shifts poly(A) site choice, as demonstrated by IgM heavy-chain switching, genome-wide APA changes in a mouse D50A knock-in, and 3′UTR shortening of specific transcripts that affects mRNA stability and m6A deposition (PMID:8945520, PMID:21119002, PMID:32816001, PMID:37816727). Loss of CstF-64 causes aberrant polyadenylation of histone mRNAs, cell-cycle arrest, loss of pluripotency in embryonic stem cells, and failure of endoderm differentiation, establishing it as essential for both housekeeping RNA processing and developmental gene regulation (PMID:9885564, PMID:24957598, PMID:25460602).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1996 High

    Establishing that CstF-64 is the rate-limiting factor for CstF assembly and APA-mediated immunoglobulin class switching resolved how a stoichiometric change in a single polyadenylation factor could redirect gene expression.

    Evidence Reconstituted in vitro polyadenylation with overexpression in B cells and gel-shift affinity measurements

    PMID:8945520

    Open questions at the time
    • Mechanism by which CstF-64 levels are themselves regulated during B-cell activation
    • Whether other APA targets respond similarly to CstF-64 dosage
  2. 1996 High

    Showing that CstF-64 concentrates in transcription-dependent nuclear 'cleavage bodies' linked its function to active transcription sites rather than a diffuse nuclear pool.

    Evidence Immunofluorescence, immunogold EM, and transcription inhibition with α-amanitin/DRB

    PMID:8654386

    Open questions at the time
    • Identity of signals that recruit CstF-64 to cleavage bodies
    • Whether cleavage body localization is required for processing efficiency
  3. 1998 High

    Genetic depletion of CstF-64 in DT40 cells demonstrated that it is essential for viability, with graded reduction causing IgM mRNA loss, G0/G1 arrest, and apoptosis — proving CstF-64 is not merely a polyadenylation accessory but a cell-growth regulator.

    Evidence Regulatable transgene replacement in DT40 chicken B cells with cell-cycle and viability assays

    PMID:9885564

    Open questions at the time
    • Which specific mRNA targets mediate the cell-cycle arrest phenotype
    • Whether the growth arrest is solely APA-dependent or involves additional functions
  4. 2003 High

    Solving the NMR structure of the CstF-64 RRM revealed that UU dinucleotide recognition occurs within a defined pocket and that the C-terminal α-helix unfolds upon RNA binding to expose the hinge domain, providing the first structural model for how RNA recognition triggers polyadenylation complex assembly.

    Evidence NMR structure determination of CstF-64 RRM with RNA-binding assays

    PMID:12773396

    Open questions at the time
    • Structure of the full-length protein or CstF holocomplex
    • How the conformational change is transmitted to downstream factors
  5. 2005 High

    NMR relaxation dynamics showed that the RNA-binding surface of the RRM becomes mobile on the μs–ms timescale upon binding GU-rich RNA, establishing that sequence discrimination relies on dynamic rather than static complementarity.

    Evidence NMR relaxation experiments comparing free and RNA-bound CstF-64 RRM with multiple RNA substrates

    PMID:15769465

    Open questions at the time
    • Whether dynamics-based discrimination operates identically in the context of the full CstF complex
    • Thermodynamic decomposition of the selectivity mechanism
  6. 2006 High

    Determination of the C-terminal domain structure as a three-helix bundle and identification of its interaction with Pcf11 distinguished CstF-64's role in 3′-end cleavage from its dispensability in transcription termination.

    Evidence NMR structure of the CTD, mutagenesis, and yeast functional assays for processing vs. termination

    PMID:17116658

    Open questions at the time
    • Whether the human ortholog uses the same surface for Pcf11/PCF11 interaction
    • Whether additional partners bind this domain
  7. 2009 High

    Mapping the hinge domain as the site of mutually exclusive binding to CstF-77 (for nuclear import and polyadenylation) or symplekin (for histone 3′ processing) defined how a single protein partitions between two distinct 3′-end processing pathways.

    Evidence Reciprocal separation-of-function mutants analyzed by SLAP assay, histone processing assay, and nuclear/cytoplasmic fractionation

    PMID:19887456 PMID:21119002

    Open questions at the time
    • Whether switching between CstF-77 and symplekin is regulated by post-translational modification
    • Structural basis of mutual exclusivity
  8. 2009 High

    Demonstration that enterovirus 71 3Cpro cleaves CstF-64 at specific sites to shut down host polyadenylation — rescuable by recombinant CstF-64 — established CstF-64 as a viral target for host gene expression shutoff.

    Evidence In vitro cleavage with wild-type/mutant 3Cpro, serial mutagenesis, polyadenylation rescue assay

    PMID:19779565

    Open questions at the time
    • Whether other viruses target CstF-64 by analogous mechanisms
    • In vivo relevance during natural infection
  9. 2014 High

    CstF-64 knockout in mouse ESCs revealed its requirement for proper histone mRNA 3′ processing, pluripotency maintenance, and endoderm differentiation, extending its biological role from constitutive RNA processing to developmental competence.

    Evidence CstF-64 KO ESCs with histone mRNA polyadenylation assay, cell-cycle analysis, lineage differentiation, and conditioned-medium rescue

    PMID:24957598 PMID:25460602

    Open questions at the time
    • Which specific histone mRNA or APA changes drive the pluripotency loss
    • Whether tauCstF-64 can partially compensate in vivo
  10. 2020 High

    A D50A missense mutation in the RRM altered its electrostatic potential and RNA affinity, changing poly(A) site usage in >1300 genes critical for brain development in mice, directly linking RRM biophysics to genome-wide APA and organismal phenotype.

    Evidence NMR of mutant RRM, reporter C/P assay, D50A knock-in mouse with genome-wide poly(A) site profiling

    PMID:32816001

    Open questions at the time
    • Precise neurological phenotype and behavioral consequences in the mouse model
    • Whether similar mutations occur in human neurodevelopmental disease
  11. 2022 High

    Biophysical dissection showed that electrostatic attraction dominates CstF-64 RRM–RNA binding with enthalpy–entropy compensation, and that a trade-off exists between high-affinity RNA binding and efficient cleavage/polyadenylation in vivo.

    Evidence NMR, ITC/SPR thermodynamics, mutagenesis, in vivo C/P assays

    PMID:35090899

    Open questions at the time
    • How the affinity–efficiency trade-off is tuned under different physiological conditions
    • Role of post-translational modifications in modulating RRM electrostatics
  12. 2023 Medium

    CSTF2 was shown to co-transcriptionally influence m6A deposition by slowing RNA Pol II elongation, revealing a previously unrecognized link between polyadenylation factor binding and epitranscriptomic modification.

    Evidence MeRIP-seq in PDAC tissues, Pol II elongation rate assays, CSTF2 manipulation, IGF2BP2 RIP

    PMID:37816727

    Open questions at the time
    • Whether elongation-rate modulation is a general property of CSTF2 or context-specific
    • Direct measurement of Pol II speed changes at single-gene resolution
    • Independent replication in non-cancer cells
  13. 2025 Medium

    Studies in pancreatic cancer and renal fibrosis showed CSTF2-driven 3′UTR shortening of specific mRNAs (PGK1, CXCL10, FGF2) alters their stability, m6A landscape, and downstream signaling, illustrating how CSTF2-mediated APA reprograms gene expression in disease contexts.

    Evidence RIP, APA assays, poly(A) tail length assays, knockdown/overexpression, xenografts, organoids, and UUO mouse model

    PMID:36113752 PMID:39514400 PMID:39972059

    Open questions at the time
    • Whether CSTF2 is a direct therapeutic target or a downstream effector
    • Genome-wide specificity of CSTF2-mediated APA changes in these disease settings
    • Independent validation of the YTHDC1–CSTF2 recruitment axis

Open questions

Synthesis pass · forward-looking unresolved questions
  • No high-resolution structure of the full CstF complex or of CstF-64 bound simultaneously to RNA and a protein partner exists; the mechanisms that regulate CstF-64 protein levels, its post-translational modifications, and the logic by which it selects specific poly(A) sites genome-wide remain incompletely defined.
  • Full CstF complex structure
  • Regulation of CstF-64 protein turnover
  • Genome-wide rules for poly(A) site selectivity by CstF-64 in vivo

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 7 GO:0098772 molecular function regulator activity 6 GO:0140098 catalytic activity, acting on RNA 3
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 1
Pathway
R-HSA-8953854 Metabolism of RNA 7 R-HSA-1266738 Developmental Biology 2 R-HSA-1640170 Cell Cycle 2 R-HSA-74160 Gene expression (Transcription) 2
Partners
AFF1AFF4CPSF2CSTF3IGF2BP2PCF11SYMPKYTHDC1
Complex memberships
CstF (cleavage stimulation factor)symplekin–CPSF–CstF histone processing complex

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 CstF-64 is limiting for formation of intact CstF complex, CstF has higher affinity for the IgM μm poly(A) site than the μs site, and overexpression of CstF-64 is sufficient to switch IgM heavy chain expression from membrane-bound to secreted form in a reconstituted in vitro processing reaction. Reconstituted in vitro polyadenylation/processing assay, overexpression in B cells, gel-shift/affinity assays Cell High 8945520
1996 CstF-64 and CPSF-100 are concentrated in discrete nuclear foci ('cleavage bodies') closely associated with coiled bodies; transcription inhibition causes complete co-localization of cleavage bodies with coiled bodies, indicating a transcription-dependent dynamic interaction. Immunofluorescence, monoclonal antibody labeling, electron microscopy immunogold double-labeling, transcription inhibition with α-amanitin/DRB The EMBO journal High 8654386
1998 Reducing CstF-64 concentration 10-fold specifically and dramatically reduces IgM heavy chain mRNA accumulation; further reduction causes reversible G0/G1 cell cycle arrest, and depletion causes apoptotic cell death, demonstrating CstF-64 plays roles in regulating gene expression and cell growth in B cells. Gene disruption and regulatable transgene replacement in DT40 B cell line; cell growth and cell cycle assays Molecular cell High 9885564
2003 The N-terminal RRM of CstF-64 recognizes GU-rich downstream elements; the C-terminal helix of the RRM unfolds upon RNA binding and extends into the hinge domain where interactions with other polyadenylation complex factors occur, suggesting this conformational change initiates polyadenylation complex assembly. UU dinucleotides are specifically recognized within an RRM pocket. NMR structure determination of CstF-64 RRM domain, RNA-binding assays The EMBO journal High 12773396
2005 The protein-RNA interface of the CstF-64 RRM acquires significant mobility on the micro-to-millisecond timescale upon binding GU-rich RNA, while the free protein is uniformly rigid; this dynamic binding is proposed as the mechanism enabling discrimination between GU-rich and non-GU-rich RNAs. NMR relaxation dynamics experiments of free and RNA-bound CstF-64 RRM Journal of molecular biology High 15769465
2006 The C-terminal domain of CstF-64 (and yeast ortholog Rna15) folds into a three-helix bundle with an uncommon topological arrangement; a cluster of conserved exposed residues is essential for interaction with Pcf11 (yeast), and this interaction is critical for 3'-end processing but dispensable for transcription termination. NMR structure determination, mutagenesis, yeast functional assays (3'-end processing and transcription termination) The Journal of biological chemistry High 17116658
2009 The hinge domain of CstF-64 is essential for interaction with CstF-77; this interaction is required for nuclear localization of CstF-64, suggesting that nuclear import of a preformed CstF complex is an essential step in polyadenylation. SLAP (stem-loop luciferase assay for polyadenylation) in vivo assay, domain mutagenesis, nuclear/cytoplasmic fractionation The Journal of biological chemistry High 19887456
2009 Enterovirus 71 3Cpro cleaves CstF-64 at position 251 in the P/G-rich domain and at multiple sites near position 500 in the C-terminus; this cleavage inhibits host cell 3'-end pre-mRNA processing and polyadenylation, and this impairment is rescued by adding purified recombinant CstF-64. In vitro cleavage assay with wild-type and catalytic mutant 3Cpro, serial mutagenesis of CstF-64, in vitro polyadenylation assay with nuclear extracts, rescue with purified CstF-64 PLoS pathogens High 19779565
2009 CstF-64 interaction with CstF-77 is required for nuclear accumulation of CstF-64, whereas interaction with symplekin is limiting for histone RNA 3' processing but relatively unimportant for cleavage/polyadenylation; CstF-64 and symplekin bind mutually exclusively to the hinge domain. Identification of CstF-64 and symplekin mutants that distinguish these interactions; nuclear localization assays; histone 3' processing assays Molecular biology of the cell High 21119002
2000 A variant form of CstF-64 (tauCstF-64, encoded by autosomal Cstf2t on chromosome 19) is expressed specifically in meiotic and postmeiotic male germ cells; it contains a Pro→Ser substitution in the RNA-binding domain and significant changes in the CstF-77 interaction region, suggesting altered polyadenylation specificities. cDNA cloning, chromosomal mapping, immunoblot with antibody reactivity and proteolytic digest pattern comparison The Journal of biological chemistry Medium 11113135
2007 CstF-64 and tauCstF-64 RNA-binding domains show differential affinities for RNA polymers: CstF-64 has higher affinity for poly(U) while tauCstF-64 has higher affinity for poly(GU); the region C-terminal to the RRM contributes to RNA sequence recognition. RNA cross-linking assay with Kd quantification, site-directed mutagenesis of the RRM The Biochemical journal Medium 17029590
2001 In C. elegans, CstF-64 forms a complex with the SL2 snRNP (but not SL1 or other U snRNAs); SL2 RNA stem/loop III is required for both SL2 identity and complex formation with CstF-64, providing a molecular framework for coupling of 3' end formation and trans-splicing in polycistronic pre-mRNA processing. Immunoprecipitation with anti-CstF-64 antibody, SL2 RNA mutational analysis in vivo and in vitro Genes & development Medium 11581161
2001 Elevated levels of CstF-64 in male germ cells enhance selection of the proximal poly(A) site on TB-RBP pre-mRNA, increasing the 1 kb mRNA isoform; CstF-64 preferentially binds to a distal site that produces the 3 kb mRNA, and overexpression shifts poly(A) site selection toward the 1 kb form. RNA cross-linking/binding assay, overexpression experiment with isoform quantification Molecular reproduction and development Medium 11241784
2014 CstF-64 is required for correct histone mRNA 3' end processing in mouse embryonic stem cells; loss of CstF-64 results in increased polyadenylation of histone mRNAs, slower growth, loss of pluripotency, and lengthened G1 phase. CstF-64 knockout mouse ESCs, histone mRNA polyadenylation assay, cell cycle analysis, pluripotency marker assays Nucleic acids research High 24957598
2014 CstF-64 is essential for endoderm differentiation in mouse ESCs; loss of CstF-64 abolishes endodermal lineage differentiation and prevents cardiomyocyte formation, which can be rescued by conditioned medium from extraembryonic endodermal stem cells. CstF-64 knockout mouse ESCs, lineage marker analysis, cardiomyocyte differentiation assay, XEN cell conditioned medium rescue experiment Stem cell research Medium 25460602
2018 The carboxy-terminus of CstF-77 (last 30 amino acids) enhances cleavage/polyadenylation by increasing the stability of the CstF-64 RRM, thereby altering the affinity of the complex for RNA; excess CstF-64 not bound to CstF-77 localizes to the cytoplasm, potentially via interaction with cytoplasmic RNAs. Reverse genetics, NMR studies of recombinant CstF-64 RRM-Hinge and CstF-77 domains, nuclear/cytoplasmic localization assays Nucleic acids research High 30257008
2018 CSTF2 induces 3'UTR shortening of RAC1 by cotranscriptional recruitment to the GUAAU motif at the proximal polyadenylation site, which attenuates recruitment of transcription elongation factors AFF1 and AFF4, causing defects in transcriptional elongation and promoting use of the proximal poly(A) site. RNA-seq, ChIP, RIP, CSTF2 overexpression/knockdown, polyadenylation site usage assays in UCB cells Cancer research Medium 30143523
2020 A missense mutation in the CstF-64 RRM (p.D50A) reduces C/P efficiency by altering amino acid side chain positions, changing the electrostatic potential of the RRM and resulting in greater affinity for RNA; in mice, this mutation alters polyadenylation sites in over 1300 genes critical for brain development. Reporter gene C/P assay, NMR structural analysis of mutant RRM, mouse model with D50A knock-in, genome-wide poly(A) site analysis Nucleic acids research High 32816001
2022 Electrostatic attraction is the dominant factor in CstF-64 RRM binding to U-rich RNA; binding involves enthalpy-entropy compensation supported by changes in picosecond-to-nanosecond timescale dynamics; competition between fast, high-affinity RNA binding and efficient correct C/P exists in vivo. NMR spectroscopy, mutagenesis, biophysical assays (ITC/SPR), in vivo C/P assays Biophysical journal High 35090899
2023 CSTF2 co-transcriptionally regulates m6A installation by slowing RNA Pol II elongation rate during gene transcription; CSTF2-regulated m6As are recognized by IGF2BP2, an m6A reader that stabilizes mRNAs. Transcriptomic m6A profiling (MeRIP-seq) in PDAC tissues, CSTF2 manipulation with RNA Pol II elongation rate assays, IGF2BP2 RIP Nature communications Medium 37816727
2024 The CSTF2 RRM domain binds U-rich RNA through a multistep binding process involving differences in picosecond-to-nanosecond timescale dynamics and structural changes in the C-terminal α-helix. NMR titration, spin relaxation experiments, paramagnetic relaxation enhancement measurements, rigid-body docking Biochemistry High 39305233
2025 CSTF2 shortens the 3'UTR of PGK1 pre-mRNA by binding near the proximal polyadenylation site, causing loss of m6A modification sites; this prevents YTHDF2-mediated mRNA degradation and increases PGK1 protein to enhance glycolysis under hypoxia. YTHDC1 recognizes hypoxia-induced m6A near the proximal poly(A) site and recruits CSTF2 to enhance 3'UTR shortening. RIP, APA site usage assays, m6A mapping, CSTF2 knockdown/overexpression, xenograft models, patient-derived organoids, small-molecule screen Cancer research Medium 39514400
2025 CSTF2 promotes PolyA polymerase alpha (PAPα) binding to the 3'UTR of CXCL10 RNA, resulting in shortened poly(A) tails and reduced CXCL10 mRNA stability; this diminishes CXCL10-mediated recruitment of innate αβ T cells, suppressing anti-tumor immunity in PDAC. RIP, poly(A) tail length assay, CSTF2 knockdown, CXCL10 mRNA stability assay, tumor infiltration analysis Cell death and differentiation Medium 39972059
2022 CSTF2 promotes 3'UTR shortening and upregulation of FGF2 mRNA by inducing use of the proximal polyadenylation site, stabilizing FGF2 mRNA through miRNA evasion; FGF2 in turn enhances CSTF2 expression forming a positive feedback loop that drives epithelial-mesenchymal transition in tubular epithelial cells. CSTF2 knockdown/overexpression, APA site usage assays, mRNA stability assay, in vivo UUO mouse model, antisense oligonucleotide treatment Biochimica et biophysica acta. Molecular basis of disease Medium 36113752

Source papers

Stage 0 corpus · 39 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1996 The polyadenylation factor CstF-64 regulates alternative processing of IgM heavy chain pre-mRNA during B cell differentiation. Cell 355 8945520
1998 Levels of polyadenylation factor CstF-64 control IgM heavy chain mRNA accumulation and other events associated with B cell differentiation. Molecular cell 193 9885564
2003 Recognition of GU-rich polyadenylation regulatory elements by human CstF-64 protein. The EMBO journal 126 12773396
2009 Enterovirus 71 3C protease cleaves a novel target CstF-64 and inhibits cellular polyadenylation. PLoS pathogens 124 19779565
1996 The RNA 3' cleavage factors CstF 64 kDa and CPSF 100 kDa are concentrated in nuclear domains closely associated with coiled bodies and newly synthesized RNA. The EMBO journal 84 8654386
2005 A 57-nucleotide upstream early polyadenylation element in human papillomavirus type 16 interacts with hFip1, CstF-64, hnRNP C1/C2, and polypyrimidine tract binding protein. Journal of virology 62 15767428
2018 CSTF2-Induced Shortening of the RAC1 3'UTR Promotes the Pathogenesis of Urothelial Carcinoma of the Bladder. Cancer research 60 30143523
2005 Protein and RNA dynamics play key roles in determining the specific recognition of GU-rich polyadenylation regulatory elements by human Cstf-64 protein. Journal of molecular biology 57 15769465
2010 Interactions of CstF-64, CstF-77, and symplekin: implications on localisation and function. Molecular biology of the cell 51 21119002
2006 The C-terminal domains of vertebrate CstF-64 and its yeast orthologue Rna15 form a new structure critical for mRNA 3'-end processing. The Journal of biological chemistry 49 17116658
2006 A multispecies comparison of the metazoan 3'-processing downstream elements and the CstF-64 RNA recognition motif. BMC genomics 42 16542450
2000 The gene for a variant form of the polyadenylation protein CstF-64 is on chromosome 19 and is expressed in pachytene spermatocytes in mice. The Journal of biological chemistry 39 11113135
2011 Characterization of a cleavage stimulation factor, 3' pre-RNA, subunit 2, 64 kDa (CSTF2) as a therapeutic target for lung cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 37 21813631
2001 A complex containing CstF-64 and the SL2 snRNP connects mRNA 3' end formation and trans-splicing in C. elegans operons. Genes & development 34 11581161
2001 Overexpression of the CstF-64 and CPSF-160 polyadenylation protein messenger RNAs in mouse male germ cells. Biology of reproduction 28 11369601
2018 The structural basis of CstF-77 modulation of cleavage and polyadenylation through stimulation of CstF-64 activity. Nucleic acids research 27 30257008
2003 Developmental distribution of the polyadenylation protein CstF-64 and the variant tauCstF-64 in mouse and rat testis. Biology of reproduction 26 14681198
2009 The hinge domain of the cleavage stimulation factor protein CstF-64 is essential for CstF-77 interaction, nuclear localization, and polyadenylation. The Journal of biological chemistry 24 19887456
2009 A family of splice variants of CstF-64 expressed in vertebrate nervous systems. BMC molecular biology 22 19284619
2002 The gene CSTF2T, encoding the human variant CstF-64 polyadenylation protein tauCstF-64, lacks introns and may be associated with male sterility. Genomics 22 12408968
2023 CSTF2 mediated mRNA N6-methyladenosine modification drives pancreatic ductal adenocarcinoma m6A subtypes. Nature communications 20 37816727
2001 Elevated levels of the polyadenylation factor CstF 64 enhance formation of the 1kB Testis brain RNA-binding protein (TB-RBP) mRNA in male germ cells. Molecular reproduction and development 19 11241784
2014 CstF-64 supports pluripotency and regulates cell cycle progression in embryonic stem cells through histone 3' end processing. Nucleic acids research 18 24957598
2007 Polyadenylation proteins CstF-64 and tauCstF-64 exhibit differential binding affinities for RNA polymers. The Biochemical journal 18 17029590
2020 A missense mutation in the CSTF2 gene that impairs the function of the RNA recognition motif and causes defects in 3' end processing is associated with intellectual disability in humans. Nucleic acids research 17 32816001
2022 CSTF2 Promotes Hepatocarcinogenesis and Hepatocellular Carcinoma Progression via Aerobic Glycolysis. Frontiers in oncology 13 35875122
2014 CstF-64 is necessary for endoderm differentiation resulting in cardiomyocyte defects. Stem cell research 13 25460602
2014 High-throughput sequencing of RNA isolated by cross-linking and immunoprecipitation (HITS-CLIP) to determine sites of binding of CstF-64 on nascent RNAs. Methods in molecular biology (Clifton, N.J.) 9 24590791
2025 CSTF2 Supports Hypoxia Tolerance in Hepatocellular Carcinoma by Enabling m6A Modification Evasion of PGK1 to Enhance Glycolysis. Cancer research 8 39514400
2022 Alternative polyadenylation writer CSTF2 forms a positive loop with FGF2 to promote tubular epithelial-mesenchymal transition and renal fibrosis. Biochimica et biophysica acta. Molecular basis of disease 7 36113752
2022 The RNA-binding protein CSTF2 regulates BAD to inhibit apoptosis in glioblastoma. International journal of biological macromolecules 7 36521710
2022 Electrostatic Interactions between CSTF2 and pre-mRNA Drive Cleavage and Polyadenylation. Biophysical journal 4 35090899
2014 The stem-loop luciferase assay for polyadenylation (SLAP) method for determining CstF-64-dependent polyadenylation activity. Methods in molecular biology (Clifton, N.J.) 3 24590783
2024 The role of CSTF2 in cancer: from technology to clinical application. Cell cycle (Georgetown, Tex.) 2 38166492
2025 CSTF2-impeded innate αβ T cell infiltration and activation exacerbate immune evasion of pancreatic cancer. Cell death and differentiation 1 39972059
2025 The role of CSTF2 in gastric cancer: implications for therapy. European journal of medical research 0 41310899
2024 Human CSTF2 RNA Recognition Motif Domain Binds to a U-Rich RNA Sequence through a Multistep Binding Process. Biochemistry 0 39305233
2024 The host gene CSTF2 regulates HBV replication via HBV PRE-induced nuclear export. Acta biochimica et biophysica Sinica 0 39722572
2023 Detection of CSTF2 by nano fluorescent probe and its correlation with malignant biological characteristics in liver cancer. American journal of cancer research 0 38058835