Affinage

CSTF2

Cleavage stimulation factor subunit 2 · UniProt P33240

Length
577 aa
Mass
61.0 kDa
Annotated
2026-06-09
39 papers in source corpus 22 papers cited in narrative 22 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

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 that recognizes GU/U-rich downstream sequence elements in pre-mRNAs and is rate-limiting for the efficiency and site selection of 3'-end cleavage and polyadenylation (PMID:8945520, PMID:12773396). Its N-terminal RRM engages GU-rich RNA through predominantly electrostatic contacts, with the C-terminal helix unfolding upon binding and the protein-RNA interface acquiring micro-to-millisecond mobility that permits recognition of diverse GU-rich sequences while discriminating against non-GU RNAs (PMID:12773396, PMID:15769465, PMID:35090899). The hinge domain anchors CstF-64 into the complex by binding CstF-77, an interaction required for nuclear import and for full RNA-binding activity, and which is mutually exclusive with symplekin binding that instead drives histone mRNA 3'-end processing (PMID:19887456, PMID:21119002, PMID:30257008). Because CstF-64 is present at limiting concentration, its abundance sets a regulatory lever for alternative poly(A) site selection, exemplified by the switch from membrane-bound to secreted IgM heavy chain during B cell differentiation, and its depletion arrests the cell cycle and triggers apoptosis (PMID:8945520, PMID:9885564). CstF-64 supports embryonic stem cell pluripotency and cell cycle progression by promoting correct non-polyadenylated processing of replication-dependent histone mRNAs and gates endoderm-dependent cardiac differentiation (PMID:24957598, PMID:25460602). Beyond canonical processing, CSTF2 acts co-transcriptionally to shorten 3'UTRs (e.g., RAC1, PGK1) by binding proximal poly(A) sites and modulating RNA Pol II elongation, with downstream effects on m6A deposition recognized by readers such as IGF2BP2, YTHDF2, and YTHDC1, linking it to mRNA stability, glycolysis, and tumor immunity (PMID:30143523, PMID:37816727, PMID:39514400). A missense mutation (p.D50A) in the RRM that alters its electrostatic potential and RNA binding causes X-linked intellectual disability and shifts poly(A) site usage across more than 1300 brain-expressed genes (PMID:32816001).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 1996 High

    Established that CstF-64 abundance, rather than mere presence, governs poly(A) site choice — explaining how a constitutive processing factor can act as a developmental switch.

    Evidence Reconstituted in vitro processing, overexpression in B cell lines, and affinity measurements at IgM heavy chain poly(A) sites

    PMID:8945520

    Open questions at the time
    • Mechanism by which CstF-64 levels are repressed in primary B cells not resolved
    • Generalizability to other alternative poly(A) site genes not yet tested
  2. 1996 High

    Localized the 3'-cleavage machinery to transcription-dependent subnuclear foci, linking CstF-64 to active transcription sites.

    Evidence Immunofluorescence, immunogold EM, BrU nascent RNA labeling, and transcription inhibition

    PMID:8654386

    Open questions at the time
    • Functional significance of cleavage body foci for processing efficiency unclear
  3. 1998 High

    Showed CstF-64 has unexpected roles beyond housekeeping 3'-end processing by linking its dosage to cell cycle progression and survival.

    Evidence Regulatable transgene replacing endogenous CstF-64 in DT40 cells with cell cycle and apoptosis readouts

    PMID:9885564

    Open questions at the time
    • Which target mRNAs drive the G0/G1 arrest and apoptosis not identified
    • Direct vs indirect effects not separated
  4. 2000 Medium

    Identified a germ-cell paralog (tauCstF-64/Cstf2t) that compensates for X-inactivation of CstF-64 during spermatogenesis, revealing tissue-specific specialization of the subunit.

    Evidence cDNA cloning, chromosomal mapping, immunoblot, 2D-PAGE, and proteolytic mapping

    PMID:11113135

    Open questions at the time
    • Functional consequences of the RRM Pro→Ser substitution not characterized in this study
    • Single-lab characterization
  5. 2001 Medium

    Connected CstF-64 to trans-splicing in C. elegans through specific association with the SL2 snRNP, expanding its role beyond cis 3'-end formation.

    Evidence Reciprocal IP and mutational dissection of SL2 RNA stem-loops with in vivo trans-splicing assays

    PMID:11581161

    Open questions at the time
    • Relevance to mammalian CstF-64 function unknown
    • Molecular contacts mediating SL2 association not mapped
  6. 2003 High

    Defined the structural basis of GU-rich element recognition and proposed an RNA-induced conformational change in the RRM C-terminal helix that initiates complex assembly.

    Evidence NMR structure of the RRM free and RNA-bound with mutagenesis of RNA contacts

    PMID:12773396

    Open questions at the time
    • Coupling between helix unfolding and downstream factor recruitment not directly demonstrated
  7. 2005 High

    Explained how a single RRM tolerates diverse GU-rich sequences by showing binding induces interface mobility rather than rigid lock-and-key recognition.

    Evidence NMR relaxation dynamics of the RRM free and bound to two GU-rich RNAs

    PMID:15769465

    Open questions at the time
    • Functional link between dynamics and in vivo poly(A) site selection not established at this stage
  8. 2006 High

    Separated the C-terminal domain's role in 3'-end processing (via Pcf11) from transcription termination, dissecting distinct functions of the subunit.

    Evidence NMR structure of C-terminal domains, surface mutagenesis, and in vitro processing assays with Rna15 mutants

    PMID:17116658

    Open questions at the time
    • Conservation of the Pcf11 interaction surface in human CstF-64 not directly tested here
  9. 2007 Medium

    Quantified differential RNA-binding specificity between CstF-64 and tauCstF-64, mapping determinants to a region C-terminal to the RBD rather than a single residue.

    Evidence RNA cross-linking Kd measurements across homopolymers with RBD mutagenesis

    PMID:17029590

    Open questions at the time
    • In vivo consequences of differential affinity for poly(A) site choice not assessed
    • Single-lab assay
  10. 2009 High

    Established the hinge domain as essential for CstF-77 binding and nuclear import, defining preformed-complex nuclear entry as a required step in polyadenylation.

    Evidence SLAP reporter assay with domain deletions, Co-IP, and IF localization

    PMID:19887456

    Open questions at the time
    • Import receptor/pathway for the CstF complex not identified
  11. 2009 High

    Revealed CstF-64 as a target of viral subversion, with EV71 3C protease cleaving and inactivating it to shut down host 3'-end processing.

    Evidence In vitro cleavage with site mapping, polyadenylation assay on protease-treated extract, and recombinant rescue

    PMID:19779565

    Open questions at the time
    • In vivo contribution of CstF-64 cleavage to viral replication during infection not quantified
  12. 2010 High

    Showed the hinge mediates mutually exclusive CstF-77 versus symplekin binding, partitioning CstF-64 between canonical poly(A) processing and histone mRNA 3'-end processing.

    Evidence Interaction-discriminating mutants, reciprocal Co-IP, complementation, and processing assays

    PMID:21119002

    Open questions at the time
    • How the choice between CstF-77 and symplekin is regulated in cells not defined
  13. 2014 Medium

    Linked CstF-64 to stem cell biology by showing it enforces correct non-polyadenylated histone mRNA processing required for pluripotency and cell cycle, and gates endoderm-dependent cardiac differentiation.

    Evidence CstF-64 knockout ESCs with histone mRNA, cell cycle, pluripotency, and differentiation assays plus conditioned-medium rescue

    PMID:24957598 PMID:25460602

    Open questions at the time
    • Direct vs secondary effects on histone processing not fully separated
    • Single-lab studies
  14. 2018 Medium

    Demonstrated co-transcriptional 3'UTR shortening as a CSTF2 function, acting by attenuating elongation factor recruitment to favor proximal poly(A) sites, with cancer phenotypes.

    Evidence RNA-seq, ChIP for CSTF2 and AFF1/AFF4, 3'UTR isoform analysis, and migration/invasion assays on RAC1

    PMID:30143523

    Open questions at the time
    • Mechanism of elongation factor attenuation not structurally defined
    • Single-lab
  15. 2018 High

    Showed CstF-77 binding allosterically enhances CstF-64 RNA-binding activity by stabilizing the RRM, coupling complex assembly to affinity.

    Evidence NMR of RRM-Hinge with CstF-77 CTD, reverse genetics, binding assays, and IF localization

    PMID:30257008

    Open questions at the time
    • Quantitative contribution of this enhancement to in vivo site selection not measured
  16. 2020 High

    Provided a direct disease link, showing an RRM missense mutation that increases RNA-binding on-rate reduces processing efficiency and causes X-linked intellectual disability with genome-wide poly(A) site shifts.

    Evidence Reporter C/P assay, NMR of D50A RRM, and genome-wide poly(A) site analysis in knock-in mice

    PMID:32816001

    Open questions at the time
    • How altered poly(A) site usage translates to neuronal dysfunction not resolved
  17. 2022 High

    Defined electrostatics as the dominant binding force and revealed a competition between fast high-affinity RNA binding and correct cleavage/polyadenylation, reframing the D50A defect mechanistically.

    Evidence Surface-charge mutagenesis, NMR, ITC/SPR, and in vivo C/P reporter

    PMID:35090899

    Open questions at the time
    • Structural intermediate driving the affinity-vs-efficiency tradeoff not directly visualized
  18. 2024 High

    Refined the binding mechanism to a multistep process involving ps-ns dynamics and C-terminal helix structural change, extending the dynamic recognition model.

    Evidence NMR titration, spin relaxation, paramagnetic relaxation enhancement, and rigid-body docking

    PMID:39305233

    Open questions at the time
    • Atomic-resolution bound-state structure not obtained
  19. 2025 Medium

    Connected CSTF2-driven 3'UTR shortening to m6A biology and disease, showing it removes or remodels m6A sites recognized by reader proteins to control mRNA stability, glycolysis, and anti-tumor immunity.

    Evidence RIP/RIP-seq, m6A-seq, poly(A) tail length assays, reader co-IPs, KO mouse and xenograft models for CXCL10 and PGK1

    PMID:37816727 PMID:39514400 PMID:39972059

    Open questions at the time
    • Direct causal chain from elongation modulation to specific m6A site loss not fully reconstituted
    • Single-lab studies per target

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CstF-64 abundance, post-translational state, and competition between high-affinity binding and efficient processing are integrated to control alternative poly(A) site choice genome-wide in different cell types remains unresolved.
  • No genome-wide model linking CstF-64 dosage to tissue-specific APA outcomes
  • Regulation of CstF-64 levels in vivo poorly defined
  • Atomic structure of the RNA-bound complex incomplete

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 5 GO:0140098 catalytic activity, acting on RNA 4 GO:0060090 molecular adaptor activity 3
Localization
GO:0005634 nucleus 2 GO:0005654 nucleoplasm 1 GO:0005829 cytosol 1
Pathway
R-HSA-8953854 Metabolism of RNA 4 R-HSA-1643685 Disease 3 R-HSA-74160 Gene expression (Transcription) 2
Partners
CSTF3IGF2BP2PAPOLAPCF11SYMPKYTHDC1YTHDF2
Complex memberships
CstF complex

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 CstF-64 is a limiting subunit of the CstF complex; its accumulation is specifically repressed in primary B cells, and overexpression of CstF-64 is sufficient to switch IgM heavy chain pre-mRNA processing from the membrane-bound (µm) to secreted (µs) form. CstF has higher affinity for the µm poly(A) site, and the µm site is stronger in a reconstituted in vitro processing reaction. Reconstituted in vitro polyadenylation/processing assay, overexpression in B cell lines, affinity measurements Cell High 8945520
1998 A 10-fold decrease in CstF-64 concentration in the DT40 B cell line specifically and dramatically reduces IgM heavy chain mRNA accumulation; further reduction causes reversible G0/G1 cell cycle arrest, and depletion leads to apoptotic cell death, demonstrating unexpected roles for CstF-64 in regulating gene expression and cell growth. Gene disruption of endogenous CstF-64 replaced with regulatable transgene in DT40 cells; cell cycle and apoptosis assays Molecular cell High 9885564
1996 CstF-64 (64 kDa subunit) and CPSF 100 kDa are concentrated in discrete nuclear foci ('cleavage bodies') closely associated with coiled bodies; these foci are transcription-dependent and contain newly synthesized RNA, revealing dynamic transcription-coupled subnuclear localization of the 3'-cleavage machinery. Immunofluorescence with monoclonal antibodies, alpha-amanitin/DRB transcription inhibition, immunogold electron microscopy, BrU labeling of nascent RNA The EMBO journal High 8654386
2003 The N-terminal RNA recognition motif (RRM) of CstF-64 recognizes GU-rich downstream sequence elements; the C-terminal helix of the RRM unfolds upon RNA binding and extends into the hinge domain where interactions with other polyadenylation assembly factors occur, suggesting this conformational change initiates assembly of the polyadenylation complex. Consecutive U residues are required for strong CstF-GU interaction. NMR structure determination of the RRM domain free and RNA-bound; mutagenesis of RNA contacts The EMBO journal High 12773396
2005 The protein-RNA interface of CstF-64 RRM acquires significant micro-to-millisecond timescale mobility upon binding GU-rich RNA, while the free protein is uniformly rigid. This dynamic behavior at the binding interface is proposed to allow binding to diverse GU-rich sequences while discriminating against non-GU-rich RNAs. NMR relaxation dynamics measurements of CstF-64 RRM free and bound to two GU-rich RNA sequences Journal of molecular biology High 15769465
2006 The C-terminal domains of CstF-64 and its yeast orthologue Rna15 fold into a three-helix bundle with an uncommon topological arrangement. This domain mediates interaction with Pcf11, and this interaction is critical for mRNA 3'-end processing but dispensable for transcription termination. NMR structure determination of C-terminal domains; mutagenesis of conserved surface residues; in vitro 3'-end processing assays with Rna15 mutants The Journal of biological chemistry High 17116658
2009 The hinge domain of CstF-64 is essential for interaction with CstF-77 and for nuclear localization; nuclear import of a preformed CstF complex is an essential step in polyadenylation. Loss of the hinge domain abolishes CstF-64-dependent polyadenylation activity as measured by a reporter assay. SLAP (stem-loop luciferase assay for polyadenylation) with CstF-64 domain deletion/mutation constructs; co-immunoprecipitation; immunofluorescence localization The Journal of biological chemistry High 19887456
2009 EV71 3C protease cleaves CstF-64 at position 251 (N-terminal P/G-rich domain) and at multiple sites near position 500 (C-terminus). This cleavage inactivates CstF-64 and inhibits host cell 3'-end pre-mRNA processing and polyadenylation; impairment is rescued by adding purified recombinant CstF-64 protein. In vitro cleavage assay with recombinant 3Cpro and CstF-64; site-directed mutagenesis to map cleavage sites; in vitro polyadenylation assay with 3Cpro-treated nuclear extract; rescue by recombinant CstF-64 PLoS pathogens High 19779565
2010 CstF-64 binds CstF-77 and symplekin mutually exclusively through its hinge domain. The CstF-64–symplekin interaction is limiting for histone RNA 3'-end processing but relatively unimportant for cleavage/polyadenylation. Nuclear accumulation of CstF-64 depends on its binding to CstF-77 but not to symplekin. CstF-64τ can compensate for loss of CstF-64 but has lower affinity for CstF-77 and is less stable. Identification of CstF-64 and symplekin mutants that distinguish the two interactions; co-immunoprecipitation; complementation assays in cell lines; 3'-end processing assays Molecular biology of the cell High 21119002
2000 A variant form of CstF-64, termed tauCstF-64, is encoded by an autosomal gene (Cstf2t) on mouse chromosome 19 and is specifically expressed in meiotic and postmeiotic germ cells to compensate for X-chromosome inactivation of the somatic CstF-64. The tauCstF-64 protein contains a Pro→Ser substitution in its RNA-binding domain and significant changes in the region interacting with CstF-77. cDNA cloning; chromosomal mapping; immunoblot; 2D-PAGE; antibody reactivity; proteolytic digest pattern comparison The Journal of biological chemistry Medium 11113135
2001 In C. elegans, CstF-64 forms a complex with the SL2 snRNP (but not SL1 or other U snRNAs), linking mRNA 3'-end formation with SL2-specific trans-splicing. Stem/loop III of SL2 RNA is required for both SL2 identity and association with CstF-64. Immunoprecipitation of complex with anti-CstF-64 antibody; mutational analysis of SL2 RNA stem-loops; in vivo trans-splicing assays Genes & development Medium 11581161
2007 CstF-64 RBD has higher affinity for poly(U) than tauCstF-64 RBD, while tauCstF-64 has higher affinity for poly(GU). A region C-terminal to the RBD (not Pro-41 alone) is important for RNA sequence recognition and differential affinity. RNA cross-linking Kd measurements with poly(G), poly(A), poly(C), poly(U), and poly(GU) ribopolymers; mutagenesis of CstF-64 RBD residues The Biochemical journal Medium 17029590
2014 CstF-64 supports ESC pluripotency and cell cycle progression by promoting correct 3'-end processing (non-polyadenylation) of replication-dependent histone mRNAs; loss of CstF-64 results in increased histone mRNA polyadenylation, lengthened G1, and loss of pluripotency. τCstF-64 partially compensates and is recruited to the histone mRNA 3'-end processing complex. CstF-64 knockout ESCs; RT-PCR and Northern analysis of histone mRNA polyadenylation; cell cycle analysis; pluripotency marker assays; τCstF-64 knockdown in Cstf2-deficient ESCs Nucleic acids research Medium 24957598
2018 The carboxy-terminus of CstF-77 enhances CstF-64 RNA binding activity by altering how the RRM of CstF-64 engages RNA, increasing RRM stability and thus the affinity of the CstF complex for RNA. CstF-64 nuclear localization depends on CstF-77 binding; excess CstF-64 accumulates in the cytoplasm, possibly by interacting with cytoplasmic RNAs. NMR spectroscopy of recombinant CstF-64 RRM-Hinge and CstF-77 CTD; reverse genetics; RNA binding assays; immunofluorescence localization Nucleic acids research High 30257008
2018 CSTF2 promotes 3'UTR shortening of RAC1 by cotranscriptionally binding to a GUAAU motif at the proximal polyadenylation site of RAC1, which attenuates recruitment of transcription elongation factors AFF1 and AFF4, causing defects in elongation and favoring proximal poly(A) site usage. RNA sequencing; chromatin immunoprecipitation (ChIP) for CSTF2 and transcription elongation factors; 3'UTR isoform analysis; CSTF2 knockdown/overexpression with migration/invasion assays Cancer research Medium 30143523
2020 A missense mutation in the RRM of CSTF2 (p.D50A) causes intellectual disability in males. This mutation changes the electrostatic potential of the RRM, leading to greater (altered on-rate) RNA binding affinity and reduced C/P efficiency, altering polyadenylation sites in over 1300 brain-expressed genes. Reporter gene C/P assay; NMR structure and chemical shift perturbation of D50A RRM; genome-wide poly(A) site analysis in knock-in mice Nucleic acids research High 32816001
2022 Electrostatic attraction is the dominant force in CSTF2 RRM binding to U-rich RNA; RNA binding is accompanied by enthalpy-entropy compensation and changes in picosecond-to-nanosecond timescale protein dynamics. Competition between fast high-affinity RNA binding and efficient correct C/P is demonstrated in vivo. Mutagenesis of surface-charged residues; NMR spectroscopy; biophysical binding assays (ITC, SPR); in vivo C/P reporter assay Biophysical journal High 35090899
2023 CSTF2 co-transcriptionally regulates m6A installation on target gene transcripts by slowing RNA Pol II elongation rate during transcription; CSTF2-regulated m6As are predominantly recognized by IGF2BP2, an m6A reader that stabilizes mRNAs. Transcriptomic m6A profiling (MeRIP-seq) in PDAC tissues; CSTF2 knockdown/overexpression with m6A and RNA Pol II elongation analysis; RIP for IGF2BP2 Nature communications Medium 37816727
2024 CSTF2 RRM binds U-rich RNA through a multistep binding process involving differences in ps-ns dynamics and potential structural changes in the C-terminal α-helix, as determined by NMR titration, spin relaxation, paramagnetic relaxation enhancement, and rigid-body docking. NMR titration and spin relaxation; paramagnetic relaxation enhancement; rigid-body docking Biochemistry High 39305233
2025 CSTF2 diminishes CXCL10 expression by promoting poly(A) polymerase alpha (PAPα) binding to the 3'UTR of CXCL10 RNA, resulting in shortened poly(A) tails and compromised CXCL10 RNA stability, thereby suppressing iαβT cell infiltration and anti-tumor immunity in PDAC. RIP assay for CSTF2 and PAPα binding to CXCL10 3'UTR; poly(A) tail length assay; CSTF2 KO mouse models and co-culture immune assays; Forsythoside B inhibitor targeting CSTF2 RRM Cell death and differentiation Medium 39972059
2025 CSTF2 shortens the 3'UTR of PGK1 pre-mRNA by binding near its proximal polyadenylation site, leading to loss of m6A sites that would otherwise be recognized by YTHDF2 (promoting degradation), thereby increasing PGK1 protein levels and enhancing glycolysis under hypoxia. Hypoxia-induced m6A near the proximal poly(A) site is recognized by YTHDC1, which recruits CSTF2 to further enhance PGK1 3'UTR shortening. RIP-seq for CSTF2 binding; m6A-seq; 3'UTR isoform analysis; CSTF2 KO in HCC cell lines and xenograft models; YTHDF2/YTHDC1 co-IP; masitinib inhibitor screen Cancer research Medium 39514400
2014 Loss of CstF-64 in mouse ESCs results in loss of differentiation potential toward the endodermal lineage, which is necessary for cardiomyocyte specification; endodermal signaling from conditioned medium of XEN stem cells restores cardiomyocyte differentiation in CstF-64-knockout cells, placing CstF-64 upstream of endoderm-dependent cardiac specification. CstF-64 knockout ESCs (Cstf2E6); endoderm/mesoderm/cardiac differentiation assays; conditioned medium rescue experiment; marker expression analysis Stem cell research Medium 25460602

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 356 8945520
1998 Levels of polyadenylation factor CstF-64 control IgM heavy chain mRNA accumulation and other events associated with B cell differentiation. Molecular cell 194 9885564
2003 Recognition of GU-rich polyadenylation regulatory elements by human CstF-64 protein. The EMBO journal 127 12773396
2009 Enterovirus 71 3C protease cleaves a novel target CstF-64 and inhibits cellular polyadenylation. PLoS pathogens 125 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 58 15769465
2010 Interactions of CstF-64, CstF-77, and symplekin: implications on localisation and function. Molecular biology of the cell 52 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 21 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
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 18 32816001
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
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
2025 CSTF2 Supports Hypoxia Tolerance in Hepatocellular Carcinoma by Enabling m6A Modification Evasion of PGK1 to Enhance Glycolysis. Cancer research 9 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 9 36113752
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
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

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