Affinage

PABPN1

Polyadenylate-binding protein 2 · UniProt Q86U42

Length
306 aa
Mass
32.7 kDa
Annotated
2026-06-10
100 papers in source corpus 32 papers cited in narrative 32 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PABPN1 is a nuclear poly(A)-binding protein that governs the maturation, fate, and length control of polyadenylated transcripts through its RNA-binding and poly(A) polymerase-stimulatory functions (PMID:25896913, PMID:36306357). It is recruited cotranscriptionally to nascent mRNPs and remains associated through nuclear export (PMID:12749861, PMID:19336419), and controls 3'-end processing by suppressing proximal polyadenylation sites and biasing toward distal site usage (PMID:27152426, PMID:37422193). Beyond tail-length control, PABPN1 couples polyadenylation to splicing of terminal introns bearing weak 3' splice sites in a poly(A) tail-dependent manner, acting directly by recruiting the splicing factors RBM26/RBM27 (PMID:37661812), and partners with MATR3 to coordinate alternative polyadenylation, intron retention, paraspeckle function, and A-to-I editing in muscle (PMID:28977530). PABPN1 negatively autoregulates its own expression by binding an adenosine-rich element in its 3' UTR, promoting terminal-intron retention and nuclear exosome-mediated clearance of its pre-mRNA (PMID:25963658). It forms liquid-liquid phase-separated nuclear poly(A) domains/speckles driven by its N-terminal disordered domain and RNA binding, a property essential for transcript stability and 3'UTR isoform formation in oocytes, with Pabpn1-null mice being sterile (PMID:36306357). Mitotic phosphorylation at four sites remodels poly(A) tails and tunes mRNA turnover to reset gene expression across the cell cycle (PMID:38943343). A cytoplasmic role has also been established whereby PABPN1 docks on 3'-uridylated maternal transcripts downstream of TUT4/7 and recruits the exoribonuclease DIS3L2 to drive zygotic genome activation-dependent maternal mRNA decay (PMID:34904664). PABPN1 additionally exerts an anti-apoptotic activity by regulating XIAP translation (PMID:18178579). Disease-causing N-terminal polyalanine expansions cause oculopharyngeal muscular dystrophy: expanded PABPN1 forms amyloid-like, RNA-dependent nuclear aggregates (PMID:14627730, PMID:37422193) that sequester partners including CFIm25 and hnRNP A1 (PMID:12945950, PMID:37422193), yet OPMD toxicity depends on the intrinsic RNA-binding function of PABPN1 rather than the polyalanine tract alone, and soluble expanded protein, not the insoluble aggregates, is the primary toxic species (PMID:16642034, PMID:17418585).

Mechanistic history

Synthesis pass · year-by-year structured walk · 30 steps
  1. 2001 Medium

    Established that PABPN1 oligomerization domains drive the nuclear aggregation seen with polyalanine expansion and that aggregation is mechanistically linked to cell death.

    Evidence Deletion mutagenesis with aggregation and cell-death readouts in COS-7 cells

    PMID:11689481

    Open questions at the time
    • Did not resolve whether aggregates themselves or soluble species are toxic
    • No structural basis for oligomerization
  2. 2003 Medium

    Placed PABPN1 on the cotranscriptional mRNP, showing it loads near transcription start and accompanies mRNP to the nuclear pore, framing it as an early and persistent mRNP factor.

    Evidence Cryo-immunoelectron microscopy of Balbiani ring mRNP in Chironomus tentans

    PMID:12749861

    Open questions at the time
    • Single insect model system
    • Does not define the molecular trigger for displacement at the pore
  3. 2003 Medium

    Identified hnRNP A1/A/B as PABPN1 partners and showed they are co-sequestered into mutant aggregates and patient inclusions, linking aggregation to partner depletion.

    Evidence Yeast two-hybrid, GST pull-down, Co-IP, and immunofluorescence in cells and OPMD muscle

    PMID:12945950

    Open questions at the time
    • Functional consequence of hnRNP sequestration not quantified
    • Direct interaction surface not mapped
  4. 2003 Medium

    Demonstrated biophysically that expanded polyalanine drives amyloid-like fibril formation with seeding behavior, providing a structural model for OPMD aggregation.

    Evidence In vitro recombinant protein fibrillation and structural/seeding assays

    PMID:14627730

    Open questions at the time
    • In vitro only
    • Relationship of fibrils to cellular toxicity unresolved
  5. 2005 Medium

    Showed wild-type PABPN1 is intrinsically aggregation-prone and that inclusions are dynamic rather than irreversible, reframing aggregates as exchangeable reservoirs.

    Evidence FRAP and domain-deletion analysis in HeLa and C2 cells

    PMID:15811916

    Open questions at the time
    • Does not establish whether dynamic exchange is protective or pathogenic
    • PAP-stimulation domain requirement not mechanistically dissected
  6. 2005 Medium

    Implicated HSP70/HSC70 chaperones in aggregate handling and showed pharmacological HSP70 induction reduces aggregate burden and cell death, identifying a tractable modifier.

    Evidence Pharmacological heat-shock induction with microscopy, solubility, and cell-death assays in HeLa

    PMID:16239242

    Open questions at the time
    • Cell-based only; no in vivo validation
    • Off-target effects of inducers not excluded
  7. 2006 Medium

    Established that OPMD muscle degeneration requires the RNA-binding function of PABPN1, not the polyalanine tract per se, redefining the disease as a property of PABPN1 function.

    Evidence Domain-specific mutants in a Drosophila OPMD model

    PMID:16642034

    Open questions at the time
    • Specific RNA targets driving degeneration not identified
    • Drosophila model may not capture all human muscle pathology
  8. 2007 Medium

    Resolved the toxic-species question by showing soluble expanded PABPN1, not insoluble aggregates, is the primary toxic entity.

    Evidence Live microscopy and aggregate-disruption experiments with cell-death readout in a cellular OPMD model

    PMID:17418585

    Open questions at the time
    • Molecular basis of soluble-species toxicity not defined
    • Single cellular model
  9. 2008 Medium

    Defined an anti-apoptotic function for wild-type PABPN1 through regulation of XIAP translation, partially lost in the mutant, linking PABPN1 dosage to cell survival.

    Evidence Overexpression/knockdown in cell and mouse models with XIAP and apoptosis readouts

    PMID:18178579

    Open questions at the time
    • Mechanism of XIAP translational control not detailed
    • Relevance to muscle pathology not established
  10. 2008 Medium

    Identified the SIRT1/AMPK/FoxO axis as a genetic and pharmacological modifier of mutant PABPN1 muscle toxicity.

    Evidence C. elegans genetic epistasis plus sirtinol/resveratrol treatment of mammalian cells

    PMID:18397876

    Open questions at the time
    • Direct molecular link between SIRT1 and PABPN1 not established here
    • Cross-species relevance uncertain
  11. 2009 Medium

    Showed expanded PABPN1 preferentially recruits Hsp70 and type-I arginine methyltransferases (PRMT1/PRMT3), tying conformational change to altered partner binding.

    Evidence Pull-down, patient-muscle immunofluorescence, and molecular simulation

    PMID:19641605

    Open questions at the time
    • Functional consequence of altered PRMT interaction untested
    • Simulation-based conformational claim not experimentally confirmed
  12. 2009 Medium

    Demonstrated via the fission yeast ortholog Pab2 that nuclear poly(A)-binding proteins are recruited cotranscriptionally ahead of canonical 3'-processing factors and persist on polysomes.

    Evidence RNase-sensitive ChIP, TAP-MS, and polysome fractionation in S. pombe

    PMID:19336419

    Open questions at the time
    • Ortholog-based; human conservation of polysome association not shown
    • Recruitment mechanism not defined
  13. 2013 Medium

    Established a Pab2/exosome pathway for nuclear pre-mRNA decay opposed by Nab2, defining poly(A)-binding-protein competition as a decay-versus-stability switch.

    Evidence Genetic epistasis and RNA decay assays in S. pombe

    PMID:24081329

    Open questions at the time
    • Ortholog system
    • Human equivalents of the competition not directly tested here
  14. 2013 Medium

    Mapped a PY-NLS/Kap104 import route for Pab2 while showing human PABPN1 uses an alternative/redundant import pathway, distinguishing nuclear targeting mechanisms.

    Evidence NLS mutagenesis, receptor-binding, and nuclear localization assays across yeast and human

    PMID:23279110

    Open questions at the time
    • Human import receptor not identified
    • Redundancy not mapped
  15. 2015 High

    Defined PABPN1 negative autoregulation: it binds an A-rich element in its own 3' UTR to drive terminal-intron retention and exosome-mediated clearance, establishing dosage homeostasis.

    Evidence Dosage manipulation, spliced/unspliced ratio measurement, exosome knockdown, RNA-binding analysis

    PMID:25963658

    Open questions at the time
    • Quantitative thresholds of the feedback loop not defined
    • In vivo physiological role of autoregulation untested
  16. 2015 Medium

    Showed PABPN1 and PAP cooperate to promote excision of introns removed only after polyadenylation, requiring both RNA-binding and PAP-stimulatory functions and impaired by alanine expansion.

    Evidence RNAi depletion, splicing assays, domain mutants, and exosome assays

    PMID:25896913

    Open questions at the time
    • Splicing factors recruited not yet identified at this stage
    • Genome-wide scope not quantified
  17. 2015 Medium

    Demonstrated PABPN1 suppresses TDP-43 pathology by promoting its degradation and restoring solubility/localization, extending PABPN1 function to proteostasis of an aggregation-prone RBP.

    Evidence Overexpression/knockdown in cells and Drosophila with solubility, stress-granule, and localization readouts

    PMID:26130692

    Open questions at the time
    • Mechanism of TDP-43 clearance not defined
    • Direct vs indirect effect unresolved
  18. 2016 Medium

    Linked PABPN1 dosage to muscle physiology in vivo: reduced PABPN1 shifts toward proximal poly(A) sites, upregulating Atrogin-1 and causing myofiber atrophy.

    Evidence AAV-shRNA knockdown in mouse TA muscle with poly(A) site, expression, and histological analyses

    PMID:27152426

    Open questions at the time
    • Causal chain from APA shift to atrophy not fully dissected
    • Single muscle context
  19. 2017 High

    Identified MATR3 as a PABPN1 partner in skeletal muscle and showed the pair jointly regulates APA, intron retention, paraspeckles, Neat1, and RNA editing.

    Evidence Co-IP/MS, RNAi, APA, paraspeckle, and RNA-editing assays in muscle cells

    PMID:28977530

    Open questions at the time
    • Division of labor between PABPN1 and MATR3 on specific targets unresolved
    • Interaction interface not mapped
  20. 2019 Medium

    Showed PABPN1 controls SIRT1 mRNA via APA, connecting the earlier SIRT1 modifier genetics to a direct regulatory mechanism in muscle wasting.

    Evidence Multi-omics and sirtinol pharmacological rescue in shPAB mouse muscle

    PMID:30739015

    Open questions at the time
    • Acetylome targets driving wasting not pinpointed
    • Feedback between SIRT1 and PABPN1 not fully closed
  21. 2019 Medium

    Reported expanded PABPN1 accumulation in mitochondria and interaction with the TIM23 import complex, with OXPHOS deficits, extending pathology beyond the nucleus.

    Evidence Mitochondrial fractionation, TIM23 Co-IP, and patient/mouse tissue analysis

    PMID:30894671

    Open questions at the time
    • Mechanism of mitochondrial targeting unclear
    • Causal contribution to OPMD pathology not established
  22. 2020 Medium

    Extended PABPN1 translational control to p63α via eIF4E/eIF4G modulation and APA of p63γ, embedding it in a keratinocyte-differentiation feedback loop.

    Evidence siRNA knockdown, APA, eIF4E/eIF4G Co-IP, ΔNp63α rescue, differentiation assays

    PMID:32243883

    Open questions at the time
    • Direct vs indirect effect on initiation-factor binding unresolved
    • Single tissue context
  23. 2022 High

    Established that PABPN1 drives liquid-liquid phase separation into nuclear poly(A) domains essential for oocyte transcript stability and 3'UTR isoform formation, with knockout causing sterility.

    Evidence Pabpn1 knockout mice, live phase-separation imaging, domain deletion, RNA-seq, and fertility assays

    PMID:36306357

    Open questions at the time
    • Composition and regulation of NPADs incompletely defined
    • Link between condensate formation and specific RNA fates partial
  24. 2022 High

    Revealed an unforeseen cytoplasmic function: PABPN1 docks on 3'-uridylated maternal mRNAs downstream of TUT4/7 and recruits DIS3L2 for ZGA-dependent decay, with knockout embryos arresting at morula.

    Evidence Pabpn1 knockout mice, RIP, DIS3L2 Co-IP, and maternal-mRNA decay RNA-seq

    PMID:34904664

    Open questions at the time
    • How nuclear vs cytoplasmic PABPN1 pools are partitioned unknown
    • Structural basis of uridyl-transcript recognition not defined
  25. 2023 High

    Identified the direct splicing mechanism: PABPN1 promotes excision of weak-3'SS last introns in a poly(A) tail-dependent manner by recruiting RBM26/RBM27, mapping the recruitment to RBM27 domains.

    Evidence Depletion, RNA tethering, TurboID-MS, and RBM27 Co-IP/domain mapping in HeLa and mouse cells

    PMID:37661812

    Open questions at the time
    • How RBM26/27 execute splicing downstream not detailed
    • Genome-wide intron selectivity rules incomplete
  26. 2023 Medium

    Showed ZC3H11A requires PABPN1 for nuclear speckle localization and uses shared zinc fingers for PABPN1 and viral mRNA binding, linking PABPN1 to viral mRNA polyadenylation.

    Evidence Interactome MS, Co-IP, speckle localization, and viral mRNA polyadenylation analysis

    PMID:37356722

    Open questions at the time
    • Functional role of ZC3H11A–PABPN1 complex in host mRNA processing unclear
    • Competition between viral and host RNA not quantified
  27. 2023 Medium

    Dissected PABPN1 aggregation as driven by both alanine expansion (controlling speckle mobility) and poly(A)-RNA (essential for condensation), with aggregates sequestering CFIm25 to impair APA.

    Evidence FRAP, poly(A) RNA binding, CFIm25 co-localization/function, and APA assays

    PMID:37422193

    Open questions at the time
    • Quantitative relationship between sequestration and APA defects partial
    • Reversibility of solid-like transition not tested
  28. 2023 Medium

    Showed SNRPD2 binds the EP domain of PABPN1 to disrupt its LLPS in colorectal cancer, de-repressing proximal poly(A) sites and shortening CTNNBIP1 3'UTR to promote tumor phenotypes.

    Evidence Phase-separation assays, domain-specific Co-IP, APA, and proliferation/migration assays

    PMID:38811444

    Open questions at the time
    • Generality beyond CTNNBIP1 not established
    • In vivo tumor relevance not tested
  29. 2024 High

    Established cell-cycle control of PABPN1: mitotic phosphorylation at four sites remodels poly(A) tails and tunes mRNA synthesis/decay to reset transcriptome dynamics.

    Evidence Phospho-site mutants with long-read poly(A) sequencing, TimeLapse-seq, and proliferation assays

    PMID:38943343

    Open questions at the time
    • Identity of the responsible mitotic kinases not pinned down
    • Specific affected mRNA cohorts incompletely characterized
  30. 2025 Medium

    Identified QKI as a positive regulator of PABPN1 LLPS, with its loss in colorectal cancer reducing phase separation and shifting APA toward pro-tumor isoforms.

    Evidence CRISPR/BiFC/FACS screen with QKI manipulation and APA/proliferation/migration assays

    PMID:40052530

    Open questions at the time
    • Mechanism by which QKI promotes condensation unclear
    • Therapeutic relevance untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How nuclear and cytoplasmic PABPN1 pools are spatially partitioned and switched between poly(A)-tail control, condensate formation, splicing, and DIS3L2-dependent decay remains undefined.
  • No structural model integrating RNA binding, LLPS, and partner recruitment
  • Mitotic kinases and human nuclear import receptor unidentified
  • Determinants of target selectivity across distinct functions unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 5 GO:0098772 molecular function regulator activity 3 GO:0140098 catalytic activity, acting on RNA 3 GO:0045182 translation regulator activity 2
Localization
GO:0005634 nucleus 3 GO:0005654 nucleoplasm 3 GO:0005739 mitochondrion 1 GO:0005829 cytosol 1
Pathway
R-HSA-8953854 Metabolism of RNA 5 R-HSA-1643685 Disease 4 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-1474165 Reproduction 2 R-HSA-1640170 Cell Cycle 1
Partners
DIS3L2HNRNPA1MATR3QKIRBM26RBM27SNRPD2ZC3H11A
Complex memberships
nuclear speckles / nuclear poly(A) domains (NPADs)

Evidence

Reading pass · 32 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 PABPN1 oligomerization is mediated by two potential oligomerization domains (ODs) in the protein; deletion of 6-8 amino acids in either OD prevents nuclear protein aggregation induced by polyalanine-expanded PABPN1, and prevention of aggregation significantly reduces cell death in COS-7 cells expressing mutant PABPN1. Deletion mutagenesis, exogenous expression in COS-7 cells, immunofluorescence microscopy, cell death assay Human molecular genetics Medium 11689481
2003 PABPN1 is associated with RNA polymerase II along the chromatin axis of the BR gene, suggesting it binds to the polymerase before, at, or shortly after the start of transcription; PABPN1 accompanies the released mRNP to the nuclear pore and is displaced from mRNPs during or shortly after passage through the nuclear pore. Cryo-immunoelectron microscopy on Chironomus tentans salivary gland Balbiani ring mRNP Experimental cell research Medium 12749861
2003 PABPN1 interacts with hnRNP A1 and hnRNP A/B (identified by yeast two-hybrid screen and confirmed by GST pull-down and co-immunoprecipitation); when co-expressed with mutant PABPN1 in COS-7 cells, hnRNP A1 and A/B co-localize with mutant PABPN1 in insoluble intranuclear aggregates, and hnRNP A1 is sequestered in OPMD nuclear inclusions in patient muscle. Yeast two-hybrid screen, GST pull-down, co-immunoprecipitation, immunofluorescence in COS-7 cells and patient muscle The Canadian journal of neurological sciences Medium 12945950
2003 Expanded polyalanine in PABPN1 N-terminal domain drives fibril formation with amyloid-like characteristics (antiparallel beta-sheets) in vitro; the lag-phase of fibril formation is reduced by seeding, and expansion to maximal OPMD length increases alpha-helical structure preceding fibrillation. In vitro recombinant protein assay, structural analysis (amyloid characteristics), seeding experiments Protein science Medium 14627730
2005 Normal (wild-type) PABPN1 is inherently aggregation-prone when exogenously expressed; protein domains required for stimulation of poly(A) polymerase are required for inclusion formation; FRAP experiments show both normal and expanded PABPN1 molecules move rapidly in and out of inclusions rather than being irreversibly sequestered. Exogenous expression in HeLa and C2 cells, domain deletion analysis, photobleaching (FRAP) experiments RNA Medium 15811916
2005 HSC70 and HSP70 chaperones interact with and localize to PABPN1 intranuclear inclusions; pharmacological induction of HSP70 (by ZnSO4, 8-hydroxyquinoline, ibuprofen, or indomethacin) recruits HSP70 and HSC70 into the nucleus and significantly reduces mutant PABPN1 aggregate burden and concomitant cell death. Pharmacological induction of heat shock response, confocal microscopy, solubility assay, cell death assay in HeLa cells Human molecular genetics Medium 16239242
2006 In a Drosophila model of OPMD, the RNA-binding domain of PABPN1 and its RNA-binding function are required for muscle degeneration, whereas the polyalanine tract is not absolutely required; this establishes that OPMD does not result purely from polyalanine toxicity but from an intrinsic property of PABPN1. Drosophila transgenic model, domain deletion/mutation analysis, muscle degeneration phenotype readout The EMBO journal Medium 16642034
2007 Soluble forms of expanded PABPN1 (expPABPN1), not the insoluble nuclear aggregates, are the primary toxic species; interfering with large nuclear aggregate formation increases soluble expPABPN1 and significantly exacerbates cell death, as demonstrated by live microscopy. Live microscopy, aggregate disruption experiments, cell death assay in cellular OPMD model Neurobiology of disease Medium 17418585
2008 Wild-type PABPN1 exerts an anti-apoptotic function by regulating translation of X-linked inhibitor of apoptosis (XIAP) protein; overexpression of wild-type PABPN1 reduces mutant PABPN1 toxicity and protects cells from pro-apoptotic insults, while PABPN1 knockdown increases apoptotic susceptibility. This protective activity is partially lost for mutant PABPN1. Overexpression and knockdown in cell and mouse models, XIAP protein level measurement, apoptosis assay Human molecular genetics Medium 18178579
2008 Sirtuin SIRT1/sir-2.1 pathway and AMPK (aak-2) modulate mutant PABPN1 toxicity in muscle: increased sir-2.1 dosage exacerbates muscle pathology in a daf-16/FoxO- and aak-2/AMPK-dependent manner in C. elegans, while sir-2.1 null mutants are protective. SIRT1 inhibitor sirtinol promotes survival of mammalian cells expressing mutant PABPN1. C. elegans genetics (increased/null sir-2.1 dosage, double mutants), pharmacological treatment (sirtinol, resveratrol), mammalian cell survival assay Human molecular genetics Medium 18397876
2009 Expanded PABPN1 preferentially binds Hsp70 chaperones and type I arginine methyltransferases (PRMT1 and PRMT3) compared to wild-type PABPN1; these proteins accumulate at intranuclear inclusions in OPMD patient muscle. Molecular simulations suggest polyalanine expansion transitions PABPN1 from disordered to stable helical conformation, altering these interactions. Pull-down assays, immunofluorescence in patient muscle, molecular simulation PloS one Medium 19641605
2009 Fission yeast PABPN1 ortholog Pab2 is cotranscriptionally recruited to active genes via nascent mRNPs (demonstrated by RNase-sensitive ChIP), with recruitment preceding that of typical 3'-processing/polyadenylation factors; Pab2 also associates with polysomes, suggesting it remains associated with translated mRNPs after nuclear export. Chromatin immunoprecipitation (ChIP) with RNase treatment, tandem affinity purification coupled with mass spectrometry, polysome fractionation Nucleic acids research Medium 19336419
2012 Full-length PABPN1 forms amyloid-like fibrils in vitro independently of the alanine segment; fibril formation kinetics and denaturation resistance differ from those of the N-terminal domain alone, and FTIR spectroscopy plus limited proteolysis indicate the C-terminal domain is involved in fibril formation. In vitro fibril formation assay, FTIR spectroscopy, limited proteolysis, chaotropic denaturant resistance The Journal of biological chemistry Medium 22570486
2013 Fission yeast nuclear poly(A)-binding proteins Pab2 (PABPN1 ortholog) and Nab2 have opposing roles in posttranscriptional regulation: Pab2 promotes nuclear pre-mRNA decay via the nuclear exosome subunit Rrp6, while Nab2 impedes Pab2/Rrp6-mediated decay by competing with Pab2 for polyadenylated transcripts in the nucleus. Genetic epistasis (double mutants), RNA decay assays, northern blotting in S. pombe Molecular and cellular biology Medium 24081329
2013 A proline-tyrosine nuclear localization signal (PY-NLS) is necessary and sufficient for nuclear localization of fission yeast Pab2, functioning through Kap104 (Kapβ2 ortholog); however, neither a functional PY-NLS nor Kapβ2 activity are required for nuclear import of human PABPN1, indicating alternative or redundant import pathways exist for human PABPN1. NLS deletion/mutation analysis, nuclear localization assay, recombinant protein binding to Kap104, in vivo nuclear localization of human PABPN1 Traffic Medium 23279110
2014 ARIH2 E3 ubiquitin ligase regulates PABPN1 protein accumulation and aggregation; PABPN1 controls ARIH2 mRNA levels via proximal polyadenylation site usage, forming a feed-forward regulatory loop. Masking the proximal polyadenylation site in ARIH2 3' UTR using antisense oligonucleotides elevates both ARIH2 and PABPN1 expression and restores myogenic defects. Antisense oligonucleotide treatment, protein accumulation and aggregation assay, RNA expression analysis, myogenesis assay The American journal of pathology Medium 24486325
2015 PABPN1 negatively controls its own expression (autoregulation) by binding to an adenosine-rich region in its own 3' UTR, which promotes retention of the 3'-terminal intron and clearance of intron-retained pre-mRNAs by the nuclear exosome; increased PABPN1 dosage reduces the spliced/unspliced transcript ratio and decreases endogenous PABPN1 protein levels. PABPN1 dosage manipulation, spliced/unspliced RNA ratio measurement, nuclear exosome knockdown, RNA binding analysis Molecular and cellular biology High 25963658
2015 PABPN1 and poly(A) polymerase (PAP) coordinate splicing of a subset of introns that are excised after polyadenylation; PABPN1 promotes intron excision specifically in the context of 3'-end polyadenylation (not when bound to internal A-tracts), requiring its RNA-binding function and PAP-stimulatory function. N-terminal alanine-expanded PABPN1 cannot fully rescue PABPN1 depletion effects on this pathway. PABPN1 depletion (RNAi), PAP depletion, splicing assays, RNA-binding domain mutant analysis, exosome assays Molecular and cellular biology Medium 25896913
2015 PABPN1 suppresses TDP-43 toxicity; overexpression of full-length PABPN1 (but not a truncated form lacking the nuclear localization signal) promotes degradation of pathological TDP-43, restores normal TDP-43 solubility and nuclear localization, and facilitates removal of persistent stress granules. Reduced PABPN1 enhances TDP-43 pathological phenotypes and causes cytoplasmic mislocalization of TDP-43. Overexpression and knockdown in cell culture and Drosophila models, TDP-43 solubility fractionation, stress granule dynamics assay, nuclear localization analysis Human molecular genetics Medium 26130692
2016 Reduced PABPN1 levels in mouse tibialis anterior muscle cause consistent decline in distal polyadenylation site (PAS) utilization, leading to upregulation of Atrogin-1 (a key muscle atrophy regulator), reduced proteasomal gene expression and activity, and myofiber atrophy with extracellular matrix thickening. AAV-shRNA knockdown in mouse TA muscle, poly(A) site utilization analysis, gene expression profiling, proteasomal activity assay, histological analysis PLoS genetics Medium 27152426
2017 PABPN1 interacts with Matrin 3 (MATR3) in mouse skeletal muscle (identified by co-immunoprecipitation and mass spectrometry); together PABPN1 and MATR3 regulate alternative polyadenylation, intron retention, paraspeckle morphology and function, Neat1 lncRNA levels, and adenosine-to-inosine (A-to-I) RNA editing of Ctn RNA in muscle cells. Co-immunoprecipitation, mass spectrometry, RNAi knockdown, alternative polyadenylation assay, paraspeckle morphology analysis, RNA editing assay Nucleic acids research High 28977530
2019 PABPN1 regulates SIRT1 mRNA levels via alternative polyadenylation site utilization; reduced PABPN1 leads to elevated SIRT1 deacetylase activity, decreased protein acetylation, and muscle wasting. SIRT1 deacetylase inhibition by sirtinol increases PABPN1 levels and reverses muscle wasting. Transcriptome and proteome comparison, acetylome profiling, SIRT1 expression analysis, sirtinol pharmacological treatment in shPAB mouse muscles iScience Medium 30739015
2019 Expanded PABPN1 accumulates in mitochondria and interacts with the TIM23 mitochondrial protein import complex; both wild-type (10-alanine) and expanded (18-alanine) PABPN1 accumulate in mitochondria, but the 18-alanine form decreases cell viability and induces aggresome formation. Reduced OXPHOS complex expression was detected in transgenic OPMD mouse muscle. Mitochondrial fractionation, co-immunoprecipitation with TIM23, immunofluorescence in patient muscle and mouse model, OXPHOS complex expression analysis Laboratory investigation Medium 30894671
2020 PABPN1 is necessary for p63α mRNA translation by modulating binding of translation initiation factors eIF4E and eIF4G to p63α mRNA; PABPN1 deficiency also increases p63γ mRNA through alternative polyadenylation in coding sequence. p63α (especially ΔNp63α) regulates PABPN1 transcription, forming a feedback loop that controls keratinocyte differentiation. PABPN1 siRNA knockdown, APA analysis, translation initiation factor binding assay (eIF4E/eIF4G co-IP), ectopic ΔNp63α rescue, keratinocyte differentiation assay The Journal of investigative dermatology Medium 32243883
2022 PABPN1 promotes the formation of nuclear poly(A) domains (NPADs) in mouse oocytes through liquid phase separation, driven by its N-terminal disordered domain and RNA-recognition motif; Pabpn1-null oocytes cannot form NPADs normally, have defects in transcript stability and long 3'UTR isoform formation, and Pabpn1-null mice are completely sterile with primary ovarian insufficiency. Pabpn1 knockout mouse model, live imaging of phase separation, domain deletion analysis, RNA-seq for 3'UTR isoform analysis, fertility assessment Science advances High 36306357
2022 PABPN1 has a cytoplasmic function in zygotic genome activation (ZGA)-dependent maternal mRNA clearance; cytoplasmic PABPN1 docks on 3'-uridylated transcripts downstream of TUT4/TUT7 uridyltransferases and recruits 3'-5' exoribonuclease DIS3L2 to facilitate maternal mRNA decay. Pabpn1 knockout embryos arrest at the morula stage with failure to remove Z-decay maternal mRNAs. Pabpn1 knockout mouse, RNA immunoprecipitation, DIS3L2 co-immunoprecipitation, RNA-seq of maternal mRNA decay, developmental stage analysis Nucleic acids research High 34904664
2023 PABPN1 promotes splicing of last introns with weak 3' splice sites in a polyA tail length-dependent manner; PABPN1 depletion induces retention of introns with weak 3' splice sites. Tethering PABPN1 to non-polyadenylated transcripts also promotes splicing, demonstrating a direct role. PABPN1 recruits RBM26/27 to promote splicing by interacting with the coiled-coil and RRM domain of RBM27, as established by TurboID-MS interactome analysis. PABPN1 depletion, RNA tethering assay, TurboID proximity labeling mass spectrometry, Co-IP with RBM27, splicing assays in HeLa and mouse cells EMBO reports High 37661812
2023 The RNA-binding protein ZC3H11A interacts specifically with PABPN1 and requires PABPN1 for its localization into nuclear speckles; ZC3H11A uses the same zinc finger motifs to interact with both PABPN1 and viral mRNA. Lack of ZC3H11A alters polyadenylation of HAdV-5 capsid mRNA. ZC3H11A protein interactome (mass spectrometry), co-immunoprecipitation, nuclear speckle localization assay, viral mRNA polyadenylation analysis The Journal of biological chemistry Medium 37356722
2023 PABPN1 liquid-liquid phase separation (LLPS) is disrupted by interaction of SNRPD2 with the glutamic-proline (EP) domain of PABPN1 in colorectal cancer; disruption of PABPN1 LLPS attenuates repression of proximal poly(A) sites, leading to shortened 3' UTR of CTNNBIP1 that promotes cell proliferation and migration. PABPN1 phase separation assay, Co-IP identifying SNRPD2-PABPN1 interaction (EP domain), APA analysis, cell proliferation and migration assays Science China. Life sciences Medium 38811444
2023 PABPN1 aggregation is driven by both Ala stretch expansion and poly(A)-RNA binding: Ala expansion controls PABPN1 mobility in nuclear speckles and leads to aggregation; poly(A) nucleotide is essential for early-stage condensation facilitating speckle formation and transition to solid-like aggregates. PABPN1 aggregates sequester CFIm25 in an mRNA-dependent manner, impairing CFIm25 function in alternative polyadenylation. FRAP/live imaging in nuclear speckles, poly(A) RNA binding assay, CFIm25 co-localization and function assay, APA analysis The Journal of biological chemistry Medium 37422193
2024 PABPN1 is phosphorylated by mitotic kinases at four specific sites during mitosis; phospho-inhibitory mutations decrease cell proliferation and cause widespread poly(A) tail lengthening, while phospho-mimetic mutations result in shorter poly(A) tails with increased non-A nucleotides, increased transcription, and reduced stability of a distinct mRNA cohort. Phosphorylation thus remodels poly(A) tails and increases mRNA turnover to reset gene expression programs across the cell cycle. Stable cell lines with point mutations at phosphorylation sites, long-read sequencing for poly(A) tail length, TimeLapse-seq for mRNA synthesis and decay, cell proliferation assay Nucleic acids research High 38943343
2025 QKI promotes PABPN1 liquid-liquid phase separation (LLPS) in colorectal cancer cells; QKI is downregulated and loses nuclear localization in colorectal cancer, reducing PABPN1 phase separation and thereby promoting alternative polyadenylation, cell proliferation, and migration. Identified via CRISPR/BiFC/FACS screen. CRISPR/Cas9-based screening with bimolecular fluorescence complementation (BiFC) and FACS, QKI knockdown/overexpression, APA analysis, cell proliferation and migration assays Protein & cell Medium 40052530

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2017 Identification of HuR target circular RNAs uncovers suppression of PABPN1 translation by CircPABPN1. RNA biology 704 28080204
2005 The MexGHI-OpmD multidrug efflux pump controls growth, antibiotic susceptibility and virulence in Pseudomonas aeruginosa via 4-quinolone-dependent cell-to-cell communication. Microbiology (Reading, England) 170 15817779
2002 Characterization of a new efflux pump, MexGHI-OpmD, from Pseudomonas aeruginosa that confers resistance to vanadium. Microbiology (Reading, England) 142 12177331
2001 Oligomerization of polyalanine expanded PABPN1 facilitates nuclear protein aggregation that is associated with cell death. Human molecular genetics 101 11689481
2013 PABPN1: molecular function and muscle disease. The FEBS journal 97 23601051
2006 A Drosophila model of oculopharyngeal muscular dystrophy reveals intrinsic toxicity of PABPN1. The EMBO journal 76 16642034
2009 Bortezomib induces the formation of nuclear poly(A) RNA granules enriched in Sam68 and PABPN1 in sensory ganglia neurons. Neurotoxicity research 67 19609631
2003 Functional cloning and characterization of a multidrug efflux pump, mexHI-opmD, from a Pseudomonas aeruginosa mutant. Antimicrobial agents and chemotherapy 67 12937010
2017 Nuclear poly(A) binding protein 1 (PABPN1) and Matrin3 interact in muscle cells and regulate RNA processing. Nucleic acids research 62 28977530
2015 Regulated Intron Retention and Nuclear Pre-mRNA Decay Contribute to PABPN1 Autoregulation. Molecular and cellular biology 61 25963658
2005 In vivo aggregation properties of the nuclear poly(A)-binding protein PABPN1. RNA (New York, N.Y.) 59 15811916
2005 PABPN1 overexpression leads to upregulation of genes encoding nuclear proteins that are sequestered in oculopharyngeal muscular dystrophy nuclear inclusions. Neurobiology of disease 58 15755682
2017 PABPN1 gene therapy for oculopharyngeal muscular dystrophy. Nature communications 57 28361972
2003 Myopathy phenotype in transgenic mice expressing mutated PABPN1 as a model of oculopharyngeal muscular dystrophy. Human molecular genetics 52 14645203
2016 Correlation between PABPN1 genotype and disease severity in oculopharyngeal muscular dystrophy. Neurology 51 28011929
2008 Sirtuin inhibition protects from the polyalanine muscular dystrophy protein PABPN1. Human molecular genetics 51 18397876
2019 Delivery of mesenchymal stem cells-derived extracellular vesicles with enriched miR-185 inhibits progression of OPMD. Artificial cells, nanomedicine, and biotechnology 50 31219352
2003 Trinucleotide expansions leading to an extended poly-L-alanine segment in the poly (A) binding protein PABPN1 cause fibril formation. Protein science : a publication of the Protein Society 49 14627730
2013 A decline in PABPN1 induces progressive muscle weakness in oculopharyngeal muscle dystrophy and in muscle aging. Aging 47 23793615
2003 HnRNP A1 and A/B interaction with PABPN1 in oculopharyngeal muscular dystrophy. The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques 46 12945950
2005 Induction of HSP70 expression and recruitment of HSC70 and HSP70 in the nucleus reduce aggregation of a polyalanine expansion mutant of PABPN1 in HeLa cells. Human molecular genetics 43 16239242
2003 Nuclear poly(A)-binding protein PABPN1 is associated with RNA polymerase II during transcription and accompanies the released transcript to the nuclear pore. Experimental cell research 43 12749861
2017 Novel mouse models of oculopharyngeal muscular dystrophy (OPMD) reveal early onset mitochondrial defects and suggest loss of PABPN1 may contribute to pathology. Human molecular genetics 40 28575395
2011 Deregulation of the ubiquitin-proteasome system is the predominant molecular pathology in OPMD animal models and patients. Skeletal muscle 40 21798095
2005 Oculopharyngeal muscular dystrophy (OPMD): analysis of the PABPN1 gene expansion sequence in 86 patients reveals 13 different expansion types and further evidence for unequal recombination as the mutational mechanism. Human genetics 40 15645184
2022 PABPN1 functions as a hub in the assembly of nuclear poly(A) domains that are essential for mouse oocyte development. Science advances 39 36306357
2015 Poly(A) Polymerase and the Nuclear Poly(A) Binding Protein, PABPN1, Coordinate the Splicing and Degradation of a Subset of Human Pre-mRNAs. Molecular and cellular biology 39 25896913
2009 Hsp70 chaperones and type I PRMTs are sequestered at intranuclear inclusions caused by polyalanine expansions in PABPN1. PloS one 38 19641605
2008 Wild-type PABPN1 is anti-apoptotic and reduces toxicity of the oculopharyngeal muscular dystrophy mutation. Human molecular genetics 38 18178579
2011 Antiprion drugs 6-aminophenanthridine and guanabenz reduce PABPN1 toxicity and aggregation in oculopharyngeal muscular dystrophy. EMBO molecular medicine 37 21204267
2005 Transgenic expression of an expanded (GCG)13 repeat PABPN1 leads to weakness and coordination defects in mice. Neurobiology of disease 37 15755680
2016 PABPN1-Dependent mRNA Processing Induces Muscle Wasting. PLoS genetics 36 27152426
2022 Nuclear poly(A) binding protein 1 (PABPN1) mediates zygotic genome activation-dependent maternal mRNA clearance during mouse early embryonic development. Nucleic acids research 34 34904664
2007 Soluble expanded PABPN1 promotes cell death in oculopharyngeal muscular dystrophy. Neurobiology of disease 34 17418585
2019 Inhibition of myostatin improves muscle atrophy in oculopharyngeal muscular dystrophy (OPMD). Journal of cachexia, sarcopenia and muscle 33 31066242
2013 Control of mRNA stability contributes to low levels of nuclear poly(A) binding protein 1 (PABPN1) in skeletal muscle. Skeletal muscle 33 24083404
2008 PABPN1 polyalanine tract deletion and long expansions modify its aggregation pattern and expression. Experimental cell research 33 18367172
2022 Exosome-Mediated Transfer of miR-1323 from Cancer-Associated Fibroblasts Confers Radioresistance of C33A Cells by Targeting PABPN1 and Activating Wnt/β-Catenin Signaling Pathway in Cervical Cancer. Reproductive sciences (Thousand Oaks, Calif.) 32 35334101
2006 Oculopharyngeal muscular dystrophy: a point mutation which mimics the effect of the PABPN1 gene triplet repeat expansion mutation. Journal of medical genetics 32 16648376
2011 Modeling oculopharyngeal muscular dystrophy in myotube cultures reveals reduced accumulation of soluble mutant PABPN1 protein. The American journal of pathology 30 21854744
2009 Cotranscriptional recruitment of the nuclear poly(A)-binding protein Pab2 to nascent transcripts and association with translating mRNPs. Nucleic acids research 28 19336419
2002 Characterization of outer membrane efflux proteins OpmE, OpmD and OpmB of Pseudomonas aeruginosa: molecular cloning and development of specific antisera. FEMS microbiology letters 28 12445646
2014 A novel feed-forward loop between ARIH2 E3-ligase and PABPN1 regulates aging-associated muscle degeneration. The American journal of pathology 27 24486325
2013 Poly(A) tail-mediated gene regulation by opposing roles of Nab2 and Pab2 nuclear poly(A)-binding proteins in pre-mRNA decay. Molecular and cellular biology 25 24081329
2003 Oculopharyngeal muscular dystrophy (OPMD) due to a small duplication in the PABPN1 gene. Human mutation 25 12673802
2015 PABPN1 suppresses TDP-43 toxicity in ALS disease models. Human molecular genetics 24 26130692
2023 The polyA tail facilitates splicing of last introns with weak 3' splice sites via PABPN1. EMBO reports 23 37661812
2013 A proline-tyrosine nuclear localization signal (PY-NLS) is required for the nuclear import of fission yeast PAB2, but not of human PABPN1. Traffic (Copenhagen, Denmark) 22 23279110
2021 Propofol suppresses colorectal cancer development by the circ-PABPN1/miR-638/SRSF1 axis. Analytical biochemistry 21 34453920
2012 Depletion of nuclear poly(A) binding protein PABPN1 produces a compensatory response by cytoplasmic PABP4 and PABP5 in cultured human cells. PloS one 21 23300856
2011 Reversible aggregation of PABPN1 pre-inclusion structures. Nucleus (Austin, Tex.) 19 21818414
2015 PABPN1 (GCN)11 as a Dominant Allele in Oculopharyngeal Muscular Dystrophy -Consequences in Clinical Diagnosis and Genetic Counselling. Journal of neuromuscular diseases 18 27858728
2008 Hofmeister salts and potential therapeutic compounds accelerate in vitro fibril formation of the N-terminal domain of PABPN1 containing a disease-causing alanine extension. Biochemistry 18 18205394
2018 Post-transcriptional regulation of Pabpn1 by the RNA binding protein HuR. Nucleic acids research 17 29939290
2012 PABPN1 shuts down alternative poly(A) sites. Cell research 17 22641371
2007 Nuclear compartmentalization and dynamics of the poly(A)-binding protein nuclear 1 (PABPN1) inclusions in supraoptic neurons under physiological and osmotic stress conditions. Molecular and cellular neurosciences 17 18255312
2021 Oral Potentially Malignant Disorders (OPMD): What is the clinical utility of dysplasia grade? Expert review of molecular diagnostics 16 33682567
2012 Nuclear speckles are involved in nuclear aggregation of PABPN1 and in the pathophysiology of oculopharyngeal muscular dystrophy. Neurobiology of disease 16 22249111
2017 An alanine expanded PABPN1 causes increased utilization of intronic polyadenylation sites. NPJ aging and mechanisms of disease 15 28649424
2007 Effect of oculopharyngeal muscular dystrophy-associated extension of seven alanines on the fibrillation properties of the N-terminal domain of PABPN1. The FEBS journal 15 17229142
2006 The dynamism of PABPN1 nuclear inclusions during the cell cycle. Neurobiology of disease 15 16860991
2024 Disruption of PABPN1 phase separation by SNRPD2 drives colorectal cancer cell proliferation and migration through promoting alternative polyadenylation of CTNNBIP1. Science China. Life sciences 14 38811444
2023 PABPN1 regulates mRNA alternative polyadenylation to inhibit bladder cancer progression. Cell & bioscience 14 36879298
2005 (GCG)11 founder mutation in the PABPN1 gene of OPMD Uruguayan families. Neuromuscular disorders : NMD 14 15694141
1997 Oculopharyngeal muscular dystrophy (OPMD)--report and genetic studies of an Australian kindred. Clinical genetics 14 9084936
2022 Novel read-through fusion transcript Bcl2l2-Pabpn1 in glioblastoma cells. Journal of cellular and molecular medicine 13 35894779
2019 Deacetylation Inhibition Reverses PABPN1-Dependent Muscle Wasting. iScience 13 30739015
2012 Polyalanine-independent conformational conversion of nuclear poly(A)-binding protein 1 (PABPN1). The Journal of biological chemistry 13 22570486
2017 Dysfunctional transcripts are formed by alternative polyadenylation in OPMD. Oncotarget 12 29088723
2015 Automated design of hammerhead ribozymes and validation by targeting the PABPN1 gene transcript. Nucleic acids research 12 26527730
2010 Cross-talk between canonical Wnt signaling and the sirtuin-FoxO longevity pathway to protect against muscular pathology induced by mutant PABPN1 expression in C. elegans. Neurobiology of disease 12 20227501
2007 Multiple mitochondrial DNA deletions in monozygotic twins with OPMD. Journal of neurology, neurosurgery, and psychiatry 12 17550990
2023 MiRNAs as non-invasive biomarkers in the serum of Oral Squamous Cell Carcinoma (OSCC) and Oral Potentially Malignant Disorder (OPMD) patients. Archives of oral biology 11 36657275
2020 PABPN1, a Target of p63, Modulates Keratinocyte Differentiation through Regulation of p63α mRNA Translation. The Journal of investigative dermatology 11 32243883
2012 Oculopharyngeal muscular dystrophy --an under-diagnosed disease in China? Report a China-born Chinese with PABPN1 mutation and epidemiology review of the literature. Journal of the Formosan Medical Association = Taiwan yi zhi 11 22817818
2024 Areca nut-induced metabolic reprogramming and M2 differentiation promote OPMD malignant transformation. Journal of experimental & clinical cancer research : CR 10 39160581
2022 Assessment of PABPN1 nuclear inclusions on a large cohort of patients and in a human xenograft model of oculopharyngeal muscular dystrophy. Acta neuropathologica 10 36197469
2021 Anti-prion Drugs Targeting the Protein Folding Activity of the Ribosome Reduce PABPN1 Aggregation. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics 10 33533011
2024 PABPN1 loss-of-function causes APA-shift in oculopharyngeal muscular dystrophy. HGG advances 9 38213032
2021 A Japanese case of oculopharyngeal muscular dystrophy (OPMD) with PABPN1 c.35G > C; p.Gly12Ala point mutation. BMC neurology 9 34225694
2019 Mitochondrial localization of PABPN1 in oculopharyngeal muscular dystrophy. Laboratory investigation; a journal of technical methods and pathology 9 30894671
2011 Two cases of oculopharyngeal muscular dystrophy (OPMD) with the rare PABPN1 c.35G>C; p.Gly12Ala point mutation. Neuromuscular disorders : NMD 9 21742497
2005 Oculopharyngeal muscular dystrophy with PABPN1 mutation in a Chinese Malaysian woman. Neuromuscular disorders : NMD 9 15725589
2024 Dysregulation of RNA-Exosome machinery is directly linked to major cancer hallmarks in prostate cancer: Oncogenic role of PABPN1. Cancer letters 8 38244911
2023 The RNA-binding protein ZC3H11A interacts with the nuclear poly(A)-binding protein PABPN1 and alters polyadenylation of viral transcripts. The Journal of biological chemistry 8 37356722
2023 PABPN1 promotes clear cell renal cell carcinoma progression by suppressing the alternative polyadenylation of SGPL1 and CREG1. Carcinogenesis 8 37452741
2020 Cytoskeletal disorganization underlies PABPN1-mediated myogenic disability. Scientific reports 8 33077830
2019 Established PABPN1 intranuclear inclusions in OPMD muscle can be efficiently reversed by AAV-mediated knockdown and replacement of mutant expanded PABPN1. Human molecular genetics 8 31294444
2016 Characterization of PABPN1 expansion mutations in a large cohort of Mexican patients with oculopharyngeal muscular dystrophy (OPMD). Journal of investigative medicine : the official publication of the American Federation for Clinical Research 8 27980005
2008 Two different PABPN1 expanded alleles in a Mexican population with oculopharyngeal muscular dystrophy arising from independent founder effects. The British journal of ophthalmology 8 18577654
2024 Phosphorylation of the nuclear poly(A) binding protein (PABPN1) during mitosis protects mRNA from hyperadenylation and maintains transcriptome dynamics. Nucleic acids research 6 38943343
2023 Expression of Human Papillomavirus and the p16 Gene in Oral Potentially Malignant Disorders (OPMD): a Comparative Study With Oral Squamous Cell Carcinoma. Applied immunohistochemistry & molecular morphology : AIMM 6 37036407
2023 PABPN1 aggregation is driven by Ala expansion and poly(A)-RNA binding, leading to CFIm25 sequestration that impairs alternative polyadenylation. The Journal of biological chemistry 6 37422193
2022 Characterization of a Read-through Fusion Transcript, BCL2L2-PABPN1, Involved in Porcine Adipogenesis. Genes 6 35327999
2017 Functional impact of an oculopharyngeal muscular dystrophy mutation in PABPN1. The Journal of physiology 6 28303574
2010 Structural basis for a PABPN1 aggregation-preventing antibody fragment in OPMD. FEBS letters 6 20226184
2008 A case of rare recessive oculopharyngeal muscular dystrophy (OPMD) coexisting with hereditary neuropathy with liability to pressure palsies (HNPP). Clinical neurology and neurosurgery 6 18358598
2008 Monitoring fibril formation of the N-terminal domain of PABPN1 carrying an alanine repeat by tryptophan fluorescence and real-time NMR. FEBS letters 6 18406354
2016 [Haplotype Analysis of Oculopharyngeal Muscular Dystrophy (OPMD) Locus in Yakutia]. Genetika 5 27281858
2025 BiFC and FACS-based CRISPR screening revealed that QKI promotes PABPN1 LLPS in colorectal cancer cells. Protein & cell 4 40052530

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