Affinage

HNRNPU

Heterogeneous nuclear ribonucleoprotein U · UniProt Q00839

Length
825 aa
Mass
90.6 kDa
Annotated
2026-06-10
100 papers in source corpus 42 papers cited in narrative 42 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

HNRNPU (SAF-A/hnRNP-U) is a multifunctional nuclear scaffold protein that organizes 3D genome architecture by directly contacting both chromosomal DNA and RNA and oligomerizing into a dynamic RNA-chromatin mesh (PMID:1324173, PMID:9204873, PMID:28622508). It binds scaffold/matrix attachment region (SAR/S/MAR) DNA elements through a bipartite SAR-specific domain that is structurally and functionally separable from its C-terminal RGG RNA-binding domain (PMID:1324173, PMID:8068679, PMID:9405365), and is bound directly to chromosomal DNA in vivo rather than through protein bridges (PMID:8174554, PMID:9204873). Genome-scale studies establish that HNRNPU maintains TAD boundaries, A/B compartments, chromatin loops, and lamina-associated domains, associating mainly with active chromatin and co-occupying sites with CTCF/RAD21 (PMID:29273625); this scaffolding activity depends on RGG-mediated binding to chromatin-associated RNAs and on cycles of oligomerization driven by its AAA+ ATPase domain, with oligomerization decompacting chromatin and loss or monomerization causing aberrant folding and genome damage (PMID:28622508). Through its RGG domain HNRNPU binds noncoding RNAs to control chromatin states, localizing to the inactive X via XIST RNA to maintain Xi heterochromatin (PMID:14608463, PMID:40493679) and mediating long-range Polycomb recruitment by the lncRNAs Airn, Kcnq1ot1, and Xist (PMID:40791421). As an RNA-binding regulator it binds essentially all spliceosomal snRNAs, governs U2 snRNP maturation and Cajal body morphology, and shapes global alternative splicing (PMID:22325991), while also stabilizing specific target mRNAs through 3'-UTR binding (PMID:17174306, PMID:32302342). HNRNPU function is regulated by phosphorylation of Ser59 — by DNA-PK in response to DNA double-strand breaks, where its phosphorylation status tracks NHEJ repair capacity (PMID:19351595, PMID:19844162), and by PLK1 during mitosis with PP2A-mediated dephosphorylation required for accurate chromosome segregation and mitotic exit (PMID:25986610). At sites of damage it is transiently recruited via poly(ADP-ribose) and then excluded in an ATM/ATR/DNA-PK-dependent manner as part of an anti-R-loop response (PMID:25030905), and it directly stimulates NEIL1-mediated excision of oxidized bases (PMID:22902625). In vivo conditional loss causes cell death of cortical neurons and progenitors with dysregulated splicing of survival and synaptic genes (PMID:35864088), and failures in spermatogenesis (PMID:34815802, PMID:38625792), reflecting its essential roles in genome organization and RNA processing.

Mechanistic history

Synthesis pass · year-by-year structured walk · 21 steps
  1. 1992 High

    Established HNRNPU's founding identity: it was unknown what proteins anchor chromatin loops to the nuclear scaffold; SAF-A was purified as a SAR/MAR-binding protein that mediates looped DNA structures, defining a structural role in chromatin loop organization.

    Evidence Protein purification, competition binding assays, and electron microscopy of SAR-element complexes

    PMID:1324173

    Open questions at the time
    • Sequence-specificity of SAR recognition and in vivo loop topology not resolved
    • Relationship to hnRNA metabolism unaddressed at this stage
  2. 1994 High

    Unified two protein identities and demonstrated dual nucleic-acid binding: it was unclear whether the scaffold protein and hnRNP-U were the same; UV cross-linking showed SAF-A=hnRNP-U is bound to chromosomal DNA in vivo and binds ds/ssDNA and RNA, predicting dual chromatin/hnRNA roles.

    Evidence UV cross-linking and filter-binding with diverse nucleic acid substrates; isoform purification with EM

    PMID:8068679 PMID:8174554

    Open questions at the time
    • Distinct DNA vs RNA binding sites inferred but not mapped
    • Functional consequence of isoform differences unknown
  3. 1997 High

    Defined separable DNA- and RNA-binding modules and direct DNA contact: it was unknown whether scaffold attachment and hnRNP functions reside in one domain; mutagenesis localized a bipartite SAR-specific DNA-binding domain independent of the RGG domain, and orthogonal cross-linking proved direct DNA contact.

    Evidence Domain deletion/mutation, apoptosis fractionation, formaldehyde/DMS cross-linking with protease digestion

    PMID:9204873 PMID:9405365

    Open questions at the time
    • Structural basis of bipartite domain not solved
    • How the two domains are coordinated on chromatin not addressed
  4. 2000 High

    Resolved how HNRNPU is dismantled during apoptosis: the protease and site were unknown; caspase-3 was shown to cleave at a non-canonical SALD motif (Asp-100), with D100A abolishing cleavage, defining a regulated detachment from chromatin during cell death.

    Evidence Recombinant caspase-3 assay, MS/Edman sequencing, D100A mutagenesis in vitro and in vivo

    PMID:10671544

    Open questions at the time
    • Functional consequence of cleavage for apoptotic chromatin disassembly not directly tested
  5. 2002 High

    Identified a non-degradative regulatory partnership: it was unknown how HNRNPU controls ubiquitin ligase activity; HNRNPU was shown to be the major nuclear partner of SCF(beta-TrCP), acting as a pseudosubstrate that stabilizes and nuclear-localizes the E3 and sets a substrate threshold.

    Evidence Affinity purification, reciprocal Co-IP, peptide competition, WD-region point mutation, ubiquitination assay

    PMID:11850407 PMID:11897664

    Open questions at the time
    • Physiological substrates whose threshold is set by HNRNPU not enumerated
    • Link between scaffolding and E3 sequestration unclear
  6. 2003 Medium

    Connected HNRNPU to facultative heterochromatin via RNA: the basis of its Xi enrichment was unknown; the RGG domain was shown to retain SAF-A at the Xi nuclear matrix and co-localize with XIST RNA, implicating it in Xi architecture.

    Evidence Immunofluorescence, nuclear matrix extraction, RGG-deletion constructs, XIST co-localization

    PMID:14608463

    Open questions at the time
    • Direct XIST-HNRNPU binding not biochemically demonstrated here
    • Causal contribution to silencing not tested
  7. 2006 Medium

    Extended HNRNPU into transcriptional and post-transcriptional regulation: it was unknown whether it modulates specific transcription factors and mRNAs; direct WT1 binding modulated WT1 target transcription, and 3'-UTR binding stabilized a defined panel of mRNAs.

    Evidence Endogenous Co-IP and domain mapping (WT1); RNAi with mRNA stability and 3'-UTR binding (TNF-alpha, GADD45A et al.)

    PMID:16924231 PMID:17174306

    Open questions at the time
    • Whether mRNA stabilization is direct vs scaffold-mediated not separated
    • Generality of 3'-UTR target set untested
  8. 2009 High

    Placed HNRNPU in the DNA-damage signaling network: the relevant kinase and site were unknown; Ser59 was identified as a DNA-PK phosphosite induced by double-strand breaks, with phosphorylation extent inversely tracking NHEJ repair capacity.

    Evidence Cell-free kinase assays, phospho-specific antibody, kinase inhibitors, NHEJ-deficient lines, MS site mapping

    PMID:19351595 PMID:19844162

    Open questions at the time
    • Direct effect of Ser59 phosphorylation on HNRNPU chromatin binding not yet defined
    • Downstream repair effectors unspecified at this stage
  9. 2011 High

    Revealed a mitotic, cytoplasmic role and key partners: it was unclear whether HNRNPU acts outside interphase chromatin; it was shown to localize to spindles, bind microtubules directly, co-IP with nucleolin, Aurora-A and TPX2, and be required for spindle assembly and chromosome alignment.

    Evidence RNAi, immunofluorescence, endogenous Co-IP, direct microtubule binding, depletion epistasis

    PMID:21242313

    Open questions at the time
    • How a chromatin scaffold protein is repurposed to spindles mechanistically unresolved
    • Relationship to its mitotic exclusion from chromatin not yet linked
  10. 2011 Medium

    Linked HNRNPU to the core transcription/remodeling machinery: it was unknown how it supports Pol II output; it bound the Pol II CTD and BRG1, with HNRNPU/BRG1 co-depletion abolishing global Pol II (not Pol I) transcription, and bound the Oct4 promoter in ES cells.

    Evidence ChIP, RNAi double knockdown, Co-IP, PLA, transcription assays

    PMID:21235343 PMID:22162999

    Open questions at the time
    • Whether the BRG1 interaction is direct not established
    • Mechanistic basis of joint requirement for Pol II transcription unresolved
  11. 2012 High

    Defined HNRNPU as a regulator of the splicing machinery and oxidative repair: it was unknown how broadly it controls RNA processing; CLIP-seq showed binding to all spliceosomal snRNAs with control of U2 snRNP maturation and global splicing, while direct NEIL1 binding stimulated oxidized-base excision via enhanced product release.

    Evidence CLIP-seq/RNA-seq with Cajal body assays; in vitro BER reconstitution, Kd, domain mapping, epistasis

    PMID:22325991 PMID:22902625

    Open questions at the time
    • How snRNA binding mechanistically drives U2 maturation not fully resolved
    • Connection between splicing role and chromatin scaffolding not bridged here
  12. 2014 High

    Resolved HNRNPU dynamics at damage sites: it was unknown how it behaves at lesions; live imaging revealed biphasic PAR-dependent recruitment then ATM/ATR/DNA-PK-dependent exclusion of transcription-associated SAF-A, functioning in an anti-R-loop mechanism.

    Evidence Laser micro-irradiation, live imaging, PAR-binding, kinase inhibitors, DNA:RNA hybrid reporter

    PMID:25030905

    Open questions at the time
    • Direct link between Ser59 phosphorylation and the exclusion phase not established here
    • Which RNA species mediate R-loop suppression unspecified
  13. 2015 High

    Distinguished mitotic from damage-related Ser59 control: it was unclear what regulates Ser59 in mitosis; PLK1 (not DNA-PK) phosphorylates Ser59 and PP2A dephosphorylates it, with both required for accurate segregation and mitotic exit.

    Evidence Phospho-antibody, kinase inhibitors, PLK1 Co-IP, phosphatase identification, S59A phenotypes

    PMID:25986610

    Open questions at the time
    • Substrate(s) downstream of Ser59 phospho-cycling in mitosis unknown
    • How the same site integrates damage vs mitotic inputs unresolved
  14. 2016 Medium

    Connected Ser59 phosphorylation to repair pathway choice: it was unknown how HNRNPU coordinates competing repair pathways; DNA-PK-phosphorylated SAF-A transiently releases NEIL1 from chromatin, relieving Ku-mediated glycosylase inhibition only when dephosphorylated, prioritizing NHEJ over BER at clustered lesions.

    Evidence In vitro glycosylase inhibition assays, D59 phosphomimetic, chromatin fractionation after IR

    PMID:27303920

    Open questions at the time
    • In vitro reconstitution not confirmed at endogenous chromatin in cells
    • Single-lab finding awaiting independent replication
  15. 2017 High

    Provided the unifying mechanistic model for genome organization: it was unknown how HNRNPU physically shapes the genome; RGG-mediated caRNA binding plus AAA+ ATPase-driven oligomerization cycles form a chromatin mesh that decompacts chromatin, while loss/monomerization causes aberrant folding and damage, and genome-wide assays confirmed maintenance of TADs, compartments, loops and LADs.

    Evidence Domain mutagenesis, Hi-C, live imaging, oligomerization/ATP assays; conditional KO with Hi-C/DamID/ChIP-seq in hepatocytes

    PMID:28622508 PMID:29273625

    Open questions at the time
    • Structure of the oligomeric mesh not determined
    • How ATPase cycling is regulated in vivo unclear
  16. 2018 Medium

    Showed enhancer-RNA-guided coactivator recruitment: it was unknown whether HNRNPU bridges eRNAs to coactivators; HPSE eRNA binding facilitated HNRNPU-p300 super-enhancer enrichment and chromatin looping to activate target genes.

    Evidence Co-IP, ChIP, chromatin conformation capture, gain/loss-of-function

    PMID:29511351

    Open questions at the time
    • Direct eRNA-HNRNPU binding mode not mapped
    • Generality beyond the HPSE locus untested
  17. 2020 Medium

    Expanded cytoplasmic and RNA-trafficking roles: it was unclear whether HNRNPU acts in the cytoplasm; it directly binds IL-6 3'-UTR in the cytoplasmic fraction and retains/stabilizes miR-30c-5p in the nucleus to limit its vesicular export, while hepatic loss disrupted chromatin accessibility and TrkB isoform expression.

    Evidence HITS-CLIP with fractionation; RIP/EMSA/miR-pulldown; conditional KO RNA-seq/ChIP-seq with rescue

    PMID:31469911 PMID:32302342 PMID:32944175

    Open questions at the time
    • Nucleocytoplasmic partitioning control not defined
    • Single-lab disease-context findings
  18. 2022 High

    Linked HNRNPU to replication, ubiquitin-dependent chromatin condensation, repair condensates, and tissue development: its roles in S-phase, CTCF-cohesin modulation, class-switch recombination and neurodevelopment were unknown; studies showed it promotes origin licensing/fork progression, that CDC20 ubiquitination drives CTCF-cohesin association, that it facilitates C-NHEJ S-S joining via G-quadruplex/R-loop control in LLPS-sensitive condensates, and that its loss kills cortical neurons/progenitors with splicing dysregulation.

    Evidence DNA fiber/MCM loading assays; AP-MS, Co-IP, domain mapping, condensation assays; conditional KO CSR with G4/R-loop and LLPS-inhibitor assays; in vivo cortical truncation with RNA-seq and rescue

    PMID:34888666 PMID:35864088 PMID:35954396 PMID:36943867

    Open questions at the time
    • Mechanistic integration of these roles with the oligomeric mesh model not established
    • Several findings single-lab and context-specific
  19. 2023 Medium

    Identified a lipid-binding capacity within the SAP domain: it was unknown that HNRNPU contacts phosphoinositides; a lysine-rich polybasic motif (aa 9–24) directly bound polyphosphoinositides, implying dual DNA/PPIn functions for the SAP domain.

    Evidence Quantitative interactomics, direct PPIn binding assay, deletion mutagenesis

    PMID:37038481

    Open questions at the time
    • Functional role of PPIn binding undefined
    • Single-study, single-lab observation
  20. 2024 Medium

    Defined RNA-binding requirements in germline development and a cytoplasmic disease axis: it was unknown which transcripts HNRNPU regulates in spermatogenesis; conditional loss in prospermatogonia caused splicing defects in Vrk1/Slx4/Dazl and SSC-pool failure, while circMYO9B-driven cytoplasmic translocation stabilized KDM1A to promote VEGFA/angiogenesis.

    Evidence Conditional KO, single-cell transcriptomics, RNA-binding/splicing assays; Co-IP, fractionation, ubiquitination assay, in vivo wound model

    PMID:38625792 PMID:39725699

    Open questions at the time
    • Direct vs indirect splicing targets not fully separated
    • Disease-context mechanism single-lab
  21. 2025 High

    Dissected domain-specific contributions to Xi maintenance, dynamics, and lncRNA-directed Polycomb recruitment: it was unclear which domains and residues drive each activity; allelic reconstitution showed the SAP domain (with S14/S26) and a Xi-localization signal control XIST localization and dynamics, while the ATPase and RGG domains maintain XIST/heterochromatin and splicing, α-satellite RNA reestablishes chromatin association after mitosis, and HNRNPU is required for Airn/Kcnq1ot1/Xist-directed Polycomb modifications.

    Evidence Allelic reconstitution, FRAP, XIST FISH, heterochromatin ChIP, splicing analysis; α-satellite RNA depletion with segregation assays; RIP and PRC modification assays (two preprints)

    PMID:40219970 PMID:40493679 PMID:40791421 PMID:41473319

    Open questions at the time
    • ATP-binding vs hydrolysis effects on Xi only partially resolved
    • Two of the lncRNA/ATPase findings are preprints awaiting peer review

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the distinct activities — ATPase-driven oligomeric chromatin mesh, snRNA/splicing regulation, lncRNA-directed heterochromatin, DNA-repair condensates, and Ser59 phospho-switching — are integrated into a single regulated protein remains the central open question.
  • No high-resolution structure of the oligomeric RNA-chromatin mesh
  • Mechanism coupling phosphorylation/ubiquitination state to scaffold assembly unresolved
  • Whether cytoplasmic and nuclear functions are coordinated or independent unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 5 GO:0003677 DNA binding 4 GO:0005198 structural molecule activity 3 GO:0140110 transcription regulator activity 3 GO:0008092 cytoskeletal protein binding 1 GO:0008289 lipid binding 1 GO:0140657 ATP-dependent activity 1
Localization
GO:0000228 nuclear chromosome 3 GO:0005634 nucleus 3 GO:0005654 nucleoplasm 2 GO:0005829 cytosol 2 GO:0005856 cytoskeleton 1
Pathway
R-HSA-73894 DNA Repair 5 R-HSA-1640170 Cell Cycle 4 R-HSA-4839726 Chromatin organization 4 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-8953854 Metabolism of RNA 3 R-HSA-5357801 Programmed Cell Death 2 R-HSA-69306 DNA Replication 1
Partners
AURKABRG1/SMARCA4BTRCCDC20DDX5NEIL1TPX2WT1
Complex memberships
53BP1-shieldin/C-NHEJ complexSCF(beta-TrCP) ubiquitin ligase (pseudosubstrate partner)SWI/SNF (BRG1-associated)

Evidence

Reading pass · 42 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 SAF-A (HNRNPU) was identified as a novel nuclear DNA-binding protein and constituent of the nuclear matrix/scaffold. The purified 120 kDa protein binds at multiple sites to human SAR (scaffold attachment region) elements, with binding sites residing in A/T-stretches. The protein forms large aggregates and mediates formation of looped DNA structures, suggesting a structural role in organizing chromatin loop domains. Protein purification, competition binding assays with synthetic polynucleotides, electron microscopy The EMBO journal High 1324173
1994 SAF-A is identical to hnRNP-U. UV cross-linking demonstrated the protein is bound to chromosomal DNA in vivo. In vitro, the protein binds both double-stranded and single-stranded DNA and RNA, likely at different binding sites, indicating dual roles in chromatin organization and hnRNA metabolism. UV cross-linking, filter-binding experiments with diverse nucleic acid substrates European journal of biochemistry High 8174554
1994 Two isoforms of hnRNP-U (form 1 and form 2) were purified and shown to differ in primary structure. Both isoforms bind double- and single-stranded DNA and RNA, form higher-ordered nucleic acid/protein complexes, and specifically bind and aggregate the human SAR element. The two isoforms differ morphologically: form 1 forms long unbranched filamentous DNA complexes while form 2 forms spherical aggregates (~35 nm diameter). Chromatographic purification, electron microscopy, nucleic acid binding assays Biochemistry High 8068679
1997 SAF-A possesses a novel bipartite SAR-specific DNA-binding domain that is independent of its C-terminal RGG RNA-binding domain. During apoptosis, caspase-dependent cleavage occurs within this bipartite DNA-binding domain, causing loss of DNA-binding activity and detachment from nuclear structural sites without affecting hnRNP complex association, indicating the two functional domains are separable. Domain deletion/mutation analysis, apoptosis induction, subcellular fractionation The EMBO journal High 9405365
1997 hnRNP-U/SAF-A is directly bound to chromosomal DNA in vivo, as demonstrated by formaldehyde cross-linking followed by CsCl density gradient purification. Dimethylsulfate cross-linking and limited protease digestion established that hnRNP-U contacts DNA directly rather than through bridging to other proteins. Formaldehyde cross-linking, CsCl density gradient centrifugation, dimethylsulfate cross-linking, limited protease digestion, western blotting Biochemistry High 9204873
2000 Caspase-3 cleaves SAF-A at Asp-100 within the non-canonical sequence SALD (rather than the canonical DEXD motif) in vitro and in vivo during apoptosis. A D100A point mutation abrogates cleavage by recombinant caspase-3 in vitro and during apoptosis in vivo, confirming SALD as a novel caspase-3 cleavage site. Recombinant caspase-3 in vitro cleavage assay, MALDI-TOF mass spectrometry, Edman sequencing, site-directed mutagenesis (D100A), in vivo apoptosis assay The Journal of biological chemistry High 10671544
2001 hnRNP-U/SAF-A represses glucocorticoid receptor (GR)-dependent transcription. A construct lacking the GR-binding domain of hnRNP-U acts as a dominant negative factor that enhances GR-driven transcription. The repressive effect depends on relative concentrations of GR, hnRNP-U and GR DNA-binding sites, suggesting hnRNP-U acts as a storage site for intranuclear GR. Transient transfection of hnRNP-U deletion constructs, reporter gene assays in Ltk(-) cells The Journal of steroid biochemistry and molecular biology Medium 11530285
2002 hnRNP-U is the major nuclear binding partner of the SCF(β-TrCP) ubiquitin ligase subunit β-TrCP/E3RS. hnRNP-U occupies E3RS stoichiometrically, stabilizes the E3 component, and is responsible for its nuclear localization. hnRNP-U acts as a pseudosubstrate—binding via the WD region in an E3-substrate-type interaction but not being targeted for degradation—and dissociates from E3RS upon competition by high-affinity substrate, enabling substrate ubiquitination. Affinity purification, Co-IP, competition with pIκBα peptide, point mutation in WD region Genes & development High 11850407
2002 An episomally replicating plasmid (pEPI-1) containing a S/MAR element binds exclusively to hnRNP-U/SAF-A in the nuclear matrix, as demonstrated by cis-diamminedichloroplatinum II cross-linking and southwestern analysis. Immunoprecipitation of the cross-linked DNA-protein complex confirmed that pEPI-1 is bound to hnRNP-U/SAF-A in vivo, providing the basis for episome mitotic stability. Cross-linking with cis-diamminedichloroplatinum II, nuclear matrix co-purification, southwestern analysis, immunoprecipitation EMBO reports Medium 11897664
2003 SAF-A is enriched at the inactive X chromosome (Xi) territory through its RGG RNA-binding domain. After removal of DNA and chromatin proteins, SAF-A remains with the nuclear matrix at the Xi. The enrichment depends on the RGG domain, raising the possibility that SAF-A interaction with XIST RNA contributes to Xi silencing through local changes in nuclear architecture. Immunofluorescence, nuclear matrix extraction, domain-deletion constructs, XIST RNA co-localization Chromosoma Medium 14608463
2006 hnRNP-U directly interacts with the Wilms' tumour protein WT1 without requiring other proteins or nucleic acids; the interaction involves the zinc-fingers of WT1 and the middle domain of hnRNP-U. hnRNP-U modulates WT1 transcriptional activation of a bona fide WT1 target gene. Co-IP of endogenous proteins, domain deletion/interaction mapping, transcriptional reporter assay Oncogene Medium 16924231
2006 hnRNP-U enhances expression of specific genes including TNF-α, GADD45A, HEXIM1, HOXA2, IER3, NHLH2, and ZFY by binding to and stabilizing their mRNAs, likely through binding to 3' UTR sequences. RNAi knockdown, mRNA stability assays, 3' UTR binding FEBS letters Medium 17174306
2008 SAF-A binds to the 3'-flanking region of the Bmal1 promoter with circadian timing in vivo (detected by in vivo footprinting), and this rhythmic binding correlates with circadian Bmal1 transcription. The RORE region of the Bmal1 promoter resides in GC-rich open chromatin, and the 3'-flanking region inhibits rhythmic transcription in reporter assays. In vivo DNase I footprinting, in vitro reporter gene assay Molecular and cellular biology Medium 18332112
2009 hnRNP-U/SAF-A is phosphorylated at Ser59 specifically by DNA-PK in vitro and in cells in response to DNA double-strand breaks. This was identified using a cell-free system for dissecting DNA damage kinase substrates. Cell-free kinase assay, in vitro phosphorylation, in vivo phosphorylation after DNA damage induction, site identification Biochemical and biophysical research communications High 19351595
2009 SAF-A is phosphorylated at Ser59 in a sequence context matching a 'S-hydrophobic' consensus exclusively by DNA-PK in response to DSB-inducing agents. The extent and duration of phosphorylation inversely correlates with the capacity of cells to repair DSBs by NHEJ, linking SAF-A phosphorylation status to DSB repair efficacy. Phospho-specific antibody, kinase inhibitor experiments, NHEJ-deficient cell lines, mass spectrometry-based site mapping Cell cycle (Georgetown, Tex.) High 19844162
2011 SAF-A localizes to mitotic spindles, spindle midzone, and cytoplasmic bridge. SAF-A depletion causes mitotic delay, chromosome misalignment, and spindle assembly defects. SAF-A co-immunoprecipitates with nucleolin, Aurora-A, and TPX2; co-localizes with TPX2 and Aurora-A at spindle poles and microtubules. SAF-A can bind microtubules directly and contributes to Aurora-A targeting to mitotic spindle microtubules. Elimination of TPX2 or Aurora-A abolishes SAF-A association with the mitotic spindle. RNAi, immunofluorescence, co-immunoprecipitation, direct microtubule binding assay Journal of cell science High 21242313
2011 SAF-A binds the Oct4 proximal promoter in ES cells and dissociates upon early differentiation. SAF-A depletion decreases Oct4 expression even with LIF. SAF-A interacts with the CTD of RNA polymerase II independently of CTD phosphorylation and mRNA. SAF-A exists in complexes with Sox2, Oct4, and STAT3 in ES cells, with complex numbers decreasing upon LIF withdrawal. ChIP, RNAi, co-immunoprecipitation of endogenous proteins, reporter assay Cellular reprogramming Medium 21235343
2011 SAF-A interacts with BRG1 (the ATPase subunit of the SWI/SNF chromatin remodeling complex) in mouse ES cells. Dual depletion of SAF-A and BRG1 abolishes global RNA Pol II transcription while leaving RNA Pol I transcription unaffected, establishing that both are jointly required for RNA Pol II-mediated transcription. Co-immunoprecipitation, in situ proximity ligation assay, co-localization, RNAi double knockdown, transcription assay PloS one Medium 22162999
2012 hnRNP U regulates U2 snRNP maturation and Cajal body morphology. CLIP-seq reveals that hnRNP-U binds virtually all classes of regulatory noncoding RNAs including all snRNAs required for splicing of both major and minor intron classes. hnRNP-U depletion causes global alternative splicing changes, establishing it as a regulator of the core splicing machinery. RNAi screen, CLIP-seq (genome-wide), RNA-seq (genome-wide), Cajal body morphology assay Molecular cell High 22325991
2012 hnRNP-U directly interacts with NEIL1 DNA glycosylase via NEIL1's C-terminal domain (dispensable for enzymatic activity). hnRNP-U stimulates NEIL1 base excision activity for oxidized bases primarily by enhancing product release. hnRNP-U and NEIL1 epistatically protect cells from low-level oxidative damage. The interacting regions in hnRNP-U map to both N and C termini. In-cell association increases after oxidative stress. Co-immunoprecipitation, in vitro base excision repair assay, domain mapping, FLAG-IP from human cells, epistasis analysis (hnRNP-U and NEIL1 double depletion), Kd measurement The Journal of biological chemistry High 22902625
2014 SAF-A exhibits biphasic dynamics at DNA damage sites: rapid transient recruitment via binding to Poly(ADP-ribose) (PAR), followed by prolonged exclusion dependent on ATM, ATR, and DNA-PK activity. Exclusion reflects dissociation of transcription-associated SAF-A from chromatin. The RNA-binding domain of SAF-A recapitulates this biphasic behavior. SAF-A exclusion is part of an anti-R-loop mechanism at damaged transcribed sites. Laser micro-irradiation, live-cell imaging, PAR binding assay, kinase inhibitor experiments, R-loop reporter (live imaging of DNA:RNA hybrids) Nucleic acids research High 25030905
2015 SAF-A Ser59 is phosphorylated by PLK1 (not DNA-PKcs) during mitosis. SAF-A interacts with PLK1 in nocodazole-arrested cells. Ser59 is dephosphorylated by PP2A during mitosis. Cells expressing S59A SAF-A show misaligned chromosomes, lagging chromosomes, polylobed nuclei, and delayed mitotic exit, demonstrating that both phosphorylation by PLK1 and dephosphorylation by PP2A at Ser59 are required for accurate mitosis. Phospho-specific antibody, kinase inhibitors, Co-IP with PLK1, phosphatase identification, S59A point mutation cell lines, mitotic phenotype analysis Molecular and cellular biology High 25986610
2016 SAF-A phosphorylated at Ser59 by DNA-PK early after ionizing radiation is linked to transient release of chromatin-bound NEIL1, preventing base excision repair (BER) from proceeding prematurely. Dephosphorylated SAF-A relieves Ku-mediated inhibition of DNA glycosylases in vitro, but the phosphomimetic D59 mutant does not. This establishes a temporal coordination mechanism where SAF-A and Ku cooperate to prioritize NHEJ over BER at clustered genome lesions. In vitro DNA glycosylase inhibition assay, phosphomimetic mutant (D59), DNA-PK phosphorylation, chromatin fractionation after IR Oncotarget Medium 27303920
2017 SAF-A oligomerizes with chromatin-associated RNAs (caRNAs) via its RGG domain to regulate interphase chromatin structure in a transcription-dependent manner. The AAA+ ATPase domain of SAF-A mediates cycles of oligomerization in response to ATP binding and hydrolysis. SAF-A oligomerization decompacts large-scale chromatin structure, while SAF-A loss or monomerization promotes aberrant chromosome folding and genome damage accumulation. Domain mutagenesis (RGG, ATPase), Hi-C, live-cell imaging, biochemical oligomerization assays, ATP hydrolysis assays, genome damage readouts Cell High 28622508
2017 HNRNPU is required for maintaining 3D genome architecture in mouse hepatocytes. HNRNPU depletion increases LAD (lamina-associated domain) coverage, causes global chromatin condensation, compartment switching (7.5% of genome), decreased TAD boundary strengths at A/B compartment borders, and reduced chromatin loop intensities. HNRNPU mainly associates with active chromatin, and 80% of HNRNPU ChIP peaks coincide with CTCF or RAD21 binding. In situ Hi-C, DamID, ChIP-seq, RNA-seq, conditional knockout in hepatocytes Genome research High 29273625
2018 HPSE eRNA binds hnRNPU to facilitate its interaction with p300, promoting their enrichment on a super enhancer, resulting in chromatin looping between the super enhancer and HPSE promoter, p300-mediated transactivation of EGR1, and subsequent HPSE upregulation. Co-immunoprecipitation, ChIP, chromatin conformation capture, gain/loss-of-function experiments Oncogene Medium 29511351
2020 hnRNPU retains miR-30c-5p in the nucleus and prevents its export into large extracellular vesicles. Binding of miR-30c-5p to hnRNPU was confirmed by RNA-immunoprecipitation, EMSA, and miR-pulldown. Nuclear binding stabilizes miR-30c-5p, reducing cytoplasmic availability for vesicular export. hnRNPU-dependent miR-30c-5p export reduced cellular migration and pro-angiogenic gene expression in recipient cells. Gain/loss-of-function, RNA-immunoprecipitation, EMSA, miR-pulldown, nanoparticle tracking analysis, electron microscopy Journal of extracellular vesicles Medium 32944175
2020 hnRNPU deficiency in mouse hepatocytes disrupts liver chromatin accessibility and stimulates expression of a truncated TrkB isoform (TRKB-T1) that promotes inflammatory signaling and stress-induced cell death. BDNF treatment reduced membrane TRKB-T1 and protected mice from diet-induced NASH, linking hnRNPU-chromatin regulation to disease-specific signaling. Hepatocyte-specific conditional knockout, RNA-seq, ChIP-seq, BDNF treatment rescue experiment Hepatology Medium 31469911
2020 In HeLa cells, hnRNPU directly binds the 3'-UTR of IL-6 mRNA, and this interaction occurs specifically in the cytoplasmic fraction, suggesting a role for cytoplasmic hnRNPU in mRNA stability control distinct from its nuclear functions. Optimized HITS-CLIP (BrdU-CLIP), subcellular fractionation, CLIP validation PloS one Medium 32302342
2021 hnRNPU interacts with WT1 and SOX9 in Sertoli cells and enhances expression of Sox8 and Sox9 by directly binding to their promoter regions. Conditional knockout of hnRNPU in murine Sertoli cells causes rapid depletion of both Sertoli and germ cells and failure of spermatogonia proliferation and migration, leading to male sterility. Conditional knockout (Cre/loxP), luciferase reporter assay, ChIP-qPCR, RNA-seq, co-immunoprecipitation Theranostics Medium 34815802
2022 HNRNPU loss of function leads to rapid cell death of both postmitotic neurons and neural progenitors in the developing mouse cortex, with neural progenitors being more sensitive. HNRNPU truncation causes dysregulation of gene expression and alternative splicing of genes involved in cell survival, cell motility, and synapse formation. Pharmaceutical and genetic agents partially rescued loss of cortical structures, radial migration defects, and neural progenitor cell death. Conditional truncation in mouse cortex, RNA-seq, alternative splicing analysis, pharmacological rescue, cell death assays Nature communications High 35864088
2022 HNRNPU promotes antibody class-switch recombination (CSR) by facilitating C-NHEJ-mediated S-S joining through the 53BP1-shieldin complex. HNRNPU binds switch region RNA/DNA G-quadruplexes and regulates R-loop and ssDNA accumulation. HNRNPU interacts with both C-NHEJ and R-loop complexes in an RNA-dependent manner. Recruitment of HNRNPU and C-NHEJ factors is sensitive to liquid-liquid phase separation inhibitors, suggesting DNA-repair condensate formation. Conditional knockout in B cells, CSR assay, Co-IP, G-quadruplex binding assay, LLPS inhibitor treatment, ssDNA/R-loop detection Cell reports Medium 36943867
2022 CDC20-mediated ubiquitination of hnRNPU promotes its interaction with the CTCF-cohesin complex, modulating chromatin condensation. The molecular domain on hnRNPU required for CDC20 interaction was mapped to amino acid residues 461–653. Dysregulation of the CDC20-hnRNPU axis contributes to altered chromatin condensation, tumor progression, and drug resistance. Affinity purification/mass spectrometry, Co-IP, immunostaining, domain mapping, DAPI/H2B-mCherry chromatin condensation assay Cancers Medium 35954396
2022 SAF-A promotes origin licensing in G1 phase, origin activation frequency in S phase, and consistent replication fork progression. SAF-A depletion causes reduced MCM loading, decreased origin activation, inconsistent fork progression, blurred replication timing domain boundaries, and elevated γ-H2AX formation leading to cellular quiescence. DNA fiber assay, origin licensing assay (MCM loading), single-cell replication timing, γ-H2AX immunostaining, siRNA depletion Journal of cell science Medium 34888666
2022 hnRNPU promotes TNBC cell proliferation and migration via association with DDX5. The HNRNPU-DDX5 complex prevents intron retention of MCM10 pre-mRNA (reducing nonsense-mediated decay) and activates Wnt/β-catenin signaling. Additionally, the HNRNPU-DDX5 complex promotes transcription of LMO4 from its transcriptional start site, activating PI3K-Akt-mTOR signaling. CRISPR screen, RNAi, Co-IP of endogenous proteins, splicing analysis, transcriptional reporter, Western blot Cell death & disease Medium 36347834
2023 SAF-A/hnRNPU directly interacts with polyphosphoinositides (PPIn) via a lysine-rich polybasic motif located at amino acids 9–24 within its SAP DNA-binding domain. Deletion of this polybasic motif prevents PPIn interaction, suggesting the SAP domain has dual functions in DNA and PPIn binding. Quantitative interactomics, direct PPIn binding assay, deletion mutagenesis microPublication biology Medium 37038481
2024 hnRNPU is required for establishing the spermatogonial stem cell (SSC) pool. Conditional loss of hnRNPU in prospermatogonia arrests spermatogenesis and sterility. hnRNPU-deficient ProSG fails to differentiate and migrate to the basement membrane. hnRNPU binds Vrk1, Slx4, and Dazl transcripts, which show aberrant alternative splicing in hnRNPU-deficient testes. Conditional knockout (Cre/loxP), single-cell transcriptomics, RNA binding analysis, alternative splicing assays Cell reports Medium 38625792
2024 circMYO9B promotes translocation of hnRNPU from nucleus to cytoplasm, which destabilizes CBL and reduces ubiquitination/degradation of KDM1A, thereby promoting VEGFA expression in endothelial cells and angiogenesis in diabetic wound healing. Co-IP, subcellular fractionation, protein stability assay, ubiquitination assay, in vivo diabetic wound healing model Communications biology Medium 39725699
2025 α-Satellite RNAs bind SAF-A and are required for recruitment of SAF-A back to chromatin upon mitotic exit. Both α-satellite RNA and SAF-A are required for chromosome segregation fidelity; depletion of either causes chromosome missegregation. SAF-A is globally excluded from chromatin during mitosis and α-satellite RNAs are required for its reestablishment, with both also aiding nuclear lamina reassembly. SAF-A RNA binding identification, RNAi depletion of α-satellite RNA or SAF-A, chromosome missegregation assays, live-cell imaging, nuclear lamina reassembly assay Nucleic acids research Medium 40219970
2025 The SAF-A SAP domain (N-terminal DNA-binding domain) and its serines S14 and S26 are required for: XIST RNA localization and XIST-dependent histone modifications on the inactive X chromosome; normal protein nuclear dynamics; and cell proliferation. The SAP domain is not required for global gene expression but plays only a minor role in mRNA splicing. A Xi localization signal resides in the SAP domain. SAF-A is highly dynamic, interacting with nascent transcripts as part of this dynamic movement rather than as a static nuclear scaffold component. Allelic reconstitution, FRAP/protein dynamics assays, XIST RNA FISH, histone modification ChIP, splicing analysis, proliferation assays PLoS genetics High 40493679
2025 The SAF-A ATPase domain and RGG repeats both control SAF-A nuclear dynamics. The RGG repeats mediate interaction with nascent transcripts. Both the ATPase domain and RGG repeats are required for maintaining XIST RNA and facultative heterochromatin marks on the Xi, for proper mRNA splicing, and for cell proliferation. Mutations blocking ATP binding vs. ATP hydrolysis have distinct effects on Xi maintenance. Allelic reconstitution, FRAP, XIST FISH, ChIP for heterochromatin marks, splicing analysis (RNA-seq), proliferation assays bioRxivpreprint Medium 41473319
2025 HNRNPU is required for long-range Polycomb recruitment by the lncRNAs Airn, Kcnq1ot1, and Xist. RNA immunoprecipitation showed enriched and correlated HNRNPU association with all three lncRNAs. HNRNPU depletion impaired PRC-directed histone modifications induced by all three lncRNAs without being necessary for proper localization of Airn or Kcnq1ot1. RNA-immunoprecipitation from formaldehyde-crosslinked cells, HNRNPU knockdown, PRC-directed histone modification assays (ChIP), lncRNA localization assays bioRxivpreprint Medium 40791421

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1992 Characterization of SAF-A, a novel nuclear DNA binding protein from HeLa cells with high affinity for nuclear matrix/scaffold attachment DNA elements. The EMBO journal 231 1324173
2017 SAF-A Regulates Interphase Chromosome Structure through Oligomerization with Chromatin-Associated RNAs. Cell 172 28622508
1994 Nucleic-acid-binding properties of hnRNP-U/SAF-A, a nuclear-matrix protein which binds DNA and RNA in vivo and in vitro. European journal of biochemistry 159 8174554
2012 Regulation of DNA-end resection by hnRNPU-like proteins promotes DNA double-strand break signaling and repair. Molecular cell 156 22365830
2014 DNA damage triggers SAF-A and RNA biogenesis factors exclusion from chromatin coupled to R-loops removal. Nucleic acids research 151 25030905
2012 Nuclear matrix factor hnRNP U/SAF-A exerts a global control of alternative splicing by regulating U2 snRNP maturation. Molecular cell 144 22325991
1997 The novel SAR-binding domain of scaffold attachment factor A (SAF-A) is a target in apoptotic nuclear breakdown. The EMBO journal 126 9405365
2003 Scaffold attachment factor A (SAF-A) is concentrated in inactive X chromosome territories through its RGG domain. Chromosoma 114 14608463
2017 The nuclear matrix protein HNRNPU maintains 3D genome architecture globally in mouse hepatocytes. Genome research 103 29273625
2022 Targeting HNRNPU to overcome cisplatin resistance in bladder cancer. Molecular cancer 101 35130920
2002 Pseudosubstrate regulation of the SCF(beta-TrCP) ubiquitin ligase by hnRNP-U. Genes & development 101 11850407
2010 The Trithorax group protein Ash2l and Saf-A are recruited to the inactive X chromosome at the onset of stable X inactivation. Development (Cambridge, England) 99 20150277
2018 HPSE enhancer RNA promotes cancer progression through driving chromatin looping and regulating hnRNPU/p300/EGR1/HPSE axis. Oncogene 93 29511351
2002 An episomally replicating vector binds to the nuclear matrix protein SAF-A in vivo. EMBO reports 90 11897664
1997 The scaffold/matrix attachment region binding protein hnRNP-U (SAF-A) is directly bound to chromosomal DNA in vivo: a chemical cross-linking study. Biochemistry 82 9204873
2020 The RNA-binding protein hnRNPU regulates the sorting of microRNA-30c-5p into large extracellular vesicles. Journal of extracellular vesicles 77 32944175
2006 hnRNP-U enhances the expression of specific genes by stabilizing mRNA. FEBS letters 73 17174306
2010 Four patients with speech delay, seizures and variable corpus callosum thickness sharing a 0.440 Mb deletion in region 1q44 containing the HNRPU gene. European journal of medical genetics 72 20382278
2017 Heterozygous HNRNPU variants cause early onset epilepsy and severe intellectual disability. Human genetics 71 28393272
2017 Genetic and phenotypic dissection of 1q43q44 microdeletion syndrome and neurodevelopmental phenotypes associated with mutations in ZBTB18 and HNRNPU. Human genetics 68 28283832
1994 Purification of two isoforms of hnRNP-U and characterization of their nucleic acid binding activity. Biochemistry 58 8068679
2020 HNF4A-AS1/hnRNPU/CTCF axis as a therapeutic target for aerobic glycolysis and neuroblastoma progression. Journal of hematology & oncology 54 32216806
2010 B23 acts as a nucleolar stress sensor and promotes cell survival through its dynamic interaction with hnRNPU and hnRNPA1. Oncogene 50 20101230
2012 Enhancement of NEIL1 protein-initiated oxidized DNA base excision repair by heterogeneous nuclear ribonucleoprotein U (hnRNP-U) via direct interaction. The Journal of biological chemistry 49 22902625
2008 Identifying functional neighborhoods within the cell nucleus: proximity analysis of early S-phase replicating chromatin domains to sites of transcription, RNA polymerase II, HP1gamma, matrin 3 and SAF-A. Journal of cellular biochemistry 47 18618731
2000 Apoptotic cleavage of scaffold attachment factor A (SAF-A) by caspase-3 occurs at a noncanonical cleavage site. The Journal of biological chemistry 45 10671544
2020 hnRNPU/TrkB Defines a Chromatin Accessibility Checkpoint for Liver Injury and Nonalcoholic Steatohepatitis Pathogenesis. Hepatology (Baltimore, Md.) 42 31469911
2017 De novo mutations in HNRNPU result in a neurodevelopmental syndrome. American journal of medical genetics. Part A 42 28944577
2017 Clinical and molecular characterization of de novo loss of function variants in HNRNPU. American journal of medical genetics. Part A 40 28815871
2023 piRNA-1742 promotes renal cell carcinoma malignancy by regulating USP8 stability through binding to hnRNPU and thereby inhibiting MUC12 ubiquitination. Experimental & molecular medicine 35 37332045
2022 Heterogeneous nuclear ribonucleoprotein U (HNRNPU) safeguards the developing mouse cortex. Nature communications 35 35864088
2021 hnRNPU in Sertoli cells cooperates with WT1 and is essential for testicular development by modulating transcriptional factors Sox8/9. Theranostics 35 34815802
2018 The role of nuclear matrix protein HNRNPU in maintaining the architecture of 3D genome. Seminars in cell & developmental biology 35 29981443
2009 hnRNP-U is a specific DNA-dependent protein kinase substrate phosphorylated in response to DNA double-strand breaks. Biochemical and biophysical research communications 34 19351595
2021 The role of SAF-A/hnRNP U in regulating chromatin structure. Current opinion in genetics & development 32 34823151
2006 hnRNP-U directly interacts with WT1 and modulates WT1 transcriptional activation. Oncogene 32 16924231
2001 Specificity of SAF-A and lamin B binding in vitro correlates with the satellite DNA bending state. Journal of cellular biochemistry 32 11573239
2009 Cell nonhomologous end joining capacity controls SAF-A phosphorylation by DNA-PK in response to DNA double-strand breaks inducers. Cell cycle (Georgetown, Tex.) 31 19844162
2023 circ-hnRNPU inhibits NONO-mediated c-Myc transactivation and mRNA stabilization essential for glycosylation and cancer progression. Journal of experimental & clinical cancer research : CR 30 37993881
2021 MicroRNA-132-3p alleviates neuron apoptosis and impairments of learning and memory abilities in Alzheimer's disease by downregulation of HNRNPU stabilized BACE1. Cell cycle (Georgetown, Tex.) 28 34585626
2008 Rhythmic SAF-A binding underlies circadian transcription of the Bmal1 gene. Molecular and cellular biology 27 18332112
2011 The nuclear scaffold protein SAF-A is required for kinetochore-microtubule attachment and contributes to the targeting of Aurora-A to mitotic spindles. Journal of cell science 25 21242313
2001 Effects of the heterogeneous nuclear ribonucleoprotein U (hnRNP U/SAF-A) on glucocorticoid-dependent transcription in vivo. The Journal of steroid biochemistry and molecular biology 25 11530285
2021 HNRNPU promotes the progression of hepatocellular carcinoma by enhancing CDK2 transcription. Experimental cell research 24 34737140
2011 SAF-A has a role in transcriptional regulation of Oct4 in ES cells through promoter binding. Cellular reprogramming 24 21235343
2024 Microglial circ-UBE2K exacerbates depression by regulating parental gene UBE2K via targeting HNRNPU. Theranostics 23 38994030
2022 HNRNPU promotes the progression of triple-negative breast cancer via RNA transcription and alternative splicing mechanisms. Cell death & disease 23 36347834
2024 hnRNPU is required for spermatogonial stem cell pool establishment in mice. Cell reports 22 38625792
2023 HNRNPU facilitates antibody class-switch recombination through C-NHEJ promotion and R-loop suppression. Cell reports 22 36943867
2022 Long Noncoding RNA lncRHL Regulates Hepatic VLDL Secretion by Modulating hnRNPU/BMAL1/MTTP Axis. Diabetes 22 35771993
2020 The splicing regulatory factor hnRNPU is a novel transcriptional target of c-Myc in hepatocellular carcinoma. FEBS letters 22 33040326
2014 A genomic copy number variant analysis implicates the MBD5 and HNRNPU genes in Chinese children with infantile spasms and expands the clinical spectrum of 2q23.1 deletion. BMC medical genetics 22 24885232
2022 Nuclear organization by satellite DNA, SAF-A/hnRNPU and matrix attachment regions. Seminars in cell & developmental biology 21 35484025
2022 LncRNA IL21-AS1 interacts with hnRNPU protein to promote IL21 overexpression and aberrant differentiation of Tfh cells in systemic lupus erythematosus. Clinical and translational medicine 21 36447054
2017 Expression Profiling Identifies the Noncoding Processed Transcript of HNRNPU with Proliferative Properties in Pancreatic Ductal Adenocarcinoma. Non-coding RNA 20 29657295
2018 An episode of acute encephalopathy with biphasic seizures and late reduced diffusion followed by hemiplegia and intractable epilepsy observed in a patient with a novel frameshift mutation in HNRNPU. Brain & development 19 29858110
2015 Phosphorylation of SAF-A/hnRNP-U Serine 59 by Polo-Like Kinase 1 Is Required for Mitosis. Molecular and cellular biology 19 25986610
2020 Analysis of the nucleocytoplasmic shuttling RNA-binding protein HNRNPU using optimized HITS-CLIP method. PloS one 18 32302342
2024 MSC-derived exosomal circMYO9B accelerates diabetic wound healing by promoting angiogenesis through the hnRNPU/CBL/KDM1A/VEGFA axis. Communications biology 17 39725699
2023 Neurodevelopmental deficits and cell-type-specific transcriptomic perturbations in a mouse model of HNRNPU haploinsufficiency. PLoS genetics 17 37782669
2011 SAF-A forms a complex with BRG1 and both components are required for RNA polymerase II mediated transcription. PloS one 17 22162999
2023 DNA methylation episignature and comparative epigenomic profiling of HNRNPU-related neurodevelopmental disorder. Genetics in medicine : official journal of the American College of Medical Genetics 16 37120726
2019 The Superoanterior Fasciculus (SAF): A Novel White Matter Pathway in the Human Brain? Frontiers in neuroanatomy 16 30890921
2000 Specific interaction of mouse major satellite with MAR-binding protein SAF-A. European journal of cell biology 16 11139148
1994 hnRNP-U/SAF-A is encoded by two differentially polyadenylated mRNAs in human cells. Biochimica et biophysica acta 16 7509195
2021 HNRNPU-AS1 Regulates Cell Proliferation and Apoptosis via the MicroRNA 205-5p/AXIN2 Axis and Wnt/β-Catenin Signaling Pathway in Cervical Cancer. Molecular and cellular biology 15 34309414
2021 SAF-A mutants disrupt chromatin structure through dominant negative effects on RNAs associated with chromatin. Mammalian genome : official journal of the International Mammalian Genome Society 14 34859278
2016 Scaffold attachment factor A (SAF-A) and Ku temporally regulate repair of radiation-induced clustered genome lesions. Oncotarget 14 27303920
2023 Germline pathogenic variants in HNRNPU are associated with alterations in blood methylome. European journal of human genetics : EJHG 13 37407733
2023 RNA-binding protein hnRNPU regulates multiple myeloma resistance to selinexor. Cancer letters 13 37984724
1991 Analysis of the promoter region of saf, a Streptomyces griseus gene that increases production of extracellular enzymes. Gene 13 1761232
2024 LncRNA evf-2 Exacerbates Podocyte Injury in Diabetic Nephropathy by Inducing Cell Cycle Re-entry and Inflammation Through Distinct Mechanisms Triggered by hnRNPU. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 12 39470303
2022 CDC20-Mediated hnRNPU Ubiquitination Regulates Chromatin Condensation and Anti-Cancer Drug Response. Cancers 11 35954396
2022 Characterization and functional analysis of chicken dsRNA binding protein hnRNPU. Developmental and comparative immunology 9 36044969
2020 Adult-Onset Myopathy with Constitutive Activation of Akt following the Loss of hnRNP-U. iScience 9 32659719
2022 SAF-A promotes origin licensing and replication fork progression to ensure robust DNA replication. Journal of cell science 8 34888666
2022 Evidence of shared transcriptomic dysregulation of HNRNPU-related disorder between human organoids and embryonic mice. iScience 8 36594023
2021 De novo frameshift variants of HNRNPU in patients with early infantile epileptic encephalopathy: Two case reports and literature review. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience 8 33914968
2009 SAF-A/hnRNP-U localization in interphase and metaphase. Cytogenetic and genome research 8 19556781
2025 hnRNPU-mediated pathogenic alternative splicing drives gastric cancer progression. Journal of experimental & clinical cancer research : CR 7 39773744
2022 HnRNPU-AS1 inhibits the proliferation, migration and invasion of HCC cells and induces autophagy through miR-556-3p/ miR-580-3p/SOCS6 axis. Cancer biomarkers : section A of Disease markers 7 35275521
2015 Genomic regions targeted by DNA topoisomerase IIβ frequently interact with a nuclear scaffold/matrix protein hnRNP U/SAF-A/SP120. Journal of cellular biochemistry 7 25418483
2025 Chromatin-associated α-satellite RNA maintains chromosome stability by reestablishing SAF-A in the mitotic cell cycle. Nucleic acids research 5 40219970
2023 HNRNPU's multi-tasking is essential for proper cortical development. BioEssays : news and reviews in molecular, cellular and developmental biology 5 37439444
2021 Pharmacological Treatment of Severe Breathing Abnormalities in a Case of HNRNPU Epileptic Encephalopathy. Molecular syndromology 5 34012379
1999 Identification of chURP, a nuclear calmodulin-binding protein related to hnRNP-U. European journal of biochemistry 5 10103044
2024 Circular RNA CircSLC22A23 Promotes Gastric Cancer Progression by Activating HNRNPU Expression. Digestive diseases and sciences 4 38400886
2025 Role of the SAF-A/HNRNPU SAP domain in X chromosome inactivation, nuclear dynamics, transcription, splicing, and cell proliferation. PLoS genetics 3 40493679
2024 Loss of HNRNPU in Skeletal Muscle Increases Intramuscular Infiltration of Ly6C Positive Cells, leading to Muscle Atrophy through Activation of NF-κB Signaling. Advanced biology 3 38797891
2024 The nuclear matrix protein HNRNPU restricts hepatitis B virus transcription by promoting OAS3-based activation of host innate immunity. Journal of medical virology 3 39011773
2025 The molecular axis hnRNPU/circKCNK2/EDC4/IL-11 aggravates osteolytic bone metastasis of RCC. Oncogene 2 40640337
2025 RNA-binding protein HnRNPU regulates proliferation and ferroptosis in colon adenocarcinoma by stabilizing the mRNA of system xc. Experimental & molecular medicine 2 41310105
2023 ITGA9-AS1 up-regulates ITGA9 by targeting miR-4765 and recruiting HNRNPU to affect the proliferation and apoptosis of non-small cell lung cancer cells. Cellular and molecular biology (Noisy-le-Grand, France) 2 38279497
2025 Correlated protein-RNA associations reveal a requirement for HNRNPU in long-range Polycomb recruitment by the lncRNAs Airn , Kcnq1ot1 , and Xist. bioRxiv : the preprint server for biology 1 40791421
2025 Long non-coding RNA STMN1P2 promotes breast cancer doxorubicin resistance by inhibiting pyroptosis through the hnRNPU-EZH2-TARF6-MALT1-caspase-1 pathway. Acta pharmacologica Sinica 1 40926024
2025 Role of the SAF-A/HNRNPU ATPase and RGG domains in X chromosome inactivation, nuclear dynamics, transcription, splicing, and cell proliferation. bioRxiv : the preprint server for biology 1 41473319
2024 Biological functions and clinic significance of SAF‑A (Review). Biomedical reports 1 38665420
2024 Case report: Early use of whole exome sequencing unveils HNRNPU-related neurodevelopmental disorder and answers additional clinical questions through reanalysis. Frontiers in genetics 1 38846959
2024 circUBE2G1 interacts with hnRNPU to promote VEGF-C-mediated lymph node metastasis of lung adenocarcinoma. Frontiers in oncology 1 39664183
2023 SAF-A/hnRNP U binds polyphosphoinositides via a lysine rich polybasic motif located in the SAP domain. microPublication biology 1 37038481

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