Affinage

POU4F1

POU domain, class 4, transcription factor 1 · UniProt Q01851

Length
419 aa
Mass
42.7 kDa
Annotated
2026-06-10
100 papers in source corpus 44 papers cited in narrative 44 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

POU4F1 (Brn-3a) is a class IV POU-domain transcription factor that governs survival, differentiation, and subtype identity of sensory and central neurons, and is redeployed in several non-neuronal disease contexts (PMID:8876243, PMID:17196582). It is expressed as two functionally distinct isoforms: the long form carries an N-terminal transactivation domain required for oncogenic transformation and for neuronal survival in vivo, whereas the POU domain mediates DNA binding, neurite outgrowth, and neurofilament/synaptic gene activation—two separable activities whose output depends on target-promoter context and a single critical residue in the POU homeodomain that distinguishes Brn-3a from its antagonistic paralog Brn-3b (PMID:8290353, PMID:7852360, PMID:8972215, PMID:9261145, PMID:15194866). The protein binds DNA directly at target promoters and enhancers and supports a pro-survival program by transactivating the anti-apoptotic genes Bcl-2 and Bcl-xL (PMID:9642226, PMID:11273642). This survival arm is integrated with apoptotic control through direct interaction with the POU domain: Brn-3a binds p53, p73, and HIPK2 to selectively block transactivation of pro-apoptotic targets (Bax, Noxa) while cooperating on the cell-cycle arrest gene p21, and HIPK2 promotes its DNA binding yet suppresses its transcriptional output (PMID:10329733, PMID:12203124, PMID:15492043, PMID:15598651, PMID:18421303). In sensory neuron development, Brn-3a directly maintains TrkA, TrkB, and TrkC receptor expression—acting at a TrkA enhancer cooperatively with Klf7—and operates upstream of Runx factors and Nurr1 to specify neuronal subtypes while repressing the proneural genes NeuroD1/NeuroD4; its in vivo occupancy correlates with conserved, H3-acetylated chromatin (PMID:10357931, PMID:12810599, PMID:17196582, PMID:17011544, PMID:20096094). It directs axon pathfinding and target innervation in trigeminal, spiral, habenular, and retinal ganglion neurons, defines functionally distinct RGC subtypes through a Pou4f1-Tbr1-Jam2 cascade, and cooperates with ISL1 to program cochleovestibular ganglion identity (PMID:8876243, PMID:11493560, PMID:16354917, PMID:19906978, PMID:19323995, PMID:38267260, PMID:38469155). Brn-3a negatively autoregulates its own expression via an upstream enhancer, and its activity is tuned by MEK1/2-ERK phosphorylation at serine-122 (PMID:12441296, PMID:19135033). In disease settings it serves as a Smad3 target driving macrophage-myofibroblast transition in renal fibrosis, promotes BRAF-inhibitor resistance in melanoma by transactivating MEK, and maintains basal-like breast cancer by activating CDK2/CCND1 and silencing ESR1 through a CDK2-EZH2-H3K27me3 axis (PMID:32788346, PMID:32532957, PMID:38491910).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1995 High

    Established that Brn-3a is a bifunctional transcription factor with two separable activation domains whose use is dictated by promoter context, and that the antagonist Brn-3b acts by direct heterodimerization that blocks Brn-3a DNA binding—defining the molecular basis of the Brn-3a/Brn-3b functional opposition.

    Evidence Domain-swap reporter assays plus EMSA and GST pulldown showing Brn-3b(s)–Brn-3a(l) complex formation in vitro

    PMID:7852360 PMID:8290353 PMID:8537352

    Open questions at the time
    • Endogenous stoichiometry of Brn-3a/Brn-3b heterodimers in neurons not quantified
    • Structural basis of context-dependent activation-domain choice not resolved
  2. 1996 High

    Defined the in vivo requirement for Brn-3a in specific neuronal populations and revealed it sits atop a transcription-factor hierarchy by positively regulating its paralogs in somatosensory neurons.

    Evidence Targeted Brn-3a deletion in mice with histology and analysis of Brn-3b/3c expression

    PMID:8876243

    Open questions at the time
    • Direct vs. indirect regulation of Brn-3b/3c not distinguished at this stage
    • Molecular targets causing neuronal loss not yet identified
  3. 1997 High

    Mapped neurite outgrowth and neurofilament/synaptic gene activation to the POU domain and pinpointed a single homeodomain residue that confers Brn-3a-specific activity, explaining functional divergence from Brn-3b.

    Evidence Overexpression, domain deletion, and point mutagenesis in ND7 cells with morphological and promoter-reporter readouts

    PMID:8972215 PMID:9261145

    Open questions at the time
    • Direct genomic targets mediating outgrowth in vivo not defined
    • How a single residue alters DNA/cofactor selectivity unknown
  4. 1998 High

    Identified Bcl-2 as a direct Brn-3a target, linking the transcription factor to a defined anti-apoptotic survival mechanism, and showed POU-domain interaction with the estrogen receptor extends its regulatory reach.

    Evidence EMSA, promoter-reporter assays, Western blot for endogenous BCL-2; GST pulldown and Y2H for ER interaction

    PMID:9448000 PMID:9642226

    Open questions at the time
    • In vivo requirement of the Bcl-2 site for neuronal survival not directly tested here
    • Physiological relevance of ER interaction in neurons unclear
  5. 1999 High

    Revealed that Brn-3a directly engages p53 to selectively suppress apoptosis while sparing other targets, defining a mechanism by which a neuronal survival factor restrains a pro-apoptotic transcription factor.

    Evidence GST pulldown, co-IP, EMSA, and promoter-deletion reporter assays mapping POU–p53 DNA-binding-domain interaction

    PMID:10329733

    Open questions at the time
    • Structural detail of the Brn-3a–p53 complex on DNA not resolved
    • Genome-wide scope of selective p53 antagonism not assessed at this stage
  6. 2001 Medium

    Extended the survival program to Bcl-xL and demonstrated cell-type specificity (sensory but not sympathetic neurons), establishing Brn-3a as a context-dependent neuroprotective regulator in vivo.

    Evidence Reporter assays, antisense knockdown, in vivo DRG overexpression with survival counts, and Bcl-xL promoter dissection under p53 repression

    PMID:11053412 PMID:11273642 PMID:11713302

    Open questions at the time
    • Mechanistic basis of sensory vs. sympathetic specificity not defined
    • Single-lab in vivo overexpression data
  7. 2001 High

    Separated axon-pathfinding defects from neuronal death temporally, establishing that Brn-3a controls trigeminal, spiral, and inner-ear axon guidance through downstream genes other than the semaphorin/neuropilin axis.

    Evidence Brn-3a KO with LacZ axon tracing, DiI tracing, and marker analysis with temporal staging

    PMID:11160433 PMID:11493560

    Open questions at the time
    • Direct downstream pathfinding effectors not identified
    • Mechanism distinguishing guidance from survival functions unresolved
  8. 2002 High

    Clarified that Brn-3a partitions p53 outputs—blocking apoptosis (Bax/Noxa) while cooperating on cell-cycle arrest (p21)—giving a coherent model for how it shifts cell fate decisions.

    Evidence Promoter-reporter assays, protein-level measurements, and apoptosis/cell-cycle assays; later EMSA/ChIP for Noxa promoter occupancy

    PMID:12203124 PMID:15598651

    Open questions at the time
    • How Brn-3a converts p53 from apoptotic to arrest mode at the promoter level not fully resolved
    • Generality across p53 target promoters not exhaustively mapped
  9. 2003 High

    Demonstrated direct in vivo enhancer occupancy and uncoupled transcriptional maintenance of TrkA from survival using Bax-KO epistasis, and established negative autoregulation as a dosage-control mechanism.

    Evidence EMSA, transgenic enhancer-mutagenesis reporter mice, Bax-KO epistasis, and autoregulation analysis across Brn-3a genotypes

    PMID:12441296 PMID:12810599

    Open questions at the time
    • Cofactors required for enhancer-specific occupancy in vivo not fully defined
    • Mechanism of autorepression at the chromatin level not resolved
  10. 2004 High

    Expanded the interaction network to HIPK2, p73, EWS, and EWS/Fli-1, revealing that partners can uncouple DNA binding from transcriptional output and modulate the survival/differentiation balance.

    Evidence Co-IP, EMSA, reporter assays, HIPK2 KO mouse phenotyping, and GST pulldown for EWS/EWS-Fli-1 interactions

    PMID:12432261 PMID:15021903 PMID:15194866 PMID:15492043 PMID:18421303

    Open questions at the time
    • Mechanism by which HIPK2 promotes binding yet suppresses transcription not structurally defined
    • Physiological relevance of EWS/EWS-Fli-1 interactions outside overexpression contexts uncertain
  11. 2006 High

    Provided a genome-scale view: in vivo Brn-3a occupancy tracks evolutionary conservation and active histone marks, and Brn-3a acts as a direct repressor of proneural genes, refining its role as a context-selective regulator rather than a simple activator.

    Evidence Locus-wide ChIP in embryonic trigeminal neurons combined with expression profiling and chromatin-state correlation

    PMID:17196582

    Open questions at the time
    • Determinants of in vivo site selection beyond conservation/histone state not defined
    • Repressor mechanism at NeuroD loci not mechanistically dissected
  12. 2010 High

    Placed Brn-3a in a transcriptional hierarchy upstream of Runx factors and Nurr1, establishing it as a master regulator of sensory and habenular neuron subtype specification through direct enhancer binding.

    Evidence KO and VP16-transactivator mice, in vivo ChIP at the Runx3 locus, axon tracing, and microarray epistasis for Nurr1

    PMID:17011544 PMID:19906978 PMID:20096094

    Open questions at the time
    • Combinatorial logic with Runx/Nurr1 not fully resolved
    • Direct vs. indirect targets within subtype programs not all distinguished
  13. 2012 High

    Demonstrated that Brn-3a is required for DRG subtype diversification and central afferent projections, with Runx1 as a downstream specification mediator, extending the developmental program to the spinal sensory system.

    Evidence Single and Brn-3a;Brn-3b double KO mice with marker analysis, DiI tracing, and temporal staging

    PMID:22326227

    Open questions at the time
    • Direct Runx1 regulation in DRG not shown by ChIP here
    • Effectors of central axon entry not identified
  14. 2019 High

    Distinguished a mature, post-developmental function: Pou4f1 tunes inner-hair-cell Ca2+ channel properties and the modiolar–pillar activity gradient in spiral ganglion neurons independent of its earlier survival/pathfinding roles.

    Evidence Tamoxifen-inducible conditional KO after E13 with Ca2+ imaging and patch-clamp electrophysiology

    PMID:31085606

    Open questions at the time
    • Transcriptional targets mediating the Ca2+ phenotype not identified
    • Cell-autonomous vs. retrograde signaling basis unclear
  15. 2024 High

    Defined RGC and cochleovestibular subtype programs at the level of direct binding, including a Pou4f1-Tbr1-Jam2 cascade and ISL1 cooperativity, sharpening the model of combinatorial subtype specification.

    Evidence CUT&RUN/ChIP for direct targets, conditional and double KO genetic epistasis, co-IP of ISL1-POU4F1, and enhancer reporter assays

    PMID:38267260 PMID:38469155 PMID:39715266

    Open questions at the time
    • Full target catalog of each cooperative partnership incomplete
    • Brn3a-specific functional validation in the Runx3 co-occupancy study is indirect
  16. 2025 High

    Established disease-context roles in which POU4F1 is itself regulated (Smad3 transactivation, HDAC2/TET1 chromatin control, USP18 deubiquitination) and drives fibrogenic, drug-resistance, oncogenic-proliferation, and identity programs through direct target promoters.

    Evidence ChIP/CUT&RUN at MEK, CDK2/CCND1, ESR1, STAT3, PRKAA2 loci; KO/knockdown with in vitro and xenograft/adoptive-transfer functional readouts

    PMID:32532957 PMID:32788346 PMID:35055045 PMID:37962640 PMID:38491910 PMID:40122823

    Open questions at the time
    • Whether neuronal-survival mechanisms operate identically in tumor cells not established
    • Cross-talk among the multiple disease pathways not integrated

Open questions

Synthesis pass · forward-looking unresolved questions
  • How POU4F1 selects among activation, repression, and apoptosis-modulating modes at individual loci—and how a single homeodomain residue and partner identity dictate output—remains mechanistically unresolved.
  • No structural model of Brn-3a–DNA–cofactor complexes
  • Determinants of in vivo site selection beyond conservation and histone state undefined
  • Unifying logic linking developmental and disease target programs unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 8 GO:0140110 transcription regulator activity 8
Localization
GO:0005634 nucleus 3
Pathway
R-HSA-1266738 Developmental Biology 6 R-HSA-1643685 Disease 5 R-HSA-5357801 Programmed Cell Death 5 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1640170 Cell Cycle 2
Partners
ESR1EWSR1HIPK2ISL1POU4F2RUNX3TP53TP73

Evidence

Reading pass · 44 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 Brn-3a encodes two protein isoforms (long and short); the long form containing an intact N-terminal domain (~100 aa conserved among class IV POU factors) is required for oncogenic transformation of primary fibroblasts, whereas the short form (lacking 84 N-terminal residues) cannot transform. Brn-3b can suppress the oncogenic activity of Brn-3a(l) when co-transfected, acting as an inhibitor. Focus-formation assay in primary fibroblasts; co-transfection of long vs. short isoforms and Brn-3a/Brn-3b combinations; identification of conserved N-terminal domain by sequence analysis Nucleic acids research Medium 8290353
1995 Brn-3a activates the alpha-internexin promoter via its N-terminal domain, while activation of an artificial promoter containing a synthetic Brn-3a binding site requires only the POU domain. Thus Brn-3a contains two functionally distinct transactivation domains whose activity depends on the target promoter context. Brn-3b represses the alpha-internexin promoter and blocks Brn-3a activation. Co-transfection reporter assays with chimeric Brn-3a/Brn-3b constructs in neuronal and non-neuronal cells; deletion and domain-swap analysis The Journal of biological chemistry High 7852360
1995 The short isoform of Brn-3b (Brn-3b(s)) directly interacts with Brn-3a(l) in solution, preventing Brn-3a(l) from forming stable complexes with octamer-related DNA sequences. This heterodimer is transcriptionally inactive and disrupts preformed Brn-3a(l)-DNA complexes, explaining the antagonistic functional relationship between these isoforms. EMSA (gel mobility shift assay); GST pulldown and in vitro binding studies; co-transfection transcription assays The Journal of biological chemistry High 8537352
1996 Targeted deletion of Brn-3a causes loss of neurons in the trigeminal ganglia, medial habenula, red nucleus, and inferior olivary nucleus, but not in retina or dorsal root ganglia. In trigeminal and dorsal root ganglia (but not retina), loss of Brn-3a markedly reduces expression of Brn-3b and Brn-3c, indicating that Brn-3a positively regulates these paralogous factors in somatosensory neurons. Targeted gene deletion in mice; histological analysis; immunohistochemistry; genetic epistasis (Brn-3a KO effect on Brn-3b/3c expression) Proceedings of the National Academy of Sciences of the United States of America High 8876243
1996 The two activation domains of Brn-3a have distinct activities that are dependent on the context of the binding site rather than differences in the target sequence itself. A single-stranded DNA preference for Brn-3a binding was demonstrated for two distinct Brn-3a binding sites. Co-transfection reporter assays with Brn-3a deletion constructs; EMSA with single- and double-stranded DNA; chimeric promoter analysis The Journal of biological chemistry Medium 8621561
1997 Brn-3a overexpression in undifferentiated ND7 neuronal cells induces neuronal process outgrowth and activates genes encoding synaptic proteins. These effects are primarily dependent on the POU domain (which also serves as an activation domain), and a single amino acid change in the POU homeodomain of Brn-3a to its Brn-3b equivalent abolishes neurite outgrowth induction. Brn-3b does not induce these effects. Stable overexpression of Brn-3a, Brn-3b, isolated POU domain, and point mutants in ND7 cells; morphological assessment of neurite outgrowth; co-transfection gene expression assays Molecular and cellular biology High 8972215
1997 Brn-3a overexpression coordinately upregulates all three neurofilament (NF-L, NF-M, NF-H) gene promoters, whereas Brn-3b has no effect. This activation is mediated by the POU domain, and a single amino acid change in the POU homeodomain converts Brn-3b into an activator of neurofilament promoters. Co-transfection reporter assays with neurofilament promoters; Western blot and RT-PCR for endogenous protein/mRNA; domain-swap and point mutagenesis The Journal of biological chemistry High 9261145
1998 Brn-3a directly activates the Bcl-2 P2 promoter in neuronal cells through a specific binding site in the promoter; this activation increases Bcl-2 protein levels. The Brn-3a binding site in the P2 promoter is required for maximal activation and for the response during ND7 cell differentiation. Co-transfection reporter assays; EMSA; Western blot for BCL-2 protein; stable Brn-3a overexpression lines; primary DRG neurons The Journal of biological chemistry High 9642226
1998 Brn-3a and Brn-3b POU domains interact with the DNA-binding domain of the estrogen receptor (ER) independently of ligand. In estradiol-stimulated cells, Brn-3b strongly activates an ERE-containing promoter whereas Brn-3a has a mild inhibitory effect. A single amino acid change in the first helix of the Brn-3a POU homeodomain to the Brn-3b equivalent converts its mild repression to Brn-3b-like activation. GST pulldown assay; yeast two-hybrid; co-transfection reporter assays with ERE-containing promoter; point mutagenesis of POU homeodomain Molecular and cellular biology High 9448000
1999 Brn-3a strongly activates Bcl-2 promoter activity and this activation is inhibited by p53. p53 requires DNA-binding activity for this inhibitory effect (DNA-binding mutants of p53 do not inhibit). Brn-3a and p53 bind to adjacent sites in the Bcl-2 p2 promoter and directly interact in vitro and in vivo; this interaction is mediated by the POU domain of Brn-3a and the DNA-binding domain of p53. The inhibitory effect is specific to Bcl-2 p1/p2 promoters and not observed on other Brn-3a-activated promoters. Co-transfection reporter assays; in vitro GST pulldown; co-immunoprecipitation in vivo; EMSA; promoter deletion analysis The Journal of biological chemistry High 10329733
1999 Brn-3a controls survival and differentiation of trigeminal neurons by regulating expression of all three Trk receptors. In Brn-3a-null mice, TrkC-expressing neurons are almost absent from birth, TrkB neurons are transiently elevated then lost, and TrkA expression progressively declines after E12.5, leading to massive apoptosis peaking at E15.5. Surviving neurons predominantly express c-ret and can be sustained by GDNF but not NGF, indicating Brn-3a does not regulate GDNF receptor expression. Brn-3a knockout mice; immunohistochemistry for Trk receptors; TUNEL apoptosis assay; in vitro neurotrophic factor survival assays on KO neurons; temporal staging Development (Cambridge, England) High 10357931
2001 Brn-3a is a transcriptional regulator of soma size, neuronal migration, and axon pathfinding in the inner ear. Absence of Brn-3a causes downregulation of TrkC, parvalbumin, and Brn-3b; selective loss of TrkC-expressing spiral ganglion neurons (phenocopying TrkC-/- mice); and severe retardation of axon projections to the cochlea and posterior vertical canal by E13.5, as well as misrouting of efferent axons. Brn-3a knockout mouse analysis; immunohistochemistry; DiI axon tracing; temporal staging; comparison with TrkC KO phenotype Development (Cambridge, England) High 11493560
2001 Brn-3a directly activates the Bcl-xL promoter in sensory but not sympathetic neurons; antisense reduction of Brn-3a reduces Bcl-xL expression; overexpression of Brn-3a in DRG in vivo (sciatic nerve injury model) enhances both Bcl-xL expression and neuronal survival. Co-transfection reporter assays; antisense oligonucleotides; in vivo Brn-3a overexpression via injection; Western blot; survival counting in DRG Molecular and cellular neurosciences Medium 11273642
2001 Brn-3a minimal promoter in the Bcl-xL locus is activated by Brn-3a and this activation is specifically blocked by p53. The same promoter sequences required for basal activity mediate both Brn-3a activation and p53 repression. A second upstream Bcl-xL promoter is also activated by Brn-3a and repressed by p53. Co-transfection reporter assays with Bcl-xL promoter deletions; co-expression of Brn-3a and p53 Nucleic acids research Medium 11713302
2001 Sensory axon growth defects (excessive/premature branching, failure to innervate whisker follicles) precede neuronal death in Brn-3a null mice. These defects resemble those in semaphorin 3A and neuropilin-1 null mice; however, neuropilin-1 expression is maintained in Brn-3a-null sensory neurons, indicating Brn-3a controls axon pathfinding through other downstream genes. Brn-3a KO crossed to LacZ reporter transgene; whole-mount beta-galactosidase histochemistry for axon visualization; immunohistochemistry for neuropilin-1; temporal analysis of phenotype vs. cell death The Journal of neuroscience : the official journal of the Society for Neuroscience High 11160433
2001 Overexpression of Brn-3a in cultured trigeminal and DRG sensory neurons enhances survival after NGF withdrawal and activates the endogenous Bcl-2 gene; reducing Brn-3a levels with antisense impairs survival of these neurons. The protective effect is absent in sympathetic neurons. Brn-3b can promote early-stage trigeminal neuron survival but with less temporal breadth than Brn-3a. Primary neuronal cultures from TG and DRG; overexpression via plasmid transfection; antisense reduction; NGF withdrawal survival assay; Bcl-2 protein measurement The Journal of biological chemistry Medium 11053412
2002 Brn-3a abolishes p53-mediated activation of the pro-apoptotic Bax promoter and Bax protein expression, while cooperating with p53 to maximally activate the p21(CIP1/Waf1) promoter. At the cellular level, Brn-3a antagonizes p53-induced apoptosis but cooperates with p53 to induce cell cycle arrest. Co-transfection reporter assays with Bax and p21 promoters; Western blot for Bax and p21 protein; apoptosis and cell cycle assays Oncogene Medium 12203124
2003 Brn-3a directly binds to specific sites in a 457 bp enhancer that regulates TrkA expression in embryonic sensory neurons. Mutagenesis of these Brn-3a binding sites in the enhancer abolishes appropriate reporter transgene expression in sensory neurons in vivo. Using Bax-KO mice to uncouple cell death from TrkA downregulation confirmed that Brn-3a is required for maintaining TrkA transcriptional activity independently of neurotrophin-dependent survival. EMSA; transgenic reporter mice with mutagenized enhancer; Bax-KO genetic background epistasis; in vivo transgene expression analysis Development (Cambridge, England) High 12810599
2003 Brn-3a negatively autoregulates its own expression by binding to conserved sites within an 11 kb upstream enhancer. In Brn-3a(+/-) mice, expression of the remaining allele is upregulated to near wild-type levels (gene dosage compensation), while transgenic overexpression of Brn-3a suppresses the endogenous gene. LacZ reporter transgenes; in vivo chromatin-binding analysis; comparison of Brn-3a protein levels in +/+, +/-, and -/- mice; transgenic overexpression Development (Cambridge, England) High 12441296
2003 EWS (Ewing's Sarcoma protein) interacts with Brn-3a via the POU domain and the RNA-binding domain of EWS (in vitro), and EWS inhibits Brn-3a-mediated activation of the Bcl-xL promoter. Yeast two-hybrid screen; in vitro GST pulldown; co-transfection reporter assays Cancer biology & therapy Medium 12432261
2004 HIPK2 physically interacts with Brn-3a, promotes Brn-3a DNA binding, but suppresses Brn-3a-dependent transcription of brn3a, trkA, and bcl-xL target genes. HIPK2 overexpression induces apoptosis in sensory neurons, while HIPK2 KO increases Brn-3a, TrkA, and Bcl-xL expression and reduces apoptosis in the trigeminal ganglion. Co-immunoprecipitation; EMSA; co-transfection reporter assays; HIPK2 overexpression in primary sensory neurons; HIPK2 targeted deletion mouse; immunohistochemistry; TUNEL The Journal of cell biology High 15492043
2004 Brn-3a abolishes p53-mediated transcription of the pro-apoptotic gene Noxa. EMSA studies show Brn-3a is associated with p53 when p53 is bound to the Noxa promoter. ChIP confirms Brn-3a association with the wild-type but not mutant Noxa promoter in cells. Co-expression of Brn-3a with p53 reduces endogenous Noxa protein in ND7 neuronal cells. In Brn-3a-/- embryos, both Bax and Noxa proteins are elevated at E14.5, preceding the wave of neuronal apoptosis. Co-transfection reporter assays; EMSA; ChIP; Western blot for endogenous Noxa and Bax; Brn-3a KO embryo tissue analysis The Journal of biological chemistry High 15598651
2004 The N-terminal transcriptional activation domain of Brn-3a is essential for neuronal survival in vivo, while the POU domain is essential for neurite outgrowth in vivo. These two functions are thus controlled by separable domains of the protein. In vivo gene manipulation (domain-specific Brn-3a constructs introduced into mice); neuronal survival quantification; neurite morphology assessment Neuroreport Medium 15194866
2004 EWS/Fli-1 (but not EWS alone) interacts with Brn-3a via the C-terminal POU domain. EWS/Fli-1 overexpression specifically inhibits Brn-3a-associated growth arrest and neurite outgrowth and blocks Brn-3a-dependent activation of p21 and SNAP-25 transcription, while EWS more effectively antagonizes the Bcl-2 upregulation function of Brn-3a. In vitro GST pulldown; co-transfection reporter assays for p21 and SNAP-25; neurite outgrowth and growth arrest assays in neuronal cells Oncogene Medium 15021903
2003 Rin, a neuron-specific small GTP-binding protein, physically interacts with the N-terminal domain of Brn-3a (identified by yeast two-hybrid) and modulates Brn-3a N-terminal-dependent activation of the egr-1 promoter. Yeast two-hybrid screen; co-transfection reporter assays for egr-1 promoter; N-terminal domain of Brn-3a as bait Oncogene Low 12934100
2005 Brn-3a-expressing RGCs project specifically to the principal retinothalamic/retinocollicular pathway (thalamocortical and collicular visual pathways) and are absent from RGCs serving accessory optic, pretectal, and hypothalamic (circadian) pathways. Brn-3a RGC axons preferentially project to the outer shell of the dorsal lateral geniculate nucleus contralaterally. Targeted knock-in of tau/beta-galactosidase axonal tracer into the Brn3a locus; anterograde axon tracing; Brn-3a KO analysis of laterality The Journal of neuroscience : the official journal of the Society for Neuroscience High 16354917
2006 Brn-3a is a direct repressor of NeuroD1 and NeuroD4 (pro-neurogenic genes) in embryonic sensory neurons, and also directly modulates its own expression. Locus-wide ChIP in embryonic trigeminal neurons shows that in vivo Brn-3a binding correlates with evolutionary conservation of genomic regions and with active histone modifications (H3 acetylation); not all high-affinity sites are occupied in vivo. Locus-wide ChIP in embryonic trigeminal neurons; microarray expression profiling of Brn3a-null ganglia; correlation of binding with histone marks and evolutionary conservation Developmental biology High 17196582
2006 Brn-3a and Klf7 synergistically activate the TrkA enhancer in vitro. In double Brn-3a-/-;Klf7-/- mutants, TrkA expression is severely reduced at E12.5 and completely lost by birth (more severe than either single mutant), demonstrating cooperative regulation of endogenous TrkA expression required for nociceptive sensory neuron survival. Co-transfection reporter assays (synergistic activation); Brn-3a-/-;Klf7-/- double KO mice; in vivo TrkA expression by immunohistochemistry; genetic epistasis Developmental biology High 17011544
2008 The MEK1/2-ERK1/2 signaling pathway regulates Brn-3a N-terminal transcriptional activity during retinoic acid (RA)-mediated neuronal differentiation. Phosphorylation of Brn-3a at serine-122 (and threonine-39) is required for RA-induced neurite outgrowth and N-terminal transactivation of the Galanin promoter. MEK inhibitors block both RA-induced Galanin activation and Brn-3a N-terminal activity; constitutively active MEK1 (but not MEK5) is sufficient to increase Brn-3a activity. Site-directed mutagenesis of Brn-3a (S122A, T39A); co-transfection reporter assays with Galanin promoter; pharmacological MEK inhibition; constitutively active MEK1/MEK5 expression; neurite outgrowth assay in ND7 cells Brain research Medium 19135033
2008 Brn-3a physically interacts with TAp73 and ΔNp73 isoforms and co-localizes with them in sensory neurons. Brn-3a antagonizes TAp73-mediated transactivation of pro-apoptotic Bax but cooperates with TAp73 to activate p21(CIP1/Waf1). Co-expression with ΔNp73 increases apoptotic protection. The C-terminal region (aa 425-494) of TAp73 is critical for Brn-3a to repress Bax transactivation. Co-immunoprecipitation; immunofluorescence co-localization; co-transfection reporter assays with Bax and p21 promoters; TAp73 C-terminal deletion constructs Cell death and differentiation Medium 18421303
2009 Brn-3a-expressing habenular neurons project exclusively to the interpeduncular nucleus. In Brn-3a null embryos, the fasciculus retroflexus forms correctly but habenular neurons fail to innervate their targets. Microarray analysis of Brn-3a null embryos reveals that Brn-3a regulates an extensive program of habenula-enriched genes. The orphan nuclear receptor Nurr1/Nr4a2 is downstream of Brn-3a and mediates expression of a subset of Brn-3a-regulated habenular transcripts. Brn-3a KO mice; axon tracing; microarray gene expression profiling; genetic epistasis (Nurr1 expression in Brn-3a nulls); bioinformatic analysis The Journal of neuroscience : the official journal of the Society for Neuroscience High 19906978
2009 Brn-3a and Brn-3b control overlapping but distinct aspects of RGC development. Brn-3a deletion alters dendritic stratification and the monostratified:bistratified RGC ratio with little effect on central projections. Brn-3b deletion leads to RGC transdifferentiation and loss, axon defects, and disrupted central projections affecting multiple visually driven behaviors. Both factors are thus required for programming distinct aspects of RGC diversity. Conditional KO alleles of Brn-3a and Brn-3b with visualization of individual cells; dendritic morphology and stratification analysis; anterograde axon tracing; behavioral testing (visual tasks) Neuron High 19323995
2010 Brn-3a acts upstream of Runx transcription factors to specify sensory neuron subtypes in the trigeminal ganglion. In Brn-3a-/- embryos, Runx3 expression is never initiated in TrkC+ neurons and Runx1 expression is severely reduced in TrkA+ neurons. A Brn-3a-VP16 dominant transactivator increases Runx3 mRNA, and Brn-3a binds in vivo by ChIP to a conserved upstream enhancer within H3-acetylated chromatin at the Runx3 locus. Brn-3a KO mice; Brn-3a-VP16 transgenic mice; ChIP for Brn-3a at Runx3 locus; immunohistochemistry for Trk receptors and Runx factors; histone modification analysis Neural development High 20096094
2012 Brn-3a is required for DRG sensory neuron subtype specification and for central axon projections into the spinal cord. Brn-3a-null DRGs show excessive early generation of TrkB+ and TrkC+ neurons plus double-positive (TrkA+/TrkB+ and TrkA+/TrkC+) cells, followed by loss of TrkB+, TrkC+ and parvalbumin+ neurons and increases in CGRP+ and c-ret+ neurons. TrkA+ afferents fail to enter the dorsal horn and TrkC+ proprioceptive projections to the ventral horn are impaired. Runx1 expression is dramatically downregulated, suggesting Brn-3a acts through Runx1 for specification. Brn-3a single and Brn-3a;Brn-3b double KO mice; immunohistochemistry for Trk receptors, parvalbumin, CGRP, Runx1; DiI axon tracing; temporal staging Developmental biology High 22326227
2019 Pou4f1 defines a subpopulation of modiolar-side type I spiral ganglion neurons (SGNs). Conditional deletion of Pou4f1 in SGNs after E13 (avoiding early pathfinding/apoptosis phenotypes) alters Ca2+ channel activation in inner hair cells (IHCs), increasing voltage sensitivity and eliminating the normal modiolar-to-pillar gradient of active zone Ca2+ influx strength, without changing SGN numbers, morphology, or synapse distribution. Conditional KO of Pou4f1 in SGNs (tamoxifen-inducible Cre); immunohistochemistry; Ca2+ imaging of IHC active zones; patch-clamp electrophysiology of IHC Ca2+ channels The Journal of neuroscience : the official journal of the Society for Neuroscience High 31085606
2020 Pou4f1 (Brn3a) is a Smad3 target gene and key downstream regulator of macrophage-myofibroblast transition (MMT) in renal fibrosis. ChIP confirmed Pou4f1 as a Smad3 target. Microarray defined a Pou4f1-dependent fibrogenic gene network driving TGF-β1/Smad3-induced MMT. Silencing Pou4f1 in TGF-β1-stimulated bone marrow-derived macrophages, then adoptively transferring them, prevented restoration of MMT and fibrosis in macrophage-depleted mice. ChIP (Smad3 binding to Pou4f1 locus); microarray gene expression; siRNA silencing; in vitro MMT assay; adoptive transfer of BMDMs into macrophage-depleted mice; two mouse models of renal fibrosis Proceedings of the National Academy of Sciences of the United States of America High 32788346
2020 POU4F1 promotes BRAF-inhibitor resistance in melanoma by transcriptionally activating MEK expression to re-activate the MAPK/ERK pathway and by increasing MITF expression. POU4F1 overexpression and knockdown in melanoma cells; Western blot for MEK, ERK, MITF; luciferase reporter assays for MEK promoter; xenograft mouse models Cell death & disease Medium 32532957
2022 HDAC2 represses BRN3A expression in melanocytes and melanoma by maintaining deacetylated chromatin at a distal enhancer of the BRN3A gene. Selective HDAC2 siRNA knockdown increases H3K27ac levels at this BRN3A distal enhancer (confirmed by ChIP-Seq) and upregulates BRN3A expression. siRNA knockdown of individual HDACs; ChIP-Seq for H3K27ac; pharmacological HDAC inhibitors (class-selective and isoform-selective); RT-PCR and Western blot for BRN3A International journal of molecular sciences Medium 35055045
2024 ISL1 and POU4F1 directly interact in developing cochleovestibular ganglion (CVG) neurons and cooperate to regulate expression of CVG-specific genes. Compound Isl1;Pou4f1 double KO causes near-complete loss of spiral ganglion neurons—more severe than either single KO—with defects in migration, axon pathfinding, and survival. POU4F1 directly binds cis-regulatory elements of Fgf10, Pou4f2, Epha5 (promoters) and Eya1 and Ntng2 (enhancers). Isl1 and Pou4f1 single and double KO mice; immunohistochemistry; co-immunoprecipitation of ISL1-POU4F1; ChIP for POU4F1 at target loci; gene expression profiling The Journal of neuroscience : the official journal of the Society for Neuroscience High 38267260
2024 POU4F1 is required for G1/S cell cycle progression in basal-like breast cancer (BLBC) through direct binding at the promoters of CDK2 and CCND1. POU4F1 also maintains BLBC identity by repressing ESR1 (ERα) expression through CDK2-mediated EZH2 phosphorylation and subsequent H3K27me3 modification at the ESR1 promoter. POU4F1 promoter activation in BLBC is maintained by the DNA demethylase TET1, which reconfigures bivalent chromatin to an active state. POU4F1 KO in BLBC cells; ChIP for POU4F1 at CDK2 and CCND1 promoters; cell cycle and proliferation assays; H3K27me3 ChIP at ESR1; Western blot for ERα and EZH2 phosphorylation; TET1 knockdown and DNA methylation analysis Advanced science (Weinheim, Baden-Wurttemberg, Germany) High 38491910
2023 Pou4f1 acts as a transcription factor for STAT3, directly regulating STAT3 transcription. In glioma cells, POU4F1 overexpression or STAT3 silencing suppresses XHP-induced pyroptosis, placing Pou4f1 upstream of STAT3 in this pathway. Dual-luciferase reporter assay for STAT3 promoter; co-IP of POU4F1-STAT3; Western blot; ChIP; siRNA/overexpression in glioma cell lines; in vivo glioma model Functional & integrative genomics Medium 37962640
2023 Pou4f1 directly binds to the Tbr1 locus (exon 6 and 3'UTR flanking region) and to the Jam2 promoter region; Pou4f1 is required for expression of Tbr1 and Jam2 in J-RGCs. The Pou4f1-bound element in Tbr1 exon 6 has enhancer activity capable of directing reporter expression in J-RGCs, establishing a Pou4f1-Tbr1-Jam2 transcriptional cascade for J-RGC subtype formation. CUT&RUN (Cleavage Under Targets and Tagmentation); conditional KO of Pou4f1; reporter assay for enhancer activity; immunohistochemistry for Tbr1 and Jam2; in situ hybridization Frontiers in ophthalmology High 38469155
2024 Runx3 and Brn3a co-bind to numerous genomic loci in early TrkC proprioceptive neurons, primarily at distally located enhancer regions. In activated and suppressed neuronal Runx3 high-confidence target genes, Runx3 cooperates mainly with Brn3a to regulate gene expression through these distant enhancers, while suppression of non-neuronal immune genes is managed by Runx3 without Brn3a. CUT&RUN for Runx3, Brn3a, Isl1, and H3K27Ac; ATAC-seq; RNA-seq of heterozygous vs. homozygous P2-Runx3 TrkC neurons; bioinformatic co-occupancy analysis PLoS genetics Medium 39715266
2025 USP18 stabilizes POU4F1 protein through deubiquitination. POU4F1 in turn promotes transcription of PRKAA2 (AMPK-α2) by binding its promoter (ChIP and dual-luciferase confirmed). USP18-mediated oncogenic effects in lung adenocarcinoma are reversed by POU4F1 knockdown, and POU4F1 regulates cell behaviors via PRKAA2 upregulation. Immunoprecipitation and ubiquitination assay (USP18-POU4F1 interaction); ChIP and dual-luciferase reporter for POU4F1 at PRKAA2 promoter; siRNA/overexpression; xenograft mouse model BMC cancer Medium 40122823

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 Brn3a as a marker of retinal ganglion cells: qualitative and quantitative time course studies in naive and optic nerve-injured retinas. Investigative ophthalmology & visual science 489 19264888
2009 Distinct roles of transcription factors brn3a and brn3b in controlling the development, morphology, and function of retinal ganglion cells. Neuron 220 19323995
1996 Targeted deletion of the mouse POU domain gene Brn-3a causes selective loss of neurons in the brainstem and trigeminal ganglion, uncoordinated limb movement, and impaired suckling. Proceedings of the National Academy of Sciences of the United States of America 201 8876243
2005 Brn3a-expressing retinal ganglion cells project specifically to thalamocortical and collicular visual pathways. The Journal of neuroscience : the official journal of the Society for Neuroscience 145 16354917
2020 Neural transcription factor Pou4f1 promotes renal fibrosis via macrophage-myofibroblast transition. Proceedings of the National Academy of Sciences of the United States of America 139 32788346
1999 p53 suppresses the activation of the Bcl-2 promoter by the Brn-3a POU family transcription factor. The Journal of biological chemistry 130 10329733
2001 Brn3a is a transcriptional regulator of soma size, target field innervation and axon pathfinding of inner ear sensory neurons. Development (Cambridge, England) 123 11493560
1999 POU domain factor Brn-3a controls the differentiation and survival of trigeminal neurons by regulating Trk receptor expression. Development (Cambridge, England) 107 10357931
1998 Bcl-2 transcription from the proximal P2 promoter is activated in neuronal cells by the Brn-3a POU family transcription factor. The Journal of biological chemistry 106 9642226
2009 Brn3a and Nurr1 mediate a gene regulatory pathway for habenula development. The Journal of neuroscience : the official journal of the Society for Neuroscience 101 19906978
2001 Defects in sensory axon growth precede neuronal death in Brn3a-deficient mice. The Journal of neuroscience : the official journal of the Society for Neuroscience 87 11160433
2004 Interaction of Brn3a and HIPK2 mediates transcriptional repression of sensory neuron survival. The Journal of cell biology 85 15492043
1993 Mouse Brn-3 family of POU transcription factors: a new aminoterminal domain is crucial for the oncogenic activity of Brn-3a. Nucleic acids research 84 8290353
2010 Morphologies of mouse retinal ganglion cells expressing transcription factors Brn3a, Brn3b, and Brn3c: analysis of wild type and mutant cells using genetically-directed sparse labeling. Vision research 79 20826176
2011 Brain derived neurotrophic factor maintains Brn3a expression in axotomized rat retinal ganglion cells. Experimental eye research 76 21315070
1995 Activation of the alpha-internexin promoter by the Brn-3a transcription factor is dependent on the N-terminal region of the protein. The Journal of biological chemistry 67 7852360
2004 Brn-3a transcription factor blocks p53-mediated activation of proapoptotic target genes Noxa and Bax in vitro and in vivo to determine cell fate. The Journal of biological chemistry 60 15598651
1997 The Brn-3a transcription factor induces neuronal process outgrowth and the coordinate expression of genes encoding synaptic proteins. Molecular and cellular biology 59 8972215
2012 Brn3a/Pou4f1 regulates dorsal root ganglion sensory neuron specification and axonal projection into the spinal cord. Developmental biology 58 22326227
2003 Brn3a regulation of TrkA/NGF receptor expression in developing sensory neurons. Development (Cambridge, England) 56 12810599
2003 Direct autoregulation and gene dosage compensation by POU-domain transcription factor Brn3a. Development (Cambridge, England) 55 12441296
2001 A minimal Bcl-x promoter is activated by Brn-3a and repressed by p53. Nucleic acids research 55 11713302
1998 POU transcription factors Brn-3a and Brn-3b interact with the estrogen receptor and differentially regulate transcriptional activity via an estrogen response element. Molecular and cellular biology 54 9448000
2000 Coordinated Up-regulation by hypoxia of adrenomedullin and one of its putative receptors (RDC-1) in cells of the rat blood-brain barrier. The Journal of biological chemistry 52 10980200
1997 Coordinate induction of the three neurofilament genes by the Brn-3a transcription factor. The Journal of biological chemistry 50 9261145
2000 The BRN-3A transcription factor protects sensory but not sympathetic neurons from programmed cell death/apoptosis. The Journal of biological chemistry 49 11053412
2002 The Brn-3a transcription factor inhibits the pro-apoptotic effect of p53 and enhances cell cycle arrest by differentially regulating the activity of the p53 target genes encoding Bax and p21(CIP1/Waf1). Oncogene 48 12203124
2019 Pou4f1 Defines a Subgroup of Type I Spiral Ganglion Neurons and Is Necessary for Normal Inner Hair Cell Presynaptic Ca2+ Signaling. The Journal of neuroscience : the official journal of the Society for Neuroscience 46 31085606
2001 Brn-3a activates the expression of Bcl-x(L) and promotes neuronal survival in vivo as well as in vitro. Molecular and cellular neurosciences 46 11273642
2010 Brn3a regulates neuronal subtype specification in the trigeminal ganglion by promoting Runx expression during sensory differentiation. Neural development 43 20096094
2005 Axotomy-induced early down-regulation of POU-IV class transcription factors Brn-3a and Brn-3b in retinal ganglion cells. Journal of molecular neuroscience : MN 35 15968082
2006 Brn3a and Klf7 cooperate to control TrkA expression in sensory neurons. Developmental biology 34 17011544
2014 Comparative expression analysis of POU4F1, POU4F2 and ISL1 in developing mouse cochleovestibular ganglion neurons. Gene expression patterns : GEP 33 24709358
1998 The HPV-activating cellular transcription factor Brn-3a is overexpressed in CIN3 cervical lesions. The Journal of clinical investigation 33 9541499
1998 The Brn-3a transcription factor. The international journal of biochemistry & cell biology 32 9839440
2006 Brn3a target gene recognition in embryonic sensory neurons. Developmental biology 31 17196582
2001 The closely related POU family transcription factors Brn-3a and Brn-3b are expressed in distinct cell types in the testis. The international journal of biochemistry & cell biology 30 11470235
1995 The neuronal nicotinic acetylcholine receptor alpha 2 subunit gene promoter is activated by the Brn-3b POU family transcription factor and not by Brn-3a or Brn-3c. The Journal of biological chemistry 29 7797498
1996 Alternative splicing of the Brn-3a and Brn-3b transcription factor RNAs is regulated in neuronal cells. Journal of molecular neuroscience : MN 28 8835784
2013 The neural crest transcription factor Brn3a is expressed in melanoma and required for cell cycle progression and survival. EMBO molecular medicine 27 23666755
2020 POU4F1 promotes the resistance of melanoma to BRAF inhibitors through MEK/ERK pathway activation and MITF up-regulation. Cell death & disease 25 32532957
2004 The effects of Brn-3a on neuronal differentiation and apoptosis are differentially modulated by EWS and its oncogenic derivative EWS/Fli-1. Oncogene 24 15021903
1997 High expression of the POU factor Brn3a in aggressive neuroendocrine tumors. The Journal of clinical endocrinology and metabolism 24 8989239
2014 Pou4f1 and pou4f2 are dispensable for the long-term survival of adult retinal ganglion cells in mice. PloS one 22 24736625
2010 POU4F1 is associated with t(8;21) acute myeloid leukemia and contributes directly to its unique transcriptional signature. Leukemia 22 20376082
2002 Effect of Brn-3a deficiency on parvalbumin-, calbindin D-28k-, calretinin- and calcitonin gene-related peptide-immunoreactive primary sensory neurons in the trigeminal ganglion. Neuroscience 22 12150774
2006 Brn-3a neuronal transcription factor functional expression in human prostate cancer. Prostate cancer and prostatic diseases 21 16276351
2001 The Brn-3a transcription factor plays a key role in regulating the growth of cervical cancer cells in vivo. Oncogene 21 11521202
2004 Effect of Brn-3a deficiency on parvalbumin-immunoreactive primary sensory neurons in the dorsal root ganglion. Brain research. Developmental brain research 18 15126036
2020 POU4F1 confers trastuzumab resistance in HER2-positive breast cancer through regulating ERK1/2 signaling pathway. Biochemical and biophysical research communications 16 32988584
2018 Postnatal developmental dynamics of cell type specification genes in Brn3a/Pou4f1 Retinal Ganglion Cells. Neural development 16 29958540
1998 NT-3 regulates expression of Brn3a but not Brn3b in developing mouse trigeminal sensory neurons. Brain research. Molecular brain research 16 9582431
1995 The levels of the antagonistic POU family transcription factors Brn-3a and Brn-3b in neuronal cells are regulated in opposite directions by serum growth factors. Neuroscience letters 16 7731552
1995 Short isoform of POU factor Brn-3b can form a heterodimer with Brn-3a that is inactive for octamer motif binding. The Journal of biological chemistry 16 8537352
2020 Software for Quantifying and Batch Processing Images of Brn3a and RBPMS Immunolabelled Retinal Ganglion Cells in Retinal Wholemounts. Translational vision science & technology 15 32821525
2005 Effects of Brn-3a protein and RNA expression in rat brain following low-level lead exposure during development on spatial learning and memory. Toxicology letters 15 16384672
2004 Coexpression of Brn-3a POU protein with p53 in a population of neuronal progenitor cells is associated with differentiation and protection against apoptosis. Journal of neuroscience research 15 15532030
1996 Similarities and differences among inner retinal neurons revealed by the expression of reporter transgenes controlled by Brn-3a, Brn-3b, and Brn-3c promotor sequences. Visual neuroscience 15 8903036
2024 Activation of Bivalent Gene POU4F1 Promotes and Maintains Basal-like Breast Cancer. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 14 38491910
2016 Brn3a and Brn3b knockout mice display unvaried retinal fine structure despite major morphological and numerical alterations of ganglion cells. The Journal of comparative neurology 14 27391320
2010 AML1/ETO proteins control POU4F1/BRN3A expression and function in t(8;21) acute myeloid leukemia. Cancer research 14 20460523
1996 The different activities of the two activation domains of the Brn-3a transcription factor are dependent on the context of the binding site. The Journal of biological chemistry 14 8621561
1996 The functionally antagonistic POU family transcription factors Brn-3a and Brn-3b show opposite changes in expression during the growth arrest and differentiation of human neuroblastoma cells. International journal of cancer 13 8782654
2017 Essential but partially redundant roles for POU4F1/Brn-3a and POU4F2/Brn-3b transcription factors in the developing heart. Cell death & disease 12 28594399
2008 Regulation of Brn-3a N-terminal transcriptional activity by MEK1/2-ERK1/2 signalling in neural differentiation. Brain research 12 19135033
2003 Measurement of Brn-3a levels in Pap smears provides a novel diagnostic marker for the detection of cervical neoplasia. Gynecologic oncology 12 12893201
2002 Effect of Brn-3a deficiency on nociceptors and low-threshold mechanoreceptors in the trigeminal ganglion. Brain research. Molecular brain research 12 12225879
2006 Differential regulation of different human papilloma virus variants by the POU family transcription factor Brn-3a. Oncogene 11 16247485
2015 Red nucleus and rubrospinal tract disorganization in the absence of Pou4f1. Frontiers in neuroanatomy 10 25698939
2005 Brn-3a deficiency increases tyrosine hydroxylase-immunoreactive neurons in the dorsal root ganglion. Brain research 10 15725417
2002 Brn-3a, a neuronal transcription factor of the POU gene family: indications for its involvement in cancer and angiogenesis. Molecular biotechnology 10 12405260
2002 The pro-oncoprotein EWS (Ewing's Sarcoma protein) interacts with the Brn-3a POU transcription factor and inhibits its ability to activate transcription. Cancer biology & therapy 10 12432261
2024 Comparison of Brn3a and RBPMS Labeling to Assess Retinal Ganglion Cell Loss During Aging and in a Model of Optic Neuropathy. Investigative ophthalmology & visual science 9 38587440
2001 The POU domain transcription factor Brn-3a protects cortical neurons from apoptosis. Neuroreport 9 11711852
2024 ISL1 and POU4F1 Directly Interact to Regulate the Differentiation and Survival of Inner Ear Sensory Neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience 8 38267260
2022 HDAC2 Is Involved in the Regulation of BRN3A in Melanocytes and Melanoma. International journal of molecular sciences 8 35055045
2020 Brn3a/Pou4f1 Functions as a Tumor Suppressor by Targeting c-MET/STAT3 Signaling in Thyroid Cancer. The Journal of clinical endocrinology and metabolism 8 32474599
2008 Brn-3a/POU4F1 interacts with and differentially affects p73-mediated transcription. Cell death and differentiation 8 18421303
2005 Effect of Brn-3a deficiency on primary nociceptors in the trigeminal ganglion. Neuroscience research 8 15740807
2005 Elevated expression of the Brn-3a and Brn-3b transcription factors in systemic lupus erythematosus correlates with antibodies to Brn-3 and overexpression of Hsp90. Arthritis and rheumatism 8 15818685
2005 Brn-3a is required for the generation of proprioceptors in the mesencephalic trigeminal tract nucleus. Brain research 8 16040009
2004 Doppel expression is regulated by the Brn-3a and Brn-3b transcription factors. Neuroreport 8 15094508
2003 Functional interaction between the small GTP-binding protein Rin and the N-terminal of Brn-3a transcription factor. Oncogene 8 12934100
2011 Molecular analysis of oncogenicity of the transcription factor, BRN3A, in cervical cancer cells. Journal of cancer research and clinical oncology 7 21928122
2007 Novel Brn3a cis-acting sequences mediate transcription of human trkA in neurons. Journal of neurochemistry 7 18086126
2004 EWS differentially activates transcription of the Brn-3a long and short isoform mRNAs from distinct promoters. Biochemical and biophysical research communications 7 15147979
2023 Xihuang pill facilitates glioma cell pyroptosis via the POU4F1/STAT3 axis. Functional & integrative genomics 6 37962640
2025 Deubiquitinase USP18 mediates cell migration, apoptosis and ferroptosis in lung adenocarcinoma by depending on POU4F1/PRKAA2 axis. BMC cancer 5 40122823
2022 Involvement of Brn3a-positive spinal dorsal horn neurons in the transmission of visceral pain in inflammatory bowel disease model mice. Frontiers in pain research (Lausanne, Switzerland) 5 36570085
2021 Genetic interplay between transcription factor Pou4f1/Brn3a and neurotrophin receptor Ret in retinal ganglion cell type specification. Neural development 5 34548095
2019 Establishment of resveratrol and its derivatives as neuroprotectant against monocrotophos-induced alteration in NIPBL and POU4F1 protein through molecular docking studies. Environmental science and pollution research international 5 31786755
2004 Distinct domains of Brn-3a regulate apoptosis and neurite outgrowth in vivo. Neuroreport 5 15194866
2004 [Effects of lead on the Brn-3a expression and the apoptosis in hippocampus neurons]. Wei sheng yan jiu = Journal of hygiene research 5 15208987
2003 Unaltered expression of Bcl-2 and TAG-1/axonin-1 precedes sensory apoptosis in Brn3a knockout mice. Neuroreport 5 12598723
2002 Effect of Brn-3a deficiency on CGRP-immunoreactivity in the dorsal root ganglion. Neuroreport 5 11930150
1997 Regulation of neuroblastoma growth and differentiation by the POU family transcription factors Brn-3a and Brn-3b (Review). International journal of oncology 5 21533495
2024 Runx3, Brn3a and Isl1 interplay orchestrates the transcriptional program in the early stages of proprioceptive neuron development. PLoS genetics 4 39715266
2023 Pou4f1-Tbr1 transcriptional cascade controls the formation of Jam2-expressing retinal ganglion cells. Frontiers in ophthalmology 4 38469155
2010 EWS/ETS proteins promote expression and regulate function of the homeodomain transcription factor BRN3A. Oncogene 4 20348952
2007 Brn-3a suppresses pseudorabies virus-induced cell death in sensory neurons. The Journal of general virology 4 17325346

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