Affinage

EBF3

Transcription factor COE3 · UniProt Q9H4W6

Length
596 aa
Mass
64.9 kDa
Annotated
2026-04-28
47 papers in source corpus 19 papers cited in narrative 19 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

EBF3 is a sequence-specific transcription factor that controls cell fate decisions in neuronal, mesenchymal, and hematopoietic lineages by directly binding target gene promoters to activate or repress transcription. It recognizes DNA through an atypical zinc finger/helix-loop-helix domain and functions as a homodimer or heterodimer; disease-causing mutations in the zinc finger or DNA-binding domain cause cytoplasmic mislocalization, reduced chromatin association, and impaired transcriptional activation, resulting in the neurodevelopmental disorder HADDS (hypotonia, ataxia, and delayed development syndrome) (PMID:28017370, PMID:28017373, PMID:35340043). In bone marrow, EBF3 maintains CXCL12-abundant reticular mesenchymal stem cell identity and suppresses osteoblast differentiation, while in neurons it promotes dopaminergic differentiation, regulates neocortical migration through NeuroD1 activation, and controls cerebellar and sensory neuron development (PMID:29563184, PMID:25192643, PMID:29113800). EBF3 directly activates diverse target promoters including CDKN1A/p21, Vimentin, ALOX15, CNTNAP4, and ACADL, and represses CCL24; its own expression is regulated epigenetically by EZH2-mediated H3K27 trimethylation and post-transcriptionally by m6A modification and miR-218 (PMID:17018599, PMID:34906623, PMID:37271497, PMID:38479556, PMID:42018103).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2006 High

    Establishing that EBF3 is a direct transcriptional activator of cell cycle inhibitor genes answered the fundamental question of how EBF3 exerts growth-suppressive effects — by binding the p21 promoter and inducing p21/p27-dependent cell cycle arrest and apoptosis.

    Evidence ChIP showing direct p21 promoter binding, reporter assays, and cell cycle/caspase-3 analysis upon EBF3 overexpression

    PMID:17018599

    Open questions at the time
    • Endogenous contexts where EBF3 regulates p21/p27 not defined
    • Whether EBF3-mediated apoptosis requires p21/p27 or operates through parallel targets not tested
  2. 2014 Medium

    Discovery that miR-218 targets Ebf3 during dopaminergic neuron differentiation established a post-transcriptional control layer and revealed EBF3 as a dose-sensitive regulator of terminal DA neuron fate.

    Evidence Gain- and loss-of-function in ES cell–derived DA neuron differentiation, miR-218 target validation, TH+ neuron quantification

    PMID:25192643

    Open questions at the time
    • Direct Ebf3 transcriptional targets in DA neurons not identified
    • In vivo relevance of miR-218/Ebf3 axis in DA neuron development not tested
  3. 2016 High

    Identification of de novo EBF3 mutations in patients with neurodevelopmental disease, combined with demonstration that zinc finger and DNA-binding domain mutations abolish transcriptional activation, dimerization, nuclear retention, and genome-wide chromatin occupancy, established the molecular basis of HADDS and defined EBF3 as a haploinsufficient transcription factor requiring DNA binding and dimerization for function.

    Evidence Patient genetics, luciferase transactivation, dimerization assays, subcellular fractionation, ChIP-seq, and RNA-seq in HEK293T cells

    PMID:28017370 PMID:28017372 PMID:28017373

    Open questions at the time
    • No crystal structure of the EBF3 DNA-binding domain to explain variant-specific effects
    • Neuronal cell-type–specific consequences of mutations not characterized
  4. 2017 Medium

    Showing that Ebf3 knockdown disrupts the multipolar-to-bipolar transition in migrating neocortical neurons and that NeuroD1 overexpression partially rescues this defect identified a specific downstream pathway through which EBF3 controls cortical neuron migration.

    Evidence In utero electroporation knockdown in mouse neocortex, morphological analysis, NeuroD1 rescue

    PMID:29113800

    Open questions at the time
    • Whether EBF3 directly binds NeuroD1 promoter not shown
    • Cell-autonomous vs. non-autonomous effects not distinguished
  5. 2018 High

    Conditional deletion of Ebf3 (alone and with Ebf1) in CAR/LepR+ bone marrow mesenchymal cells revealed that EBF3 maintains mesenchymal stem cell identity and prevents osteoblast differentiation, directly linking EBF3 to hematopoietic niche function.

    Evidence Conditional knockout mice with lineage tracing, histology showing osteosclerosis, HSC functional assays

    PMID:29563184

    Open questions at the time
    • Direct transcriptional targets mediating the anti-osteoblast program not identified
    • Relative contribution of EBF3 vs. EBF1 in single cells not resolved
  6. 2021 Medium

    ChIP-seq in neuronal cells revealed genome-wide enrichment of EBF3 binding at promoters of neurodevelopmental disorder genes, providing a mechanistic link between EBF3 transcriptional targets and the neurodevelopmental phenotype of HADDS patients.

    Evidence ChIP-seq in neuronal cells with statistical enrichment for NDD gene promoters

    PMID:34256850

    Open questions at the time
    • Functional validation of individual NDD gene targets not performed
    • Whether EBF3 activates or represses these NDD targets not determined
  7. 2021 Medium

    Demonstration that the EGR1/EZH2/HDAC9 complex silences EBF3 via H3K27me3 at its promoter, and that EBF3 directly activates Vimentin transcription, established an epigenetic switch controlling EBF3 expression and identified a pro-metastatic transcriptional target.

    Evidence ChIP and reporter assays at the EBF3 and Vimentin promoters, epigenetic complex characterization in nasopharyngeal carcinoma

    PMID:34906623

    Open questions at the time
    • Whether EZH2-mediated EBF3 silencing operates in normal developmental contexts not tested
    • Vimentin as sole mediator of metastatic phenotype not established
  8. 2022 Medium

    Functional testing of multiple EBF3 patient variants using Drosophila rescue and luciferase assays established a genotype-severity correlation, showing zinc finger mutations are more damaging than certain DNA-binding domain mutations.

    Evidence UAS-GAL4 rescue of Drosophila lethality with variant EBF3 constructs and luciferase transcriptional assays

    PMID:35340043

    Open questions at the time
    • Drosophila model does not recapitulate human brain-specific phenotypes
    • Structural basis for differential severity of ZNF vs. DBD variants remains computational
  9. 2023 Medium

    The Bmal1/EZH2→EBF3→ALOX15 axis in AML cells extended the epigenetic regulation paradigm and identified EBF3 as a transcriptional activator of ALOX15 that promotes ferroptosis, providing a functional context beyond development.

    Evidence ChIP at EBF3 and ALOX15 promoters, knockdown/overexpression, ferroptosis assays, xenograft model in AML

    PMID:37271497

    Open questions at the time
    • Whether EBF3-driven ferroptosis operates in non-malignant hematopoietic cells unknown
    • Specificity of Bmal1 recruitment of EZH2 to EBF3 vs. other loci not addressed
  10. 2023 High

    Conditional CXCL12 deletion from Ebf3+ cells demonstrated that the EBF3-marked CAR niche specifically maintains HSC localization and lymphoid-biased repopulating ability via CXCL12, refining the niche model.

    Evidence Conditional CXCL12 KO from Ebf3-Cre+ cells, transplantation assays, in vitro CXCL12 treatment

    PMID:37880234

    Open questions at the time
    • Whether EBF3 directly regulates CXCL12 transcription not tested
    • Heterogeneity within Ebf3+ CAR cells not resolved
  11. 2024 Medium

    Discovery that FTO-regulated m6A modification controls EBF3 mRNA stability, and that EBF3 directly activates CNTNAP4 to protect DA neurons from apoptosis, added a post-transcriptional regulatory layer and a neuroprotective target gene.

    Evidence ChIP and DNA pulldown at the CNTNAP4 promoter, CNTNAP4 knockdown rescue, MPTP Parkinson's disease mouse model

    PMID:38479556

    Open questions at the time
    • Specific m6A sites on EBF3 mRNA not mapped
    • Whether CNTNAP4 activation is relevant to HADDS neuropathology unknown
  12. 2025 Medium

    Identification of EBF3 as a transcriptional activator of ACADL (blocking YAP nuclear localization) and a repressor of CCL24 (remodeling tumor immune microenvironment) expanded the target repertoire to include Hippo pathway modulation and immune regulation.

    Evidence Promoter binding/reporter assays, rescue experiments, xenograft and syngeneic mouse models in breast and lung cancer

    PMID:41270467 PMID:42018103

    Open questions at the time
    • Whether ACADL-mediated YAP suppression is relevant to non-cancer contexts not addressed
    • Direct mechanism by which EBF3 represses (vs. activates) transcription at CCL24 not elucidated

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis of EBF3 DNA recognition and dimerization, the complete neuronal target gene program explaining HADDS pathogenesis, the mechanism by which EBF3 switches between transcriptional activation and repression, and whether EBF3's roles in mesenchymal stem cell maintenance and neuronal development share common transcriptional targets.
  • No experimentally determined structure of EBF3
  • Genome-wide target analysis in disease-relevant neuronal subtypes lacking
  • Activation vs. repression mechanism at different promoters unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 9 GO:0140110 transcription regulator activity 8
Localization
GO:0005634 nucleus 2 GO:0005694 chromosome 2
Pathway
R-HSA-74160 Gene expression (Transcription) 9 R-HSA-1266738 Developmental Biology 5 R-HSA-5357801 Programmed Cell Death 2 R-HSA-1640170 Cell Cycle 1
Partners
EBF1EZH2NEUROD1PRDM8

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 EBF3 directly binds the p21(cip1/waf1) promoter and regulates transcription from both p21(cip1/waf1) and p27(kip1) promoters, inducing cell cycle arrest and apoptosis with caspase-3 activation; cyclin-dependent kinase inhibitors p27(kip1) and p57(kip2) are persistently activated while cell survival/proliferation genes are suppressed. Reporter assays, chromatin immunoprecipitation (ChIP), overexpression with functional readouts (cell cycle analysis, caspase-3 activation) Cancer research High 17018599
2016 De novo missense variants in EBF3 affecting a conserved zinc finger motif reduce transcriptional activity and the ability to form heterodimers with wild-type EBF3, establishing that DNA binding and dimerization are required for EBF3 function in brain development. Transactivation (luciferase) assays, heterodimer formation assays with mutant proteins in cell lines, structural modeling American journal of human genetics High 28017370 28017372 28017373
2016 EBF3 missense mutations affecting the DNA-binding domain cause mislocalization of mutant proteins to the cytoplasm and reduce chromatin association, as demonstrated by subcellular fractionation; mutant EBF3 has reduced genome-wide DNA binding and gene-regulatory activity by ChIP-seq and RNA-seq. Subcellular fractionation, in situ chromatin association assay, ChIP-seq, RNA-seq, transactivation assays in HEK293T cells American journal of human genetics High 28017373
2014 Ebf3 is a target of miR-218 during dopaminergic (DA) neuron development; overexpression of Ebf3 at the neural precursor stage increases TH+ DA neuron number, while suppression reduces it, and miR-218-mediated regulation of Ebf3 controls terminal differentiation of DA neurons. Overexpression and knockdown in ES cell differentiation system, miRNA target validation, cell counting of TH+ neurons Brain research Medium 25192643
2017 Ebf3 is a target gene of the transcription factor Prdm8; Ebf3 knockdown causes severe defects in leading process formation and inhibits the multipolar-to-bipolar transition of migrating neocortical neurons. Ebf3 positively regulates NeuroD1 transcription and NeuroD1 overexpression partially rescues the migration defect. In utero electroporation-based knockdown, morphological analysis of migrating neurons, NeuroD1 overexpression rescue Biochemical and biophysical research communications Medium 29113800
2018 Ebf3 is expressed in CXCL12-abundant reticular (CAR)/LepR+ mesenchymal stem cells of bone marrow; deletion of Ebf3 in these cells impairs HSC niche function and causes osteosclerosis. Combined deletion of Ebf1 and Ebf3 leads to osteoblast differentiation of CAR cells with reduced HSC niche factor expression and complete marrow cavity occlusion, demonstrating that Ebf3 maintains mesenchymal stem cell identity and inhibits osteoblast differentiation. Conditional knockout mice, lineage tracing, histology, HSC functional assays Genes & development High 29563184
2018 EBF3-EGFP fusion protein localizes predominantly to the nucleus when expressed in HepG2 cells, establishing nuclear localization of EBF3. Fluorescence microscopy and Western blot of nuclear/cytoplasmic fractions of transfected cells Xi bao yu fen zi mian yi xue za zhi Low 18845077
2021 EBF3 directly binds the Vimentin promoter to transcriptionally upregulate it, promoting metastasis in nasopharyngeal carcinoma; EBF3 is epigenetically silenced by the EGR1/EZH2/HDAC9 complex via H3K27me3 at its promoter. ChIP, promoter reporter assays, RNA-seq, epigenetic complex characterization Cancer letters Medium 34906623
2023 Bmal1 recruits EZH2 to the EBF3 promoter to enhance H3K27me3-mediated methylation and suppress EBF3 expression; EBF3 in turn binds the ALOX15 promoter to enhance its expression and promote ferroptosis, establishing the Bmal1/EZH2 → EBF3 → ALOX15 → ferroptosis axis in AML. ChIP, promoter reporter assays, knockdown/overexpression, in vivo xenograft model, ferroptosis biochemical assays Cancer science Medium 37271497
2023 CXCL12 deletion from Ebf3+/LepR+ CAR cells markedly reduces HSCs and impairs their ability to generate B cell progenitors; CXCL12 maintains lymphoid-biased HSC repopulating ability in vitro, demonstrating that CAR cell-derived CXCL12 is required for HSC localization and lymphoid-biased maintenance. Conditional CXCL12 deletion from Ebf3+ cells, transplantation assays, in vitro CXCL12 treatment of HSCs Nature communications High 37880234
2020 Ebf3 is required in lateral plate mesenchyme cells (particularly tendon/connective tissue cells) at embryonic day 9.5–10.5 for sternum ossification; Ebf3 knockout leads to defective Runx2+ pre-osteoblast generation without affecting chondrogenesis, with upregulation of Egr1/2, Osr1 and Islet1+ cells and downregulation of Shox2. Knockout and conditional/temporal knockout mice, cell lineage analysis, gene expression profiling Development High 32398354
2024 EBF3 binds the CNTNAP4 promoter and directly activates CNTNAP4 transcription, protecting dopaminergic neurons from apoptosis in a Parkinson's disease model; m6A methylation (regulated by FTO) controls EBF3 mRNA stability and expression. Luciferase reporter assay, ChIP, DNA pulldown assay, CNTNAP4 knockdown rescue experiment, in vivo MPTP mouse model Cellular signalling Medium 38479556
2025 EBF3 transcriptionally activates ACADL by binding to its promoter, blocking nuclear YAP localization and canonical Hippo/YAP target genes (CTGF, CYR61, ANKRD1) to suppress breast cancer cell growth. Promoter binding assays, luciferase reporter, ACADL knockdown rescue, xenograft tumor model Pathology, research and practice Medium 41270467
2025 EBF3 transcriptionally represses CCL24 to remodel the tumor immune microenvironment in lung adenocarcinoma, reducing M2-like macrophage infiltration and increasing CD4+/CD8+ T cell recruitment; EBF3 also suppresses AKT and P38 phosphorylation. Overexpression/knockdown, ChIP/reporter assays for CCL24, conditioned medium macrophage polarization assay, syngeneic mouse model with immune flow cytometry, CCL24 rescue experiment Cellular oncology Medium 42018103
2025 SNORA47 interacts with EBF3 to facilitate translocation of ribosomal protein L11 (RPL11), which modulates c-Myc levels, establishing a SNORA47-EBF3-RPL11-c-Myc axis controlling breast cancer stemness. Co-immunoprecipitation/interaction assays, overexpression/knockdown with phenotypic readouts Molecular medicine Low 40264043
2022 EBF3 missense variants disrupting the zinc finger domain (ZNF) fail to restore viability in Drosophila and impair transcriptional activation in luciferase assays, whereas the recurrent DBD variant p.Arg209Trp partially rescues fly viability and preserves transcriptional activation, establishing a genotype-severity correlation. In vivo Drosophila UAS-GAL4 rescue assays, in vitro luciferase transcriptional activation assays Annals of neurology Medium 35340043
2017 Missense variants in the zinc knuckle of EBF3's DNA binding domain reduce DNA affinity, as predicted by homology-based atomic modeling and molecular dynamics simulations, consistent with experimental data for the paralogous residue in EBF1. Homology-based structural modeling, molecular dynamics simulations Cold Spring Harbor molecular case studies Low 28487885
2021 EBF3 binds promoters of neurodevelopmental disorder (NDD) genes in neuronal cells as shown by ChIP-seq, with enrichment for binding NDD genes involved in gene regulation (p=7.43×10-6, OR=1.87). ChIP-seq in neuronal cells, gene enrichment analysis Human genomics Medium 34256850
2024 In zebrafish ebf3a loss-of-function mutants, the cerebellum, hypothalamus, and hindbrain are smaller, cerebellar activity is strongly increased, and genes marking olfactory sensory neurons, the lateral line, and cerebellar Purkinje neurons are significantly downregulated, establishing Ebf3's role in sensory system and cerebellar development. Loss-of-function zebrafish mutant, RNA-sequencing, brain activity imaging, behavioral assays bioRxivpreprint Medium

Source papers

Stage 0 corpus · 47 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2018 Stem cell niche-specific Ebf3 maintains the bone marrow cavity. Genes & development 138 29563184
2016 A Syndromic Neurodevelopmental Disorder Caused by De Novo Variants in EBF3. American journal of human genetics 92 28017372
2018 Long Noncoding RNA EBF3-AS Promotes Neuron Apoptosis in Alzheimer's Disease. DNA and cell biology 84 29298096
2016 Mutations in EBF3 Disturb Transcriptional Profiles and Cause Intellectual Disability, Ataxia, and Facial Dysmorphism. American journal of human genetics 63 28017373
2016 De Novo Mutations in EBF3 Cause a Neurodevelopmental Syndrome. American journal of human genetics 58 28017370
2006 An EBF3-mediated transcriptional program that induces cell cycle arrest and apoptosis. Cancer research 55 17018599
2017 Genome-wide methylation sequencing of paired primary and metastatic cell lines identifies common DNA methylation changes and a role for EBF3 as a candidate epigenetic driver of melanoma metastasis. Oncotarget 54 28030832
2019 Characterisation of DNA methylation changes in EBF3 and TBC1D16 associated with tumour progression and metastasis in multiple cancer types. Clinical epigenetics 39 31383000
2010 HPV status-independent association of alcohol and tobacco exposure or prior radiation therapy with promoter methylation of FUSSEL18, EBF3, IRX1, and SEPT9, but not SLC5A8, in head and neck squamous cell carcinomas. Genes, chromosomes & cancer 37 20029986
2011 Aberrant DNA methylation and tumor suppressive activity of the EBF3 gene in gastric carcinoma. International journal of cancer 34 21387304
2015 Early B-cell factor 3 (EBF3) is a novel tumor suppressor gene with promoter hypermethylation in pediatric acute myeloid leukemia. Journal of experimental & clinical cancer research : CR 28 25609158
2021 Coding and noncoding variants in EBF3 are involved in HADDS and simplex autism. Human genomics 27 34256850
2017 De novo variants in EBF3 are associated with hypotonia, developmental delay, intellectual disability, and autism. Cold Spring Harbor molecular case studies 27 29162653
2014 Ebf3-miR218 regulation is involved in the development of dopaminergic neurons. Brain research 26 25192643
2013 Hypermethylation of EBF3 and IRX1 genes in synovial fibroblasts of patients with rheumatoid arthritis. Molecules and cells 24 23456299
2023 Circadian clock protein Bmal1 accelerates acute myeloid leukemia by inhibiting ferroptosis through the EBF3/ALOX15 axis. Cancer science 22 37271497
2017 Novel de novo variant in EBF3 is likely to impact DNA binding in a patient with a neurodevelopmental disorder and expanded phenotypes: patient report, in silico functional assessment, and review of published cases. Cold Spring Harbor molecular case studies 22 28487885
2023 Ebf3+ niche-derived CXCL12 is required for the localization and maintenance of hematopoietic stem cells. Nature communications 21 37880234
2018 MiR-23b-3p induces the proliferation and metastasis of esophageal squamous cell carcinomas cells through the inhibition of EBF3. Acta biochimica et biophysica Sinica 21 29750239
2021 EBF3 reactivation by inhibiting the EGR1/EZH2/HDAC9 complex promotes metastasis via transcriptionally enhancing vimentin in nasopharyngeal carcinoma. Cancer letters 19 34906623
2017 Prdm13 is required for Ebf3+ amacrine cell formation in the retina. Developmental biology 19 29258872
2017 Whole Gene Deletion of EBF3 Supporting Haploinsufficiency of This Gene as a Mechanism of Neurodevelopmental Disease. Frontiers in genetics 18 29062322
2018 The caudo-ventral pallium is a novel pallial domain expressing Gdf10 and generating Ebf3-positive neurons of the medial amygdala. Brain structure & function 16 29869132
2018 Coupled monoubiquitylation of the co-E3 ligase DCNL1 by Ariadne-RBR E3 ubiquitin ligases promotes cullin-RING ligase complex remodeling. The Journal of biological chemistry 14 30587576
2022 An Integrated Phenotypic and Genotypic Approach Reveals a High-Risk Subtype Association for EBF3 Missense Variants Affecting the Zinc Finger Domain. Annals of neurology 13 35340043
2021 Duplication/triplication mosaicism of EBF3 and expansion of the EBF3 neurodevelopmental disorder phenotype. European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society 13 34999443
2021 Clinical spectrum of individuals with de novo EBF3 variants or deletions. American journal of medical genetics. Part A 12 34050706
2017 A Prdm8 target gene Ebf3 regulates multipolar-to-bipolar transition in migrating neocortical cells. Biochemical and biophysical research communications 11 29113800
2018 Associations of Pulmonary Fibrosis with Peripheral Blood Th1/Th2 Cell Imbalance and EBF3 Gene Methylation in Uygur Pigeon Breeder's Lung Patients. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 10 29913442
2021 Neuroimaging Findings in Patients with EBF3 Mutations: Report of Two Cases. Molecular syndromology 6 34177436
2020 Transient and lineage-restricted requirement of Ebf3 for sternum ossification. Development (Cambridge, England) 6 32398354
2024 Early B Cell Factor 3 (EBF3) attenuates Parkinson's disease through directly regulating contactin-associated protein-like 4 (CNTNAP4) transcription: An experimental study. Cellular signalling 5 38479556
2023 Further delineation of EBF3-related syndromic neurodevelopmental disorder in twelve Chinese patients. Frontiers in pediatrics 5 36937983
2023 Neurologic, Neuropsychologic, and Neuroradiologic Features of EBF3-Related Syndrome. Neurology. Genetics 5 37090941
2025 Concurrent RB1 and P53 pathway disruption predisposes to the development of a primitive neuronal component in high-grade gliomas depending on MYC-driven EBF3 transcription. Acta neuropathologica 4 39821672
2021 A Novel de novo Mutation in EBF3 Associated With Hypotonia, Ataxia, and Delayed Development Syndrome in a Chinese Boy. Frontiers in genetics 4 34367240
2025 SNORA47 affects stemness and chemotherapy sensitivity via EBF3/RPL11/c-Myc axis in luminal A breast cancer. Molecular medicine (Cambridge, Mass.) 3 40264043
2024 Targeted DNA Methylation Editing Using an All-in-One System Establishes Paradoxical Activation of EBF3. Cancers 2 38473261
2024 MiR-301b-3p targets and regulates EBF3 to impact the stem-like phenotype of breast cancer cells through glycolysis. Journal of clinical biochemistry and nutrition 2 39896160
2025 A nonsense variant in the C-terminal transactivation domain of the EBF3 gene in an individual with intellectual disability and behavioural disorder: case report and literature review. Psychiatric genetics 1 40073166
2026 EBF3 suppresses lung adenocarcinoma progression and immune evasion via transcriptional repression of CCL24. Cellular oncology (Dordrecht, Netherlands) 0 42018103
2025 Generation and Characterization of a Knockout Mouse of an Enhancer of EBF3. bioRxiv : the preprint server for biology 0 39829799
2025 Generation and characterization of a knockout mouse of an enhancer of EBF3. Biology open 0 41081394
2025 EBF3 transcriptionally activates ACADL to block the Hippo/YAP signaling pathway and inhibits breast cancer progression. Pathology, research and practice 0 41270467
2024 Augmentation Cystoplasty in a Girl With Early B-cell Factor 3 (EBF3)-Related Syndrome. Cureus 0 39109108
2022 [Analysis of clinical features and EBF3 gene variant in a child with hypotonia, ataxia and developmental delay]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 0 36317217
2008 [Construction of eukaryotic expression vector for EBF3 and EGFP fusion protein and its expression in HepG2 cells]. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 0 18845077