Ask about this productRelated genes to: EBF3 Blocking Peptide
- Gene:
- EBF3 NIH gene
- Name:
- EBF transcription factor 3
- Previous symbol:
- -
- Synonyms:
- COE3, DKFZp667B0210
- Chromosome:
- 10q26.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-11
- Date modifiied:
- 2018-09-21
Related products to: EBF3 Blocking Peptide
Related articles to: EBF3 Blocking Peptide
- Hypothalamic arginine vasopressin (AVP) and oxytocin (OXT) magnocellular neurons (MCNs), share a developmental lineage. The transcription factors driving specification are yet unknown. Using gene regulatory network analysis on published single-cell RNA-sequencing data of the developing mouse hypothalamus, we identified RORA, EBF3, FOXP1, FOXP2, and BCL11B as candidate transcription factors for differential MCN specification. We modeled developmental gene expression dynamics using computational cell fate mapping, revealing enrichment of EBF3 and BCL11B in the lineage, and FOXP1 and FOXP2 in the lineage. analysis of and promoters predicted a binding site for FOXP1 and FOXP2, and assay identified regulation on both and genomic promoters. Finally, heterozygous FOXP1 knockout mice exhibited a significant reduction in AVP and OXT neuron abundance, with OXT neurons disproportionally affected. We conclude that FOXP1 participates in MCN development, while being differentially active in OXT MCNs relative to AVP MCNs. - Source: PubMed
Publication date: 2026/04/04
Berkhout Jari BTrender SophieKrabichler QuirinPodpecan YuvalFranke FelixSchubert TimBurbach PeterGrinevich ValeryAdan RogerFröhlich HenningAlthammer FerdinandMeijer Onno CMahfouz Ahmed - The transcription factor EBF3 is frequently downregulated in lung adenocarcinoma (LUAD), and its low expression is associated with poor patient prognosis. The functional significance and mechanistic basis of EBF3 in LUAD pathogenesis, particularly its potential impact on the tumor immune microenvironment, remain largely unexplored. - Source: PubMed
Publication date: 2026/04/22
Li LanYang YiRanLi DanChen ChuMaoMu XinMeiWu JiaXinYuan Jin - Congenital cranial dysinnervation disorders (CCDDs) are a group of rare, nonprogressive conditions characterized by abnormal development of the cranial motor nerves and variable ocular motility deficits, ptosis, incomitant strabismus, and facial palsy. Advances in genetics and neuroimaging have revealed that these disorders result from defects in neuronal differentiation or axon guidance of the cranial motor neurons. Duane retraction syndrome, the most common CCDD, results from the absence of the abducens nerve and innervation of the lateral rectus by oculomotor nerve axons; causative genes include CHN1, MAFB, HOXA1, SALL4, and EBF3, although most cases do not have a genetic diagnosis. Congenital fibrosis of the extraocular muscles (CFEOM), results from variants in KIF21A, PHOX2A, TUBB3, or other tubulin genes, and affects the oculomotor and trochlear nerves. Horizontal gaze palsy with progressive scoliosis (HGPPS), caused by ROBO3 loss of function, arises from failure of axonal midline crossing in the brainstem. Moebius syndrome, defined by abducens and facial nerve palsies, has no identified genetic cause and may result from non-Mendelian causes. Additional CCDDs with atypical or syndromic presentations are linked to COL25A1, ECEL1, and ACKR3, although many do not have a genetic explanation. The expanding list of CCDD-associated genes highlights shared developmental pathways, including neuronal differentiation, axon guidance, and microtubule dynamics. Improved genetic diagnosis informs prognosis and multidisciplinary management. This review synthesizes current understanding of CCDDs, emphasizing the shift from phenotypic classification to molecular subtyping, and underscores the importance of ongoing research to resolve genetically unsolved cases and refine diagnostic and therapeutic strategies. - Source: PubMed
Publication date: 2026/03/23
Aufderheide KathleenWhitman Mary C - Parkinson's disease (PD) is a widespread neurodegenerative disorder. MicroRNAs (miRNAs) have emerged as crucial regulatory molecules in the context of PD. Exploring the diagnostic significance of miR-4443 in PD and its impacts on microglial inflammatory responses. The present study enrolled 95 PD patients and 90 healthy controls. The expression levels of miR-4443 and EBF3 and their diagnostic potential for PD were analyzed using RT-qPCR and a ROC curve. LPS-treated BV2 microglial cells were utilized to simulate the neuroinflammatory process in PD pathogenesis. Cell proliferation activity was assessed using the CCK-8 assay. ELISA was employed to measure cellular pro-inflammatory cytokine levels. To confirm the putative binding between miR-4443 and EBF3, a dual-luciferase reporter assay was conducted. The expression level of miR-4443 was significantly up-regulated in the serum of PD patients, and it exhibited diagnostic potential for PD. Following LPS induction in BV2 microglial cells, miR-4443 expression was up-regulated. Overexpression of this miRNA suppressed proliferation and enhanced pro-inflammatory cytokine release. Conversely, miR-4443 knockdown reversed the resultant phenotypic changes. EBF3 was verified to have a binding relationship with miR-4443. Functional experiments indicated that miR-4443 might participate in the neuroinflammatory process of PD pathogenesis by targeting EBF3. Up-regulated miR-4443 has diagnostic significance for PD and may participate in neuroinflammation through regulating EBF3. - Source: PubMed
Publication date: 2026/01/29
Lu HuijieZhao ZhenwuLin YangLei SiyingFeng Yuyao - Transcription factors (TFs) are essential for neuronal identity, yet their potential non-cell-autonomous functions remain largely unexplored. Here, we uncover both cell- and non-cell-autonomous roles for the conserved terminal selector UNC-3 in motor neurons (MNs). UNC-3 is an ortholog of human EBF3, mutations in which cause a severe neurodevelopmental syndrome. Single-cell RNA sequencing of cholinergic MNs, which express , and downstream GABA MNs, which do not, revealed that loss disrupts neuronal identity in distinct ways across MN classes. Four cholinergic MN classes lose their molecular identity entirely, whereas the AS class retains it partially, illuminating terminal selector-driven neuronal diversification processes. Integrated transcriptomic and genomic analyses uncovered a dual cell-autonomous role for UNC-3 as both a direct activator and repressor of neuron-type-specific genes in cholinergic MNs, including repression of alternate neurotransmitter programs. Unexpectedly, loss also caused widespread transcriptional, morphological, and connectivity defects in downstream GABA MNs. Mechanistically, these non-cell-autonomous effects are mediated by cholinergic neurotransmission and include activation of the pro-regenerative bZIP TF CEBP-1 (C/EBP) and dysregulation of UNC-6/Netrin signaling. These findings redefine terminal selectors as both intrinsic and extrinsic regulators of neuronal identity and circuit assembly, offering a mechanistic framework for understanding EBF3 syndrome pathogenesis. - Source: PubMed
Publication date: 2025/12/25
Smith Jayson JTaylor Seth RDestain HonorineKim GraceHall David HWhite John GMiller David MKratsios Paschalis