EBF1

Last update 08 May 2025

Basic Info

Synonyms

COE1, Early B-cell factor, EBF

+ [6]

Introduction

Key pioneer transcription factor of B-cell specification and commitment (PubMed:27807034). Recognizes variations of the palindromic sequence 5'-ATTCCCNNGGGAATT-3'. Operates in a transcription factor network to activate B-cell-specific genes and repress genes associated with alternative cell fates. For instance, positively regulates many B-cell specific genes including BCR or CD40 while repressing genes that direct cells into alternative lineages, including GATA3 and TCF7 for the T-cell lineage. In addition to its role during lymphopoiesis, controls the thermogenic gene program in adipocytes during development and in response to environmental cold (By similarity). (Microbial infection) Acts as a chromatin anchor for Epstein-Barr virus EBNA2 to mediate the assembly of EBNA2 chromatin complexes in B-cells (PubMed:28968461). In addition, binds to the viral LMP1 proximal promoter and promotes its expression during latency (PubMed:26819314).

100 Clinical Results associated with EBF1

100 Translational Medicine associated with EBF1

0 Patents (Medical) associated with EBF1

592

Literatures (Medical) associated with EBF1

01 May 2025·BJOG: An International Journal of Obstetrics & Gynaecology

Endometriosis‐Related Genetic Factors and Their Role in Preterm Birth: A Two‐Sample Mendelian Randomisation Study

Article

Author: Kristjansson, Dana ; Ytterberg, Karin ; Flatley, Christopher ; Juodakis, Julius ; Jacobsson, Bo ; Sole‐Navais, Pol

ABSTRACTObjectiveEndometriosis affects 10% of women worldwide and is linked to adverse pregnancy outcomes, including preterm birth. Recent epidemiological and genetic studies indicate that endometriosis may influence gestational duration and the likelihood of preterm birth. This study aimed to estimate the direct genetic causal effects of endometriosis on gestational duration and preterm birth using Mendelian randomisation (MR) analysis, leveraging genetic data from recent genome‐wide association studies (GWASs).DesignA two‐sample MR study.SettingSummary statistics from published GWASs on European ancestry populations for endometriosis and gestational duration.Population or SampleInstrumental variables for endometriosis were derived from a meta‐analysis comprising 60 674 endometriosis cases and 701 926 controls.MethodsGenetic correlations and heritability estimates were calculated using linkage disequilibrium score regression. Two‐sample MR with multiplicative random‐effects inverse variance weighting assessed the primary objectives, supplemented by sensitivity analyses to validate MR assumptions.Main Outcome MeasuresPrimary outcomes were gestational duration and preterm birth, sourced from the latest GWAS data.ResultsLD score regression revealed no genetic correlation between endometriosis and either gestational duration or preterm birth. MR analysis showed no causal association between endometriosis and maternal effects on offspring gestational duration (β = 0.40, 95% CI: −0.39 to 1.19, p = 0.32) or preterm birth (OR = 0.94, 95% CI: 0.82–1.06, p = 0.36). Sensitivity analyses indicated pleiotropy but no violations of MR assumptions. Of the four loci overlapping between the gestational duration and endometriosis GWASs, three (EBF1, WNT4, and GDAP1) were identified as outliers using MR‐Presso.ConclusionsContrary to observational studies, MR analyses found no direct causal link between endometriosis and gestational duration or preterm birth. Overlaps in genomic regions suggest that the relationship may be mediated through different biological pathways.

01 Apr 2025·Cancer Letters

EBF1-induced CSRP2 boosts the progression of B-cell acute lymphocytic leukemia by inhibiting ferroptosis

Article

Author: Liu, Gexiu ; Liu, Chengcheng ; Chen, Lu ; Tang, Hailin ; Wang, Hua ; Chang, Boyang ; Zhou, Fenling

B-cell acute lymphocytic leukemia (B-ALL) is a highly aggressive malignancy with poor prognosis. Developing diagnostic markers and therapeutic targets to identify and treat B-ALL early would improve the outcomes of B-ALL patients. Here, we conducted RNA next-generation sequencing using bone marrow (BM) specimens obtained from 7 B-ALL patients and 7 healthy donors. We found cysteine and glycine-rich protein 2 (CSRP2) upregulated in B-ALL. Down-regulation of CSRP2 resulted in suppressed cell proliferation and enhanced cell apoptosis in B-ALL. In addition, inhibition of CSRP2 increased cell ferroptosis in B-ALL cells. Mechanically, we revealed that transcription factor early B cell factor 1 (EBF1) regulated CSRP2 levels in B-ALL, and inhibition of EBF1 decreased CSRP2 levels in B-ALL. In conclusion, the dysregulation EBF1 led to CSRP2 upregulation and resulting in progression of B-ALL. The EBF1/CSRP2 axis could be of great potential as therapeutic targets for B-ALL treatment.

01 Mar 2025·Current Pharmaceutical Biotechnology

Dihydroartemisinin Modulates Prostate Cancer Progression by Regulating Multiple Genes via the Transcription Factor NR2F2

Article

Author: Zu, Yuxin ; Chan, Yunhui ; Zhao, Rong ; Shao, Yong ; Zhang, Chuan

Objective:This study aimed to investigate the effect of dihydroartemisinin (DHA) on DU145 cells and the role of NR2F2 (COUP-TFII) and its potential target genes in this process.Methods:GSE122625 was used to identify differentially expressed genes (DEGs) between the DHA-treated and control groups. Protein-protein interaction (PPI) network analysis was performed to identify hub genes, and the ChEA3 database was used to identify potential transcription factors. qRT-PCR and Western blot were used to validate the expression of genes of interest and functional assays were performed to evaluate the effect of DHA on DU145 and PC-3 cells. To solidify the regulatory relationship of NR2F2 with EFNB2, EBF1, ETS1, and VEGFA, a Chromatin Immunoprecipitation (ChIP) experiment was performed.Results:We identified 85 DEGs in DU145 cells treated with DHA, and PPI network analysis identified NR2F2 as a hub gene and potential transcription factor. The regulatory network of NR2F2 and its potential target genes (EFNB2, EBF1, ETS1, and VEGFA) was constructed, and the expression of these genes was upregulated in DHA-treated cells compared to control cells. Functional assays showed that DHA treatment inhibited epithelial-mesenchymal transition, reduced inflammation, and promoted apoptosis in DU145 and PC-3 cells. Furthermore, NR2F2 knockdown receded the DHA-induced upregulation of target genes and functional changes of DU145 and PC-3 cells. The outcomes of ChIP unequivocally pointed to a positive regulatory role of NR2F2 in these gene expressions.Conclusion:Our study suggests that DHA treatment affects the functions of DU145 and PC-3 cells by regulating the expression of NR2F2 and its potential target genes, and NR2F2 may serve as a potential therapeutic target for prostate cancer.

Analysis

Perform a panoramic analysis of this field.

view full example data

AI Agents Built for Biopharma Breakthroughs

Accelerate discovery. Empower decisions. Transform outcomes.

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis