ArticleThe Journal of biological chemistry2013
Early B-cell factor 1 regulates the expansion of B-cell progenitors in a dose-dependent manner.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- B-lineage commitment is dependent on a reversible epigenetic switch.Genes & development · 2026Article
- Advances in Research on the B-Lineage Transcription Factor EBF1 in Solid Tumors.International journal of molecular sciences · 2025Review
- The chromatin reader Dido3 is a regulator of the gene network that controls B cell differentiation.Cell & bioscience · 2025Article
- Early B-Cell Factor 1: An Archetype for a Lineage-Restricted Transcription Factor Linking Development to Disease.Advances in experimental medicine and biology · 2024Review
- Transcription factor networks link B-lymphocyte development and malignant transformation in leukemia.Genes & development · 2023Review
- EBF1 primes B-lymphoid enhancers and limits the myeloid bias in murine multipotent progenitors.The Journal of experimental medicine · 2022Article
- The telomere complex and the origin of the cancer stem cell.Biomarker research · 2021Review
- Mutant U2AF1-induced alternative splicing of H2afy (macroH2A1) regulates B-lymphopoiesis in mice.Cell reports · 2021Article
- Article
- PAX5 is part of a functional transcription factor network targeted in lymphoid leukemia.PLoS genetics · 2019Article
- Molecular Regulation of Differentiation in Early B-Lymphocyte Development.International journal of molecular sciences · 2018Review
- Epistatic interactions between mutations of TACI (Clinical & translational immunology · 2017Article
- Early B Cell Progenitors Deficient for GON4L Fail To Differentiate Due to a Block in Mitotic Cell Division.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Transcription factor networks in B-cell differentiation link development to acute lymphoid leukemia.Blood · 2015Review
- Combined heterozygous loss of Ebf1 and Pax5 allows for T-lineage conversion of B cell progenitors.The Journal of experimental medicine · 2015Article
- Ebf1 in DNA repair and leukemogenesis.Blood · 2015Article
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcription factor doses are of importance for normal and malignant B-lymphocyte development; however, the understanding of underlying mechanisms and functional consequences of reduced transcription factor levels is limited. We have analyzed progenitor and B-lineage compartments in mice carrying heterozygote mutations in the E2a, Ebf1, or Pax5 gene. Although lymphoid progenitors from Ebf1 or Pax5 heterozygote mice were specified and lineage-restricted in a manner comparable with Wt progenitors, this process was severely impaired in E2a heterozygote mutant mice. This defect was not significantly enhanced upon combined deletion of E2a with Ebf1 or Pax5. Analysis of the pre-B-cell compartment in Ebf1 heterozygote mice revealed a reduction in cell numbers. These cells expressed Pax5 and other B-lineage-associated genes, and global gene expression analysis suggested that the reduction of the pre-B-cell compartment was a result of impaired pre-B-cell expansion. This idea was supported by a reduction in IL2Rα-expressing late pre-B-cells as well as by cell cycle analysis and by the finding that the complexity of the VDJ rearrangement patterns was comparable in Wt and Ebf1(+/-) pre-B-cells, although the number of progenitors was reduced. Heterozygote deletion of Ebf1 resulted in impaired response to IL7 in vitro and reduced expression levels of pre-BCR on the cell surface, providing possible explanations for the observed stage-specific reduction in cellular expansion. Thus, transcription factor doses are critical for specification as well as expansion of B-lymphoid progenitors, providing increased insight into the molecular regulation of B-cell development.
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