ArticleJournal of immunology (Baltimore, Md. : 1950)2006
E2A promotes the survival of precursor and mature B lymphocytes.
Article in Journal of immunology (Baltimore, Md. : 1950), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- A meta-analysis of Hodgkin lymphoma reveals 19p13.3 TCF3 as a novel susceptibility locus.Nature communications · 2014Pooled it
- WNT signaling in human pluripotent stem cells promotes HDAC2-dependent epigenetic programs and development of retinoic acid-responsive mesoderm.Stem cell reports · 2026Article
- TCF3 haploinsufficiency defined by immune, clinical, gene-dosage, and murine studies.The Journal of allergy and clinical immunology · 2023Article
- E2A regulates neural ectoderm fate specification in human embryonic stem cells.Development (Cambridge, England) · 2020Article
- YY1 binds to the E3' enhancer and inhibits the expression of the immunoglobulin κ gene via epigenetic modifications.Immunology · 2018Article
- Zinc transporter SLC39A10/ZIP10 facilitates antiapoptotic signaling during early B-cell development.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- E proteins in lymphocyte development and lymphoid diseases.Current topics in developmental biology · 2014Review
- Complementary regulation of early B-lymphoid differentiation by genetic and epigenetic mechanisms.International journal of hematology · 2013Review
- TiF1-gamma plays an essential role in murine hematopoiesis and regulates transcriptional elongation of erythroid genes.Developmental biology · 2013Article
- E protein transcription factors are required for the development of CD4(+) lineage T cells.Immunity · 2012Article
- Epigenetic regulation of B lymphocyte differentiation, transdifferentiation, and reprogramming.Comparative and functional genomics · 2012Article
- Stage-specific functions of E-proteins at the β-selection and T-cell receptor checkpoints during thymocyte development.Immunologic research · 2011Article
- E proteins and the regulation of early lymphocyte development.Immunological reviews · 2010Review
- Developmental trajectories in early hematopoiesis.Genes & development · 2009Article
- A tamoxifen inducible knock-in allele for investigation of E2A function.BMC developmental biology · 2009Article
- Distinct roles for E12 and E47 in B cell specification and the sequential rearrangement of immunoglobulin light chain loci.The Journal of experimental medicine · 2009Article
- E and ID proteins branch out.Nature reviews. Immunology · 2009Review
- E47 controls the developmental integrity and cell cycle quiescence of multipotential hematopoietic progenitors.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Acquisition of a functional T cell receptor during T lymphocyte development is enforced by HEB and E2A transcription factors.Immunity · 2007Article
- E2A and HEB are required to block thymocyte proliferation prior to pre-TCR expression.Journal of immunology (Baltimore, Md. : 1950) · 2007Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The basic helix-loop-helix transcription factor E2A is an essential regulator of B lymphocyte lineage commitment and is required to activate the expression of numerous B lineage-specific genes. Studies involving ectopic expression of Id proteins, which inhibit E2A as well as other basic helix-loop-helix proteins such as HEB, suggest additional roles of E2A at later stages of B cell development. We use E2A-deficient and E2A and HEB double-deficient pre-B cell lines to directly assess the function of E2A and HEB in B cell development after lineage commitment. We show that, in contrast to the established role of E2A in lineage commitment, elimination of E2A and HEB in pre-B cell lines has only a modest negative impact on B lineage gene expression. However, E2A single and E2A and HEB double-deficient but not HEB single-deficient cell lines show dramatically enhanced apoptosis upon growth arrest. To address the possible role of E2A in the regulation of B cell survival in vivo, we crossed IFN-inducible Cre-transgenic mice to E2A conditional mice. Cre-mediated E2A deletion resulted in a block in bone marrow B cell development and a significant reduction in the proportion and total number of splenic B cells in these mice. We show that Cre-mediated deletion of E2A in adoptively transferred mature B cells results in the rapid depletion of the transferred population within 24 h of Cre induction. These results reveal that E2A is not required to maintain B cell fate but is essential in promoting pre-B and B cell survival.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.