ArticleImmunity2013
Transcriptional repression of Gata3 is essential for early B cell commitment.
Article in Immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.
- Genome-wide association study implicates immune dysfunction in the development of Hodgkin lymphoma.Blood · 2018Pooled it
- Genome-wide association study of classical Hodgkin lymphoma identifies key regulators of disease susceptibility.Nature communications · 2017Pooled it
- Association of GATA3 Polymorphisms With Minimal Residual Disease and Relapse Risk in Childhood Acute Lymphoblastic Leukemia.Journal of the National Cancer Institute · 2021Trial
- Clinical and molecular characteristics ofHaematologica · 2019Trial
- B-lineage commitment is dependent on a reversible epigenetic switch.Genes & development · 2026Article
- Berberine as a natural immunomodulator of B lymphocytes.Inflammopharmacology · 2025Review
- Review
- YY1 knockout in pro-B cells impairs lineage commitment, enabling unusual hematopoietic lineage plasticity.Genes & development · 2024Article
- Concepts in B cell acute lymphoblastic leukemia pathogenesis.Journal of leukocyte biology · 2024Review
- Canalizing cell fate by transcriptional repression.Molecular systems biology · 2024Review
- Progression of Notch signaling regulation of B cells under radiation exposure.Frontiers in immunology · 2024Review
- Identification of Immune-Linked Hub Genes and Diagnostic Model Construction in Schizophrenia.Journal of molecular neuroscience : MN · 2023Article
- Tnpo3 enables EBF1 function in conditions of antagonistic Notch signaling.Genes & development · 2022Article
- EBF1 nuclear repositioning instructs chromatin refolding to promote therapy resistance in T leukemic cells.Molecular cell · 2022Article
- Noncoding genetic variation in GATA3 increases acute lymphoblastic leukemia risk through local and global changes in chromatin conformation.Nature genetics · 2022Article
- E Protein Transcription Factors as Suppressors of T Lymphocyte Acute Lymphoblastic Leukemia.Frontiers in immunology · 2022Review
- Immunoproteasome Inhibition Reduces the T Helper 2 Response in Mouse Models of Allergic Airway Inflammation.Frontiers in immunology · 2022Article
- Article
- Interactions between lineage-associated transcription factors govern haematopoietic progenitor states.The EMBO journal · 2020Article
- Novel, Non-Gene-Destructive Knock-In Reporter Mice Refute the Concept of MonoallelicJournal of immunology (Baltimore, Md. : 1950) · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The mechanisms underlying the silencing of alternative fate potentials in very early B cell precursors remain unclear. Using gain- and loss-of-function approaches together with a synthetic Zinc-finger polypeptide (6ZFP) engineered to prevent transcription factor binding to a defined cis element, we show that the transcription factor EBF1 promotes B cell lineage commitment by directly repressing expression of the T-cell-lineage-requisite Gata3 gene. Ebf1-deficient lymphoid progenitors exhibited increased T cell lineage potential and elevated Gata3 transcript expression, whereas enforced EBF1 expression inhibited T cell differentiation and caused rapid loss of Gata3 mRNA. Notably, 6ZFP-mediated perturbation of EBF1 binding to a Gata3 regulatory region restored Gata3 expression, abrogated EBF1-driven suppression of T cell differentiation, and prevented B cell differentiation via a GATA3-dependent mechanism. Furthermore, EBF1 binding to Gata3 regulatory sites induced repressive histone modifications across this region. These data identify a transcriptional circuit critical for B cell lineage commitment.
Indexed as
Identifiers
What OpenQuestion holds
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.