ArticleBlood2011
Pre-B cell receptor-mediated activation of BCL6 induces pre-B cell quiescence through transcriptional repression of MYC.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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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.
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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
40 citing papers in PubMed, 67 citations in OpenAlex.
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- Profiling the activity of the para-caspase MALT1 in B-cell acute lymphoblastic leukemia for potential targeted therapeutic application.Haematologica · 2024Article
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- Evolving insights into the genomic complexity and immune landscape of diffuse large B-cell lymphoma: opportunities for novel biomarkers.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Review
- E3 Ubiquitin Ligase Fbw7 Regulates the Survival of Mature B Cells.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
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- Ikaros antagonizes DNA binding by STAT5 in pre-B cells.PloS one · 2020Article
- Primary Chest Wall MYC/BCL6 Double-hit Lymphoma with t (3;7) (q27;p12) and t (8;14) (q24;q32) Translocations.Internal medicine (Tokyo, Japan) · 2019Article
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- Internal deletion of BCOR reveals a tumor suppressor function for BCOR in T lymphocyte malignancies.The Journal of experimental medicine · 2017Article
- An essential EBV latent antigen 3C binds Bcl6 for targeted degradation and cell proliferation.PLoS pathogens · 2017Article
- Review
- Ibrutinib inhibits pre-BCRBlood · 2017Article
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
Abstract
Initial cell surface expression of the pre-B cell receptor induces proliferation. After 2 to 5 divisions, however, large pre-BII (Fraction C') cells exit cell cycle to become resting, small pre-BII cells (Fraction D). The mechanism by which pre-BII cells exit cell cycle, however, is currently unclear. The checkpoint at the Fraction C'-D transition is critical for immunoglobulin light chain gene recombination and to prevent malignant transformation into acute lymphoblastic leukemia. Here we demonstrate that inducible activation of pre-B cell receptor signaling induces cell-cycle exit through up-regulation of the transcriptional repressor BCL6. Inducible activation of BCL6 downstream of the pre-B cell receptor results in transcriptional repression of MYC and CCND2. Hence, pre-B cell receptor-mediated activation of BCL6 limits pre-B cell proliferation and induces cellular quiescence at the small pre-BII (Fraction D) stage.
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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.