ArticleThe Journal of cell biology2007
Myc stimulates B lymphocyte differentiation and amplifies calcium signaling.
Article in The Journal of cell biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis 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
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.
- Prognostic significances of overexpression MYC and/or BCL2 in R-CHOP-treated diffuse large B-cell lymphoma: A Systematic review and meta-analysis.Scientific reports · 2018Pooled it
- A temporal map of B cell diversification mechanisms in mice.Nature immunology · 2026Article
- Review
- Antibiotic treatment limits survival of peripheral and bone marrow B-cell populations.Blood advances · 2025Article
- MYC Binding Near Transcriptional End Sites Regulates Basal Gene Expression, Read-Through Transcription, and Intragenic Contacts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Emulsion adjuvant-induced uric acid release modulates optimal immunogenicity by targeting dendritic cells and B cells.NPJ vaccines · 2025Article
- Concomitant loss of TET2 and TET3 results in T cell expansion and genomic instability in mice.Communications biology · 2024Article
- DOCK8 gene mutation alters cell subsets, BCR signaling, and cell metabolism in B cells.Cell death & disease · 2024Article
- Review
- EBF1, PAX5, and MYC: regulation on B cell development and association with hematologic neoplasms.Frontiers in immunology · 2024Review
- Differential variability analysis of single-cell gene expression data.Briefings in bioinformatics · 2023Article
- The 'omics of obesity in B-cell acute lymphoblastic leukemia.Journal of the National Cancer Institute. Monographs · 2023Article
- Calcineurin-independent NFATc1 signaling is essential for survival of Burkitt lymphoma cells.Frontiers in oncology · 2023Article
- Review
- Intensive stretch-activated CRT-PMCA1 feedback loop promoted apoptosis of myoblasts through CaApoptosis : an international journal on programmed cell death · 2022Article
- Defective bone repletion in aged Balb/cBy mice was caused by impaired osteoblastic differentiation.Journal of bone and mineral metabolism · 2022Article
- Evidence of premature lymphocyte aging in people with low anti-spike antibody levels after BNT162b2 vaccination.iScience · 2022Article
- Postmitotic G1 phase survivin drives mitogen-independent cell division of B lymphocytes.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- MYC: a multipurpose oncogene with prognostic and therapeutic implications in blood malignancies.Journal of hematology & oncology · 2021Review
- Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Deregulated expression of the Myc family of transcription factors (c-, N-, and L-myc) contributes to the development of many cancers by a mechanism believed to involve the stimulation of cell proliferation and inhibition of differentiation. However, using B cell-specific c-/N-myc double-knockout mice and E(mu)-myc transgenic mice bred onto genetic backgrounds (recombinase-activating gene 2-/- and Btk-/- Tec-/-) whereby B cell development is arrested, we show that Myc is necessary to stimulate both proliferation and differentiation in primary B cells. Moreover, Myc expression results in sustained increases in intracellular Ca2+ ([Ca2+]i), which is required for Myc to stimulate B cell proliferation and differentiation. The increase in [Ca2+]i correlates with constitutive nuclear factor of activated T cells (NFAT) nuclear translocation, reduced Ca2+ efflux, and decreased expression of the plasma membrane Ca2+-adenosine triphosphatase (PMCA) efflux pump. Our findings demonstrate a revised model whereby Myc promotes both proliferation and differentiation, in part by a remarkable mechanism whereby Myc amplifies Ca2+ signals, thereby enabling the concurrent expression of Myc- and Ca2+-regulated target genes.
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.