ArticlePloS one2014
Mitogen-induced B-cell proliferation activates Chk2-dependent G1/S cell cycle arrest.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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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Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
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- Chromatin Control of EBV Infection and Latency.Current topics in microbiology and immunology · 2025Article
- Early multiple sclerosis activity associated with TBX21+CD21loCXCR3+ B cell expansion resembling EBV-induced phenotypes.JCI insight · 2025Article
- Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression.PLoS pathogens · 2024Article
- Epstein-Barr virus reactivation induces divergent abortive, reprogrammed, and host shutoff states by lytic progression.bioRxiv : the preprint server for biology · 2024Article
- The Research Progress on Immortalization of Human B Cells.Microorganisms · 2023Review
- Chk1/2 inhibitor AZD7762 blocks the growth of preantral follicles by inducing apoptosis, suppressing proliferation, and interfering with the cell cycle in granulosa cells.Histology and histopathology · 2023Article
- Contribution of viral and bacterial infections to senescence and immunosenescence.Frontiers in cellular and infection microbiology · 2023Review
- Human Monoclonal IgE Antibodies-a Major Milestone in Allergy.Current allergy and asthma reports · 2023Review
- Immunosenescence in atherosclerosis: A role for chronic viral infections.Frontiers in immunology · 2022Review
- Epstein-Barr virus perpetuates B cell germinal center dynamics and generation of autoimmune-associated phenotypesFrontiers in immunology · 2022Article
- Monocarboxylate transporter antagonism reveals metabolic vulnerabilities of viral-driven lymphomas.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Genome instability and lymphoma.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021Article
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- A multi-omics approach to Epstein-Barr virus immortalization of B-cells reveals EBNA1 chromatin pioneering activities targeting nucleotide metabolism.PLoS pathogens · 2021Article
- C1s Inhibition by BIVV009 (Sutimlimab) Prevents Complement-Enhanced Activation of Autoimmune Human B Cells In Vitro.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- A Screen for Epstein-Barr Virus Proteins That Inhibit the DNA Damage Response Reveals a Novel Histone Binding Protein.Journal of virology · 2018Article
- Intracellular BH3 Profiling Reveals Shifts in Antiapoptotic Dependency in Human B Cell Maturation and Mitogen-Stimulated Proliferation.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
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Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
B-cell activation and proliferation can be induced by a variety of extracellular stimuli. The fate of an activated B cell following mitogen stimulation can be dictated by the strength or duration of the signal, the expression of downstream signaling components necessary to promote proliferation, and the cell intrinsic sensors and regulators of the proliferative program. Previously we have identified the DNA damage response (DDR) signaling pathway as a cell intrinsic sensor that is activated upon latent infection of primary human B cells by Epstein-Barr virus (EBV). Here we have assessed the role of the DDR as a limiting factor in the proliferative response to non-viral B-cell mitogens. We report that TLR9 activation through CpG-rich oligonucleotides induced B-cell hyper-proliferation and an ATM/Chk2 downstream signaling pathway. However, B-cell activation through the CD40 pathway coupled with interleukin-4 (IL-4) promoted proliferation less robustly and only a modest DDR. These two mitogens, but not EBV, modestly induced intrinsic apoptosis that was independent from the DDR. However, all three mitogens triggered a DDR-dependent G1/S phase cell cycle arrest preventing B-cell proliferation. The extent of G1/S arrest, as evidenced by release through Chk2 inhibition, correlated with B-cell proliferation rates. These findings have implications for the regulation of extra-follicular B-cell activation as it may pertain to the development of auto-immune diseases or lymphoma.
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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.