ArticleJournal of immunology (Baltimore, Md. : 1950)2013
The tumor promoter and NF-κB modulator Bcl-3 regulates splenic B cell development.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Article
- Clinical and transcriptomic characterization of patients with chronic lymphocytic leukemia harboring t(14;19): an ERIC study.Leukemia · 2025Article
- Direct-in-NOD genetic ablation of Bcl3 leads to complete type 1 diabetes protection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Regulation and Function of the Atypical IκBs-Bcl-3, IκBEuropean journal of immunology · 2025Review
- Article
- Early Pregnancy Regulates Expression of IkappaB Family in Ovine Spleen and Lymph Nodes.International journal of molecular sciences · 2023Article
- Loss of Bcl-3 delays bone fracture healing through activating NF-κB signaling in mesenchymal stem cells.Journal of orthopaedic translation · 2022Article
- Bcl-3: A Double-Edged Sword in Immune Cells and Inflammation.Frontiers in immunology · 2022Review
- The hepatic senescence-associated secretory phenotype promotes hepatocarcinogenesis through Bcl3-dependent activation of macrophages.Cell & bioscience · 2021Article
- The NF-κB regulator Bcl-3 restricts terminal differentiation and promotes memory cell formation of CD8+ T cells during viral infection.PLoS pathogens · 2021Article
- TACI expression and plasma cell differentiation are impaired in the absence of functional IκBNS.Immunology and cell biology · 2019Article
- Nuclear Factor-kappaB in Autoimmunity: Man and Mouse.Frontiers in immunology · 2018Review
- Negative role of TAK1 in marginal zone B-cell development incidental to NF-κB noncanonical pathway activation.Immunology and cell biology · 2016Article
- Review
- Heterozygous Mutation in IκBNS Leads to Reduced Levels of Natural IgM Antibodies and Impaired Responses to T-Independent Type 2 Antigens.Frontiers in immunology · 2016Article
- The NF-κB regulator Bcl-3 governs dendritic cell antigen presentation functions in adaptive immunity.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- The oncoprotein and transcriptional regulator Bcl-3 governs plasticity and pathogenicity of autoimmune T cells.Immunity · 2014Article
- B-1a transitional cells are phenotypically distinct and are lacking in mice deficient in IκBNS.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Plasma cell formation, secretion, and persistence: the short and the long of it.Critical reviews in immunology · 2014Review
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
Bcl-3 is an atypical member of the family of IκB proteins. Unlike the classic members, Bcl-3 functions as a nuclear transcriptional cofactor that may, depending on context, promote or suppress genes via association with p50/NF-κB1 or p52/NF-κB2 homodimers. Bcl-3 is also an oncogene, because it is a partner in recurrent translocations in B cell tumors, resulting in deregulated expression. Bcl-3 functions, however, remain poorly understood. We have investigated the role of Bcl-3 in B cells and discovered a previously unknown involvement in the splenic development of these cells. Loss of Bcl-3 in B cells resulted in significantly more marginal zone (MZ) and fewer follicular (FO) B cells. Conversely, transgenic expression of Bcl-3 in B cells generated fewer MZ and more FO B cells. Both Bcl-3(-/-) FO and MZ B cells were more responsive to LPS stimulation compared with their wild-type counterparts, including increased proliferation. By contrast, Bcl-3(-/-) FO B cells were more prone to apoptosis upon BCR stimulation, also limiting their expansion. The data reveal Bcl-3 as a regulator of B cell fate determination, restricting the MZ path and favoring the FO pathway, at least in part, via increased signal-specific survival of the latter, a finding of relevance to its tumorigenic activity.
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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.