ArticleThe Journal of experimental medicine2003
B cell-specific transgenic expression of Bcl2 rescues early B lymphopoiesis but not B cell responses in BOB.1/OBF.1-deficient mice.
Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 46 citations in OpenAlex.
- RACK1 is required for normal B cell development and signaling but not RAG1 degradation.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- The Role of the Transcriptional Coactivator BOB.1/OBF.1 in Adaptive Immunity.Advances in experimental medicine and biology · 2024Review
- Genome-wide association studies for immunoglobulin concentrations in colostrum and serum in Chinese Holstein.BMC genomics · 2022Article
- Differential Requirement of Vav Proteins for Btk-dependent and -Independent Signaling During B Cell Development.Frontiers in cell and developmental biology · 2022Article
- MCL-1 is required throughout B-cell development and its loss sensitizes specific B-cell subsets to inhibition of BCL-2 or BCL-XL.Cell death & disease · 2016Article
- The transcriptional coactivator Bob1 promotes the development of follicular T helper cells via Bcl6.The EMBO journal · 2016Article
- VprBP Is Required for Efficient Editing and Selection of Igκ+ B Cells, but Is Dispensable for Igλ+ and Marginal Zone B Cell Maturation and Selection.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Waldenström macroglobulinemia: clinical and immunological aspects, natural history, cell of origin, and emerging mouse models.ISRN hematology · 2013Review
- B-lymphopoiesis is stopped by mobilizing doses of G-CSF and is rescued by overexpression of the anti-apoptotic protein Bcl2.Haematologica · 2013Article
- Octamer-dependent transcription in T cells is mediated by NFAT and NF-κB.Nucleic acids research · 2013Article
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- The transcription factor Fli-1 modulates marginal zone and follicular B cell development in mice.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Regulation of B-cell entry into the cell cycle.Immunological reviews · 2008Review
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- BOB.1/OBF.1 controls the balance of TH1 and TH2 immune responses.The EMBO journal · 2007Article
- Oct transcription factors mediate t(14;18) lymphoma cell survival by directly regulating bcl-2 expression.Oncogene · 2006Article
- Btk expression is controlled by Oct and BOB.1/OBF.1.Nucleic acids research · 2006Article
- BAFF regulates B cell survival by downregulating the BH3-only family member Bim via the ERK pathway.The Journal of experimental medicine · 2005Article
- Autoimmune glomerulonephritis with spontaneous formation of splenic germinal centers in mice lacking the estrogen receptor alpha gene.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mice deficient for the transcriptional coactivator BOB.1/OBF.1 show several defects in B cell differentiation. Numbers of immature transitional B cells in the bone marrow are reduced and fewer B cells reach the periphery. Furthermore, germinal center B cells are absent and marginal zone (MZ) B lymphocytes are markedly reduced. Increased levels of B cell apoptosis in these mice prompted us to analyze expression and function of antiapoptotic proteins. Bcl2 expression is strongly reduced in BOB.1/OBF.1-deficient pre-B cells. When BOB.1/OBF.1-deficient mice were crossed with Bcl2-transgenic mice, B cell development in the bone marrow and numbers of B cells in peripheral lymphoid organs were normalized. However, neither germinal center B cells nor MZ B cells were rescued. Additionally, Bcl2 did not rescue the defects in signaling and affinity maturation found in BOB.1/OBF.1-deficient mice. Interestingly, Bcl2-transgenic mice by themselves show an MZ B cell defect. Virtually no functional MZ B cells were detected in these mice. In contrast, mice deficient for Bcl2 show a relative increase in MZ B cell numbers, indicating a previously undetected function of Bcl2 for this B cell compartment.
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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.