ArticleMolecular and cellular biology2002
BOB.1/OBF.1 deficiency affects marginal-zone B-cell compartment.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 50 citations in OpenAlex.
- Regulation of B cell development and lymphocyte function by transcriptional coactivator OCA-B.Frontiers in immunology · 2026Review
- OCA-B/Pou2af1 is sufficient to promote CD4Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Role of the Transcriptional Coactivator BOB.1/OBF.1 in Adaptive Immunity.Advances in experimental medicine and biology · 2024Review
- The transcriptional program during germinal center reaction - a close view at GC B cells, Tfh cells and Tfr cells.Frontiers in immunology · 2023Review
- T Cell Specific BOB.1/OBF.1 Expression Promotes Germinal Center Response and T Helper Cell Differentiation.Frontiers in immunology · 2022Article
- The BTB-ZF transcription factor Zbtb20 is driven by Irf4 to promote plasma cell differentiation and longevity.The Journal of experimental medicine · 2014Article
- Oct2 and Obf1 as Facilitators of B:T Cell Collaboration during a Humoral Immune Response.Frontiers in immunology · 2014Article
- Octamer-dependent transcription in T cells is mediated by NFAT and NF-κB.Nucleic acids research · 2013Article
- Direct interactions of OCA-B and TFII-I regulate immunoglobulin heavy-chain gene transcription by facilitating enhancer-promoter communication.Molecular cell · 2011Article
- The follicular versus marginal zone B lymphocyte cell fate decision.Nature reviews. Immunology · 2009Review
- Oct2 enhances antibody-secreting cell differentiation through regulation of IL-5 receptor alpha chain expression on activated B cells.The Journal of experimental medicine · 2008Article
- Article
- Silencing and nuclear repositioning of the lambda5 gene locus at the pre-B cell stage requires Aiolos and OBF-1.PloS one · 2008Article
- Enforced expression of the transcriptional coactivator OBF1 impairs B cell differentiation at the earliest stage of development.PloS one · 2008Article
- BOB.1/OBF.1 controls the balance of TH1 and TH2 immune responses.The EMBO journal · 2007Article
- Dysregulated TCL1 requires the germinal center and genome instability for mature B-cell transformation.Blood · 2006Article
- The Ets factor Spi-B is a direct critical target of the coactivator OBF-1.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Btk expression is controlled by Oct and BOB.1/OBF.1.Nucleic acids research · 2006Article
- Characterization of marginal zone B cell precursors.The Journal of experimental medicine · 2005Article
- Differential requirement for OBF-1 during antibody-secreting cell differentiation.The Journal of experimental medicine · 2005Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Marginal-zone (MZ) B cells represent a first line of defense against particulate blood-borne antigens. Together with the B1 cells, they are responsible for the early response against type II T-independent antigens. The molecular pathways controlling the development of MZ B cells are only poorly understood. We found that these cells are virtually absent in mice deficient in the BOB.1/OBF.1 coactivator. Loss of these B cells was demonstrated by the lack of cells showing the appropriate cell surface phenotype but also by histological analyses and tri-nitro-phenol-Ficoll capturing. The lack of these cells is a B-cell-intrinsic defect, as shown by bone marrow complementation experiments. We also show that the expression of BOB.1/OBF.1 in peripheral B cells is required for the development of MZ B lymphocytes. Our analysis of BOB.1/OBF.1-deficient splenic B cells reveals alterations in cell motility, tumor necrosis factor receptor expression, and B-cell receptor (BCR) signaling. These changes could contribute to the loss of MZ B lymphocytes by altering the maturation of the cells. Interestingly, development of and BCR signaling in B1 B cells are completely normal in BOB.1/OBF.1 mutant mice.
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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.