ArticleThe Journal of experimental medicine1994
The B cell-specific transcription factor BSAP regulates B cell proliferation.
Article in The Journal of experimental medicine, 1994. 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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Who cites it
30 citing papers in PubMed, 137 citations in OpenAlex.
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- Roles for histone H3K4 methyltransferase activities during immunoglobulin class-switch recombination.Biochimica et biophysica acta · 2012Review
- Transcription factor Ebf1 regulates differentiation stage-specific signaling, proliferation, and survival of B cells.Genes & development · 2012Article
- An incoherent regulatory network architecture that orchestrates B cell diversification in response to antigen signaling.Molecular systems biology · 2011Article
- Vitamin A and retinoic acid in the regulation of B-cell development and antibody production.Vitamins and hormones · 2011Review
- APE/Ref-1 makes fine-tuning of CD40-induced B cell proliferation.Molecular immunology · 2008Article
- Vitamin A and immune function: retinoic acid modulates population dynamics in antigen receptor and CD38-stimulated splenic B cells.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Blimp-1-dependent repression of Pax-5 is required for differentiation of B cells to immunoglobulin M-secreting plasma cells.Molecular and cellular biology · 2002Article
- The CD23a and CD23b proximal promoters display different sensitivities to exogenous stimuli in B lymphocytes.Genes and immunity · 2002Article
- Inhibition of the function of the FcgammaRIIB by a monoclonal antibody to thymic shared antigen-1, a Ly-6 family antigen.Immunology · 2001Article
- Treatment of allergic airway inflammation and hyperresponsiveness by antisense-induced local blockade of GATA-3 expression.The Journal of experimental medicine · 2001Article
- Signaling by CD40 and its mimics in B cell activation.Immunologic research · 2001Review
- Potent induction of long-term CD8+ T cell memory by short-term IL-4 exposure during T cell receptor stimulation.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- BSAP can repress enhancer activity by targeting PU.1 function.Molecular and cellular biology · 2000Article
- Distinct factors regulate the murine RAG-2 promoter in B- and T-cell lines.Molecular and cellular biology · 1999Article
- Regulation of interleukin (IL)-12 receptor beta2 subunit expression by endogenous IL-12: a critical step in the differentiation of pathogenic autoreactive T cells.The Journal of experimental medicine · 1999Article
- Cloning and characterization of a novel membrane-associated antigenic protein of Helicobacter pylori.Infection and immunity · 1999Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The B cell-specific activator protein (BSAP) is a DNA-binding transcription factor expressed in pro-B, pre-B, and mature B cells, but not in plasma cells. In this study, we explored the role of BSAP in B cell function by assessing how the content of this protein varies in cells driven by proliferative stimuli and, conversely, how artificial manipulation of BSAP activity affects cell proliferation. We found that BSAP activity of nuclear extracts increased when B cells were activated by mitogen (lipopolysaccharide [LPS]), antigen receptor-mediated signaling (surface immunoglobulin D [IgD] cross-linking) or T cell-dependent stimulation (CD40 cross-linking). We could suppress BSAP activity by exposure of B cells to phosphorothioate oligonucleotides antisense to the BSAP translation initiation start site, whereas control oligonucleotides were virtually inactive. Antisense-induced BSAP suppression was associated with a striking reduction in LPS-induced proliferation of splenic B cells and in the spontaneous proliferation of B lymphoma cells (CH12.LX), but the antisense oligonucleotide had virtually no effect on proliferation of two cell lines lacking BSAP: the T lymphoma line EL-4 and the plasma cell line MOPC-315. Overexpression of BSAP in splenic B cells or de novo expression in MOPC-315 plasma cells induced by transfection of a BSAP expression plasmid stimulated cell proliferation. Taken together, these results suggest that BSAP activity is a rate-limiting regulator of B cell proliferation. We also found that treatment with the antisense BSAP oligonucleotide downregulated Ig class switching induced by interleukin 4 plus LPS. This effect may be secondary to reduced proliferation or could be mediated through BSAP binding sites in the IgH locus.
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