ArticleMolecular and cellular biology2000
BSAP can repress enhancer activity by targeting PU.1 function.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 64 citations in OpenAlex.
- Pax5 Negatively Regulates Osteoclastogenesis through Downregulation of Blimp1.International journal of molecular sciences · 2021Article
- RAG-Mediated DNA Breaks Attenuate PU.1 Activity in Early B Cells through Activation of a SPIC-BCLAF1 Complex.Cell reports · 2019Article
- Role of mir-15a/16-1 in early B cell development in a mouse model of chronic lymphocytic leukemia.Oncotarget · 2016Article
- E2A Antagonizes PU.1 Activity through Inhibition of DNA Binding.BioMed research international · 2016Article
- A novel pax5-binding regulatory element in the igκ locus.Frontiers in immunology · 2014Article
- B-lineage transcription factors and cooperating gene lesions required for leukemia development.Leukemia · 2013Review
- YY1 controls immunoglobulin class switch recombination and nuclear activation-induced deaminase levels.Molecular and cellular biology · 2012Article
- A developmentally controlled competitive STAT5-PU.1 DNA binding mechanism regulates activity of the Ig κ E3' enhancer.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- The long winding road toward understanding the molecular mechanisms for B-cell suppression by 2,3,7,8-tetrachlorodibenzo-p-dioxin.Toxicological sciences : an official journal of the Society of Toxicology · 2011Review
- Highly cooperative recruitment of Ets-1 and release of autoinhibition by Pax5.Journal of molecular biology · 2009Article
- Predicting combinatorial binding of transcription factors to regulatory elements in the human genome by association rule mining.BMC bioinformatics · 2007Article
- Overexpression of a hematopoietic transcriptional regulator EDAG induces myelopoiesis and suppresses lymphopoiesis in transgenic mice.Leukemia · 2007Article
- B cell activator PAX5 promotes lymphomagenesis through stimulation of B cell receptor signaling.The Journal of clinical investigation · 2007Article
- The transcriptional repressor GFI-1 antagonizes PU.1 activity through protein-protein interaction.The Journal of biological chemistry · 2007Article
- B-Lymphoma cells with epigenetic silencing of Pax5 trans-differentiate into macrophages, but not other hematopoietic lineages.Experimental cell research · 2007Article
- Epigenetic histone modifications do not control Igkappa locus contraction and intranuclear localization in cells with dual B cell-macrophage potential.Journal of immunology (Baltimore, Md. : 1950) · 2006Article
- Epstein-Barr virus EBNA-3C is targeted to and regulates expression from the bidirectional LMP-1/2B promoter.Journal of virology · 2006Article
- Maturation stage-specific regulation of megakaryopoiesis by pointed-domain Ets proteins.Blood · 2006Article
- The mechanism of repression of the myeloid-specific c-fms gene by Pax5 during B lineage restriction.The EMBO journal · 2006Article
- Long-range interactions between three transcriptional enhancers, active Vkappa gene promoters, and a 3' boundary sequence spanning 46 kilobases.Molecular and cellular biology · 2005Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
PU.1 and BSAP are transcription factors crucial for proper B-cell development. Absence of PU.1 results in loss of B, T, and myeloid cells, while absence of BSAP results in an early block in B-cell differentiation. Both of these proteins bind to the immunoglobulin kappa chain 3' enhancer, which is developmentally regulated during B-cell differentiation. We find here that BSAP can repress 3' enhancer activity. This repression can occur in plasmacytoma lines or in a non-B-cell line in which the enhancer is activated by addition of the appropriate enhancer binding transcription factors. We show that the transcription factor PU.1 is a target of the BSAP-mediated repression. Although PU.1 and BSAP can physically interact through their respective DNA binding domains, this interaction does not affect DNA binding. When PU.1 function is assayed in isolation on a multimerized PU.1 binding site, BSAP targets a portion of the PU.1 transactivation domain (residues 7 to 30) for repression. The BSAP inhibitory domain (residues 358 to 385) is needed for this repression. Interestingly, the coactivator protein p300 can eliminate this BSAP-mediated repression. We also show that PU.1 can inhibit BSAP transactivation and that this repression requires PU.1 amino acids 7 to 30. Transfection of p300 resulted in only a partial reversal of PU.1-mediated repression of BSAP. When PU.1 function is assayed in the context of the immunoglobulin kappa chain 3' enhancer and associated binding proteins, BSAP represses PU.1 function by a distinct mechanism. This repression does not require the PU.1 transactivation or PEST domains and cannot be reversed by p300 expression. The possible roles of BSAP and PU.1 antagonistic activities in hematopoietic development are discussed.
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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.