ArticleMolecular and cellular biology2005
Bruton's tyrosine kinase regulates immunoglobulin promoter activation in association with the transcription factor Bright.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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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.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- Post-transcriptional (re)programming of B lymphocyte development: From bench to bedside?Advances in immunology · 2024Review
- ARID3a from the ARID family: structure, role in autoimmune diseases and drug discovery.Acta pharmacologica Sinica · 2023Review
- Bruton's Tyrosine Kinase Inhibition as an Emerging Therapy in Systemic Autoimmune Disease.Drugs · 2021Review
- Targeting BTK Signaling in the Microenvironment of Solid Tumors as a Feasible Cancer Therapy Option.Cancers · 2021Review
- p65BTK Is a Novel Biomarker and Therapeutic Target in Solid Tumors.Frontiers in cell and developmental biology · 2021Review
- ARID3a expression in human hematopoietic stem cells is associated with distinct gene patterns in aged individuals.Immunity & ageing : I & A · 2020Article
- New Frontiers: ARID3a in SLE.Cells · 2019Review
- The Transcription Factor ARID3a Is Important for In Vitro Differentiation of Human Hematopoietic Progenitors.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Perspectives on fetal derived CD5+ B1 B cells.European journal of immunology · 2015Review
- Review
- Lin28b promotes fetal B lymphopoiesis through the transcription factor Arid3a.The Journal of experimental medicine · 2015Article
- Differential expression of the transcription factor ARID3a in lupus patient hematopoietic progenitor cells.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- The Bright Side of Hematopoiesis: Regulatory Roles of ARID3a/Bright in Human and Mouse Hematopoiesis.Frontiers in immunology · 2014Review
- Construction of human activity-based phosphorylation networks.Molecular systems biology · 2013Article
- The transcription factor Bright plays a role in marginal zone B lymphocyte development and autoantibody production.Molecular immunology · 2011Article
- Characterization of a new ARID family transcription factor (Brightlike/ARID3C) that co-activates Bright/ARID3A-mediated immunoglobulin gene transcription.Molecular immunology · 2011Article
- The herpes simplex virus immediate-early ubiquitin ligase ICP0 induces degradation of the ICP0 repressor protein E2FBP1.Journal of virology · 2011Article
- The ARID family transcription factor bright is required for both hematopoietic stem cell and B lineage development.Molecular and cellular biology · 2011Article
- Loss of Bright/ARID3a function promotes developmental plasticity.Stem cells (Dayton, Ohio) · 2010Article
- Bruton's tyrosine kinase revealed as a negative regulator of Wnt-beta-catenin signaling.Science signaling · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Bright (B-cell regulator of immunoglobulin heavy chain transcription) binding to immunoglobulin heavy chain loci after B-cell activation is associated with increased heavy chain transcription. Our earlier reports demonstrated that Bright coimmunoprecipitates with Bruton's tyrosine kinase (Btk) and that these proteins associate in a DNA-binding complex in primary B cells. B cells from immunodeficient mice with a mutation in Btk failed to produce stable Bright DNA-binding complexes. In order to determine if Btk is important for Bright function, a transcription activation assay was established and analyzed using real-time PCR technology. Cells lacking both Bright and Btk were transfected with Bright and/or Btk along with an immunoglobulin heavy chain reporter construct. Immunoglobulin gene transcription was enhanced when Bright and Btk were coexpressed. In contrast, neither Bright nor Btk alone led to activation of heavy chain transcription. Furthermore, Bright function required both Btk kinase activity and sequences within the pleckstrin homology domain of Btk. Bright was not appreciably phosphorylated by Btk; however, a third tyrosine-phosphorylated protein coprecipitated with Bright. Thus, the ability of Bright to enhance immunoglobulin transcription critically requires functional Btk.
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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.