ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Transgenic mice expressing dominant-negative bright exhibit defects in B1 B cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
The trial behind it
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
20 citing papers in PubMed, 21 citations in OpenAlex.
- ARID3a from the ARID family: structure, role in autoimmune diseases and drug discovery.Acta pharmacologica Sinica · 2023Review
- TLR engagement induces ARID3a in human blood hematopoietic progenitors and modulates IFNα production.Cellular immunology · 2020Article
- 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
- Global miRNA expression analysis identifies novel key regulators of plasma cell differentiation and malignant plasma cell.Nucleic acids research · 2017Article
- Arid3a regulates mesoderm differentiation in mouse embryonic stem cells.Journal of stem cell therapy and transplantation · 2017Article
- A Role for the Transcription FactorFrontiers in immunology · 2017Article
- 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
- Disease activity in systemic lupus erythematosus correlates with expression of the transcription factor AT-rich-interactive domain 3A.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Role of tissue-specific AT-rich DNA sequence-binding proteins in lymphocyte differentiation.International journal of hematology · 2014Review
- The Bright Side of Hematopoiesis: Regulatory Roles of ARID3a/Bright in Human and Mouse Hematopoiesis.Frontiers in immunology · 2014Review
- Transgenic expression of survivin compensates for OX40-deficiency in driving Th2 development and allergic inflammation.European journal of immunology · 2013Article
- Spatial congregation of STAT binding directs selective nuclear architecture during T-cell functional differentiation.Genome research · 2013Article
- Article
- CCL5-independent helper T lymphocyte responses to immuno-dominant pneumococcal surface protein A epitopes.Vaccine · 2012Article
- The transcription factor Bright plays a role in marginal zone B lymphocyte development and autoantibody production.Molecular immunology · 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
- Signalling of the BCR is regulated by a lipid rafts-localised transcription factor, Bright.The EMBO journal · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The transcription factor Bright up-regulates Ig H chain production from select V region promoters and requires Bright dimerization, Bruton's tyrosine kinase (Btk), and the Btk substrate, TFII-I, for this activity. Defects in Btk cause X-linked immunodeficiency disease in mice and humans. Btk-deficient mice exhibit decreased serum IgM production, B cell developmental blocks, absence of peritoneal B1 cells, and subnormal immune responses against Ags, including phosphorylcholine, which confer protection against Streptococcus pneumoniae. Transgenic mice expressing dominant-negative Bright share similarities with Btk-deficient mice, including decreased serum IgM, poor anti-phosphorylcholine responses, and slightly reduced numbers of mature B cells. Although dominant-negative Bright mice developed B1 B cells, these were functionally deficient in Ig secretion. These data suggest a mechanistic explanation for the abnormal responses to phosphorylcholine observed in Btk-deficient mice, and indicate that Bright functions in a subset of Btk-dependent pathways in vivo, particularly those responses dominated by B1 B cells.
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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.