ArticleMolecular cancer2007
Bright/ARID3A contributes to chromatin accessibility of the immunoglobulin heavy chain enhancer.
Article in Molecular cancer, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 43 citations in OpenAlex.
- IRP1/ARID3A complex promotes pancreatic cancer chemoresistance by suppressing CYGB-related ferroptosis.Genes & diseases · 2026Article
- Pharmacologic Modulation of ARID3A with Rimegepant Reactivates Type I Interferon Signaling and Sensitizes Triple-Negative Breast Cancer to PD-1 Blockade.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ARID3a from the ARID family: structure, role in autoimmune diseases and drug discovery.Acta pharmacologica Sinica · 2023Review
- Article
- Hepatic ARID3A facilitates liver cancer malignancy by cooperating with CEP131 to regulate an embryonic stem cell-like gene signature.Cell death & disease · 2022Article
- Article
- Deficiencies in the DNA Binding Protein ARID3a Alter Chromatin Structures Important for Early Human Erythropoiesis.ImmunoHorizons · 2021Article
- Lipid Rafts Interaction of the ARID3A Transcription Factor with EZRIN and G-Actin Regulates B-Cell Receptor Signaling.Diseases (Basel, Switzerland) · 2021Article
- FOXP1 Interacts with MyoD to Repress its Transcription and Myoblast Conversion.Journal of cellular signaling · 2021Article
- Immune network dysregulation precedes clinical diagnosis of asthma.Scientific reports · 2020Article
- An Insight into Reprogramming Barriers to iPSC Generation.Stem cell reviews and reports · 2020Review
- 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
- Article
- Positional specificity of different transcription factor classes within enhancers.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Advances and Limitations of Current Epigenetic Studies Investigating Mammalian Axonal Regeneration.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Review
- Arid3a regulates mesoderm differentiation in mouse embryonic stem cells.Journal of stem cell therapy and transplantation · 2017Article
- Article
- Arid3b Is Critical for B Lymphocyte Development.PloS one · 2016Article
- Repressors of reprogramming.World journal of stem cells · 2015Review
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 1 institution in 1 country.
Funding
Abstract
Bright/ARID3A is a nuclear matrix-associated transcription factor that stimulates immunoglobulin heavy chain (IgH) expression and Cyclin E1/E2F-dependent cell cycle progression. Bright positively activates IgH transcriptional initiation by binding to ATC-rich P sites within nuclear matrix attachment regions (MARs) flanking the IgH intronic enhancer (Emu). Over-expression of Bright in cultured B cells was shown to correlate with DNase hypersensitivity of Emu. We report here further efforts to analyze Bright-mediated Emu enhancer activation within the physiological constraints of chromatin. A system was established in which VH promoter-driven in vitro transcription on chromatin- reconstituted templates was responsive to Emu. Bright assisted in blocking the general repression caused by nucleosome assembly but was incapable of stimulating transcription from prebound nucleosome arrays. In vitro transcriptional derepression by Bright was enhanced on templates in which Emu is flanked by MARs and was inhibited by competition with high affinity Bright binding (P2) sites. DNase hypersensitivity of chromatin-reconstituted Emu was increased when prepackaged with B cell nuclear extract supplemented with Bright. These results identify Bright as a contributor to accessibility of the IgH enhancer.
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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.