ArticleMolecular and cellular biology2006
A regulated nucleocytoplasmic shuttle contributes to Bright's function as a transcriptional activator of immunoglobulin genes.
Article in Molecular and cellular biology, 2006. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
20 citing papers in PubMed, 30 citations in OpenAlex.
- Arid3c identifies an uncharacterized subpopulation of V2 interneurons during embryonic spinal cord development.Frontiers in cellular neuroscience · 2024Article
- ARID3a from the ARID family: structure, role in autoimmune diseases and drug discovery.Acta pharmacologica Sinica · 2023Review
- Lipid Rafts Interaction of the ARID3A Transcription Factor with EZRIN and G-Actin Regulates B-Cell Receptor Signaling.Diseases (Basel, Switzerland) · 2021Article
- Article
- Crucial Role of Increased Arid3a at the Pre-B and Immature B Cell Stages for B1a Cell Generation.Frontiers in immunology · 2019Article
- Competitive Promoter-Associated Matrix Attachment Region Binding of the Arid3a and Cux1 Transcription Factors.Diseases (Basel, Switzerland) · 2017Article
- Arid3a regulates mesoderm differentiation in mouse embryonic stem cells.Journal of stem cell therapy and transplantation · 2017Article
- Arid3b Is Critical for B Lymphocyte Development.PloS one · 2016Article
- Perspectives on fetal derived CD5+ B1 B cells.European journal of immunology · 2015Review
- Lin28b promotes fetal B lymphopoiesis through the transcription factor Arid3a.The Journal of experimental medicine · 2015Article
- Arid3a is essential to execution of the first cell fate decision via direct embryonic and extraembryonic transcriptional regulation.Genes & development · 2014Article
- Recent advances in the ARID family: focusing on roles in human cancer.OncoTargets and therapy · 2014Review
- Article
- 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
- Heterogeneous nuclear ribonucleoprotein K: altered pattern of expression associated with diagnosis and prognosis of prostate cancer.British journal of cancer · 2009Article
- Signalling of the BCR is regulated by a lipid rafts-localised transcription factor, Bright.The EMBO journal · 2009Article
- SUMOylation of DRIL1 directs its transcriptional activity towards leukocyte lineage-specific genes.PloS one · 2009Article
- Bright/ARID3A contributes to chromatin accessibility of the immunoglobulin heavy chain enhancer.Molecular cancer · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Bright/ARID3a has been implicated in mitogen- and growth factor-induced up-regulation of immunoglobulin heavy-chain (IgH) genes and in E2F1-dependent G1/S cell cycle progression. For IgH transactivation, Bright binds to nuclear matrix association regions upstream of certain variable region promoters and flanking the IgH intronic enhancer. While Bright protein was previously shown to reside within the nuclear matrix, we show here that a significant amount of Bright resides in the cytoplasm of normal and transformed B cells. Leptomycin B, chromosome region maintenance 1 (CRM1) overexpression, and heterokaryon experiments indicate that Bright actively shuttles between the nucleus and the cytoplasm in a CRM1-dependent manner. We mapped the functional nuclear localization signal to the N-terminal region of REKLES, a domain conserved within ARID3 paralogues. Residues within the C terminus of REKLES contain its nuclear export signal, whose regulation is primarily responsible for Bright shuttling. Growth factor depletion and cell synchronization experiments indicated that Bright shuttling during S phase of the cell cycle leads to an increase in its nuclear abundance. Finally, we show that shuttle-incompetent Bright point mutants, even if sequestered within the nucleus, are incapable of transactivating an IgH reporter gene. Therefore, regulation of Bright's cellular localization appears to be required for its function.
Indexed as
Identifiers
What OpenQuestion holds
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.