ArticleOncogene1999
The Bcl-3 oncoprotein acts as a bridging factor between NF-kappaB/Rel and nuclear co-regulators.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers, 1 of them a synthesis that pooled it.
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
146 citing papers in PubMed, 1 synthesis or guideline pooled it, 316 citations in OpenAlex.
- Lack of association between BARD1 Cys557Ser variant and breast cancer risk: a meta-analysis of 11,870 cases and 7,687 controls.Journal of cancer research and clinical oncology · 2011Pooled it
- PF4 drives mechanical overload-induced temporomandibular joint osteoarthritis through TLR2-dependent activation of NF-κB.Journal of translational medicine · 2026Article
- NF-κB Signaling in Prostate Cancer Progression: Inflammatory Mediators, Survival Pathways, and Regulatory Axes.Cancers · 2026Review
- Unveiling the multifaceted roles of BCL3: biological functions and disease implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Pirin Transcriptionally Regulates PLA2G4A To Inhibit Ferroptosis in Colorectal Cancer via Lipid Profile Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Pirin does not bind to p65 or regulate NFκB-dependent gene expression but does modulate cellular quercetin levels.Molecular pharmacology · 2025Article
- Regulation and Function of the Atypical IκBs-Bcl-3, IκBEuropean journal of immunology · 2025Review
- Article
- Pirin does not bind to p65 or regulate NFκB-dependent gene expression but does modulate cellular quercetin levels.bioRxiv : the preprint server for biology · 2024Article
- New insights into the pharmacological inhibition of SRF activity: Key inhibitory targets and mechanisms.Vascular pharmacology · 2024Review
- Versatile function of NF-ĸB in inflammation and cancer.Experimental hematology & oncology · 2024Review
- NF-κB in biology and targeted therapy: new insights and translational implications.Signal transduction and targeted therapy · 2024Review
- Pirin Inhibits FAS-Mediated Apoptosis to Support Colorectal Cancer Survival.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Multifaceted roles for BCL3 in cancer: a proto-oncogene comes of age.Molecular cancer · 2024Review
- Effects of a Pirin-like protein on strain growth and spinosad biosynthesis in Saccharopolyspora spinosa.Applied microbiology and biotechnology · 2023Article
- Genetic Determinants ofAntibiotics (Basel, Switzerland) · 2023Article
- Regulatory mechanisms and therapeutic potential of JAB1 in neurological development and disorders.Molecular medicine (Cambridge, Mass.) · 2023Review
- Pirin is a prognostic marker of human melanoma that dampens the proliferation of malignant cells by downregulating JARID1B/KDM5B expression.Scientific reports · 2023Article
- Role of the redox state of the Pirin-bound cofactor on interaction with the master regulators of inflammation and other pathways.PloS one · 2023Article
86 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proto-oncoprotein Bcl-3 is a member of the IkappaB family and is present predominantly in the nucleus. To gain insight into specific nuclear functions of Bcl-3 we have isolated proteins that interact with its ankyrin repeat domain. Using the yeast two-hybrid-system we identified four novel binding partners of Bcl-3 in addition to NF-kappaB p50 and p52, previously known to associate with Bcl-3. The novel Bcl-3 interactors Jab1, Pirin, Tip60 and Bard1 are nuclear proteins which also bind to other transcription factors including c-Jun, nuclear factor I (NFI), HIV-1 Tat or the tumor suppressor and PolII holoenzyme component Brca1, respectively. Bcl-3, p50, and either Bard1, Tip60 or Pirin are sequestered into quarternary complexes on NF-kappaB DNA binding sites, whereas Jab1 enhances p50-Bcl-3-DNA complex formation. Furthermore, the histone acetylase Tip60 enhances Bcl-3-p50 activated transcription through an NF-kappaB binding site, indicating that quarternary complexes containing Bcl-3 interactors modulate NF-kappaB driven gene expression. These data implicate Bcl-3 as an adaptor between NF-kappaB p50/p52 and other transcription regulators and suggest that its gene activation function may at least in part be due to recruitment of the Tip60 histone actetylase.
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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.