ArticleThe Journal of biological chemistry2014
Inhibition of transcription by B cell Leukemia 3 (Bcl-3) protein requires interaction with nuclear factor κB (NF-κB) p50.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed.
- Macrophages tune responses to pathogen dynamics through TLR4 stimulation memory and by licensing susceptibility to IL-10.bioRxiv : the preprint server for biology · 2026Article
- NF-κB Signaling in Prostate Cancer Progression: Inflammatory Mediators, Survival Pathways, and Regulatory Axes.Cancers · 2026Review
- Article
- Regulation and Function of the Atypical IκBs-Bcl-3, IκBEuropean journal of immunology · 2025Review
- The NF-κB signaling network in the life of T cells.Frontiers in immunology · 2025Review
- Current progress of anti‑PD‑1/PDL1 immunotherapy for glioblastoma (Review).Molecular medicine reports · 2024Review
- MAP3K1 expression is associated with progression and poor prognosis of hormone receptor-positive, HER2-negative early-stage breast cancer.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Identification and Interpretation of eQTL and eGenes for Hodgkin Lymphoma Susceptibility.Genes · 2023Article
- Bcl-3: A Double-Edged Sword in Immune Cells and Inflammation.Frontiers in immunology · 2022Review
- Inhibitory feedback control of NF-κB signalling in health and disease.The Biochemical journal · 2021Review
- Target acquired: transcriptional regulators as drug targets for protozoan parasites.International journal for parasitology · 2021Review
- Transcription Coactivator BCL3 Acts as a Potential Regulator of Lipid Metabolism Through the Effects on Inflammation.Journal of inflammation research · 2021Article
- Characterization of the clinical and immunologic phenotype and management of 157 individuals with 56 distinct heterozygous NFKB1 mutations.The Journal of allergy and clinical immunology · 2020Article
- The deubiquitinase USP7 uses a distinct ubiquitin-like domain to deubiquitinate NF-ĸB subunits.The Journal of biological chemistry · 2020Article
- The role of B-Cell Lymphoma-3 (BCL-3) in enabling the hallmarks of cancer: implications for the treatment of colorectal carcinogenesis.Carcinogenesis · 2020Review
- A pipeline to create predictive functional networks: application to the tumor progression of hepatocellular carcinoma.BMC bioinformatics · 2020Article
- The IκB-protein BCL-3 controls Toll-like receptor-induced MAPK activity by promoting TPL-2 degradation in the nucleus.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- The regulation of sequence specific NF-κB DNA binding and transcription by IKKβ phosphorylation of NF-κB p50 at serine 80.Nucleic acids research · 2019Article
- Human DNA polymerase delta is a pentameric holoenzyme with a dimeric p12 subunit.Life science alliance · 2019Article
- Transcriptome Profiling of Bovine Macrophages Infected byFrontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B cell leukemia 3 (Bcl-3) is an essential negative regulator of NF-κB during Toll-like receptor and TNF receptor signaling. Bcl-3 also interacts with a number of transcriptional regulators, including homodimers of the NF-κB p50 subunit. Deletion of Bcl-3 results in increased NF-κB p50 ubiquitination and proteasomal degradation and increased inflammatory gene expression. We employed immobilized peptide array technology to define a region of p50 required for the formation of a Bcl-3·p50 homodimer immunosuppressor complex. Our data demonstrate that amino acids 359-361 and 363 of p50 are critical for interaction with Bcl-3 and essential for Bcl-3-mediated inhibition of inflammatory gene expression. Bcl-3 is unable to interact with p50 when these amino acids are mutated, rendering it incapable of inhibiting the transcriptional activity of NF-κB. Bcl-3 interaction-defective p50 is hyperubiquitinated and has a significantly reduced half-life relative to wild-type p50. Nfkb1(-/-) cells reconstituted with mutated p50 precursor p105 are hyperresponsive to TNFα stimulation relative to wild-type p105, as measured by inflammatory gene expression. Mutant p105 recapitulates a Bcl3(-/-) phenotype. This study demonstrates that interaction with p50 is necessary and sufficient for the anti-inflammatory properties of Bcl-3 and further highlights the importance of p50 homodimer stability in the control of NF-κB target gene expression.
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