ArticleFrontiers in cell and developmental biology2022
Atypical IκB Bcl3 enhances the generation of the NF-κB p52 homodimer.
Article in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- The transcription complex p52-ETS1 is essential for germinal center formation.Nature immunology · 2025Article
- Inflammation in Penile Squamous Cell Carcinoma: A Comprehensive Review.International journal of molecular sciences · 2025Review
- Integrative function of histone deacetylase 3 in inflammation.Molecular biology reports · 2024Review
- LTBP2 regulates cisplatin resistance in GC cells via activation of the NF-κB2/BCL3 pathway.Genetics and molecular biology · 2024Article
- NF-κB Pathway and Its Inhibitors: A Promising Frontier in the Management of Alzheimer's Disease.Biomedicines · 2023Review
- Review
- Altered mRNA Expression of NFKB1 and NFKB2 Genes in Penile Lichen Sclerosus, Penile Cancer and Zoon Balanitis.Journal of clinical medicine · 2022Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
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Abstract
The NF-κB family of dimeric transcription factors regulate diverse biological functions. Their cellular expression profiles differ, which lead to different concentrations in different cell/tissue types. Although the activation mechanisms of different NF-κB dimers have been widely investigated, there is limited information on specific NF-κB dimers' formation. The NF-κB p52:p52 homodimer regulates an important subset of target genes in cancer cells; however, the molecular mechanism of the generation of this specific homodimer remains unclear. Our study has revealed that the atypical IκB protein, Bcl3, plays an essential role in enhancing the p52:p52 homodimer population which is a unique mechanism to p52 within the NF-κB family. p52 was shown to heterodimerize with four other NF-κB subunits (RelA, RelB, cRel, and p50); all heterodimers, except p52:p50, are significantly more stable than the p52:p52 homodimer. Bcl3 is able to compete with all other NF-κB subunits in cells for efficient p52:p52 homodimer formation which consequently leads to the upregulation of target genes that are involved in cell proliferation, migration, and inflammation, which explain why aberrant activation of Bcl3 and p52 leads to cancer.
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