ArticleMolecular and cellular biology2000
Bcl-3 expression promotes cell survival following interleukin-4 deprivation and is controlled by AP1 and AP1-like transcription factors.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed.
- Efficient apoptosis via double-strand breaks of DNA in human epithelial cells induced by non-thermal effect of high-field broadband terahertz waves.Scientific reports · 2026Article
- CX3CL1 induces cell migration and invasion through ICAM-1 expression in oral squamous cell carcinoma cells.Journal of cellular and molecular medicine · 2023Article
- Acryl-3,5-bis(2,4-difluorobenzylidene)-4-piperidone targeting cellular JUN proto-oncogene, AP-1 transcription factor subunit inhibits head and neck squamous cell carcinoma progression.Exploration of targeted anti-tumor therapy · 2023Article
- Hepatocyte Bcl-3 protects from death-receptor mediated apoptosis and subsequent acute liver failure.Cell death & disease · 2022Article
- 2-Methoxy-1,4-naphthoquinone (MNQ) regulates cancer key genes of MAPK, PI3K, and NF-κB pathways in Raji cells.Genomics & informatics · 2022Article
- Bcl-3: A Double-Edged Sword in Immune Cells and Inflammation.Frontiers in immunology · 2022Review
- Investigating Core Signaling Pathways of Hepatitis B Virus Pathogenesis for Biomarkers Identification and Drug Discovery via Systems Biology and Deep Learning Method.Biomedicines · 2020Article
- Bcl-3 promotes Wnt signaling by maintaining the acetylation of β-catenin at lysine 49 in colorectal cancer.Signal transduction and targeted therapy · 2020Article
- Prognostic value from integrative analysis of transcription factors c-Jun and Fra-1 in oral squamous cell carcinoma: a multicenter cohort study.Scientific reports · 2017Article
- CIRBP protects H9C2 cells against myocardial ischemia through inhibition of NF-κB pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017Article
- Activator protein 1 promotes gemcitabine-induced apoptosis in pancreatic cancer by upregulating its downstream target Bim.Oncology letters · 2016Article
- Review
- Small molecule inhibitors targeting activator protein 1 (AP-1).Journal of medicinal chemistry · 2014Article
- IL-9-mediated survival of type 2 innate lymphoid cells promotes damage control in helminth-induced lung inflammation.The Journal of experimental medicine · 2013Article
- Atypical IκB proteins - nuclear modulators of NF-κB signaling.Cell communication and signaling : CCS · 2013Article
- Expression of Id proteins is regulated by the Bcl-3 proto-oncogene in prostate cancer.Oncogene · 2013Article
- TCR stimulation upregulates MS4a4B expression through induction of AP-1 transcription factor during T cell activation.Molecular immunology · 2012Article
- NF-κB, the first quarter-century: remarkable progress and outstanding questions.Genes & development · 2012Review
- Role of Bcl-3 in solid tumors.Molecular cancer · 2011Review
- JUN-CCAAT/enhancer-binding protein complexes inhibit surfactant-associated protein B promoter activity.American journal of respiratory cell and molecular biology · 2011Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have analyzed the interleukin-4 (IL-4)-triggered mechanisms implicated in cell survival and show here that IL-4 deprivation induces apoptotic cell death but does not modulate Bcl-2 or Bcl-x expression. Since Bcl-x expression is insufficient to ensure cell survival in the absence of IL-4, we speculate that additional molecules replace the antiapoptotic role of Bcl-2 and Bcl-x in an alternative IL-4-triggered pathway. Cell death is associated with Bcl-3 downregulation and Bcl-3 expression blocks IL-4 deprivation-induced apoptosis, suggesting that Bcl-3 acts as a survival factor in the absence of growth factor. To characterize the IL-4-induced regulation of murine Bcl-3 expression, we cloned the promoter of this gene. Sequencing of the promoter showed no TATA box element but did reveal binding sites for AP1, AP1-like, and SP1 transcription factors. Retardation gels showed that IL-4 specifically induces AP1 and AP1-like binding activity and that mutation of these binding sites abolishes the IL-4-induced Bcl-3 promoter activity, suggesting that these transcription factors are important in Bcl-3 promoter transactivation. IL-4 deprivation induces downregulation of Jun expression and upregulation of Fos expression, both of which are proteins involved in the formation of AP1 and AP1-like transcription factors. Overexpression of Jun family proteins transactivates the promoter and restores Bcl-3 expression in the absence of IL-4 stimulation. Taken together, these data describe a new biological role for Bcl-3 and define the regulatory pathway implicated in Bcl-3 expression.
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