ArticleFrontiers in molecular biosciences2023
Overexpression of IκB⍺ modulates NF-κB activation of inflammatory target gene expression.
Article in Frontiers in molecular biosciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
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- Focal Estrogen Therapy in Male Rats Promotes Neuronal Survival and Reduces Denervation Atrophy After Spinal Cord Injury via Modulation of β-Catenin and NF-κB.Neurochemical research · 2026Article
- Therapeutic Potential of NF-κB Inhibition in Glioblastoma: Gene Therapy Approach with rAAV-5 Mediated IκBαM Overexpression.Molecular biotechnology · 2026Article
- Mechanisms and therapeutic prospects of DNA methylation-mucosal innate immunity crosstalk in inflammatory bowel disease.Frontiers in immunology · 2026Review
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- Effects of Dietary Vitamin D Levels on Markers Related to Amyloidogenesis and Neuroinflammation in db/db Mice.Nutrients · 2025Article
- Copper-mediated MAM regulation of the NF-κB signalling pathway enhances Seneca Valley virus replication in PK-15 cells.Veterinary research · 2025Article
- [Research progress on the cGAS-STING signaling pathway in immune-mediated inflammatory diseases in children].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Review
- Decoy oligonucleotides targeting NF-κB: a promising therapeutic approach for inflammatory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Synoviocyte-chondrocyte triculture model for early-stage PTOA: fibronectin fragment-induced catabolic effectsFrontiers in bioengineering and biotechnology · 2025Article
- Molecular Mechanisms Linking Omega-3 Fatty Acids and the Gut-Brain Axis.Molecules (Basel, Switzerland) · 2024Review
- NFκB signalling in colorectal cancer: Examining the central dogma of IKKα and IKKβ signalling.Heliyon · 2024Review
- Cellular heterogeneity in TNF/TNFR1 signalling: live cell imaging of cell fate decisions in single cells.Cell death & disease · 2024Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Cells respond to inflammatory stimuli such as cytokines by activation of the nuclear factor-κB (NF-κB) signalling pathway, resulting in oscillatory translocation of the transcription factor p65 between nucleus and cytoplasm in some cell types. We investigate the relationship between p65 and inhibitor-κB⍺ (IκBα) protein levels and dynamic properties of the system, and how this interaction impacts on the expression of key inflammatory genes. Using bacterial artificial chromosomes, we developed new cell models of IκB⍺-eGFP protein overexpression in a pseudo-native genomic context. We find that cells with high levels of the negative regulator IκBα remain responsive to inflammatory stimuli and maintain dynamics for both p65 and IκBα. In contrast, canonical target gene expression is dramatically reduced by overexpression of IκBα, but can be partially rescued by overexpression of p65. Treatment with leptomycin B to promote nuclear accumulation of IκB⍺ also suppresses canonical target gene expression, suggesting a mechanism in which nuclear IκB⍺ accumulation prevents productive p65 interaction with promoter binding sites. This causes reduced target promoter binding and gene transcription, which we validate by chromatin immunoprecipitation and in primary cells. Overall, we show how inflammatory gene transcription is modulated by the expression levels of both IκB⍺ and p65. This results in an anti-inflammatory effect on transcription, demonstrating a broad mechanism to modulate the strength of inflammatory response.
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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.