ArticleNature communications2015
IκBβ enhances the generation of the low-affinity NFκB/RelA homodimer.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
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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.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- NF-κB: master regulator of cellular responses in health and disease.Immunity & inflammation · 2025Review
- Transient interactions modulate the affinity of NF-κB transcription factors for DNA.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Targeting the NF-κB pathway as a potential regulator of immune checkpoints in cancer immunotherapy.Cellular and molecular life sciences : CMLS · 2024Review
- Flow-Induced Shear Stress Primes NLRP3 Inflammasome Activation in Macrophages via Piezo1.ACS applied materials & interfaces · 2024Article
- Regulation of IkappaB Protein Expression by Early Gestation in the Thymus of Ewes.Veterinary sciences · 2023Article
- New Insights into NF-κB Signaling in Innate Immunity: Focus on Immunometabolic Crosstalks.Biology · 2023Review
- The NF-κB Transcriptional Network Is a High-Dose Vitamin C-Targetable Vulnerability in Breast Cancer.Biomedicines · 2023Review
- The NF-κB multidimer system model: A knowledge base to explore diverse biological contexts.Science signaling · 2023Review
- Optimization of BRET saturation assays for robust and sensitive cytosolic protein-protein interaction studies.Scientific reports · 2022Article
- Atypical IκB Bcl3 enhances the generation of the NF-κB p52 homodimer.Frontiers in cell and developmental biology · 2022Article
- Defining the structure of the NF-ĸB pathway in human immune cells using quantitative proteomic data.Cellular signalling · 2021Article
- An epithelialProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Review
- The Nuclear Factor Kappa B (NF-kB) signaling in cancer development and immune diseases.Genes & diseases · 2021Review
- The Effect of Novel Oleanolic Acid Oximes Conjugated with Indomethacin on the Nrf2-ARE And NF-κB Signaling Pathways in Normal Hepatocytes and Human Hepatocellular Cancer Cells.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Multiplexing information flow through dynamic signalling systems.PLoS computational biology · 2020Article
- Genome reading by the NF-κB transcription factors.Nucleic acids research · 2019Review
- Exclusivity and Compensation in NFκB Dimer Distributions and IκB Inhibition.Biochemistry · 2019Article
- Assaying Homodimers of NF-κB in Live Single Cells.Frontiers in immunology · 2019Article
- Considering Abundance, Affinity, and Binding Site Availability in the NF-κB Target Selection Puzzle.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
The NFκB family of dimeric transcription factors regulate inflammatory and immune responses. While the dynamic control of NFκB dimer activity via the IκB-NFκB signalling module is well understood, there is little information on how specific dimer repertoires are generated from Rel family polypeptides. Here we report the iterative construction-guided by in vitro and in vivo experimentation-of a mathematical model of the Rel-NFκB generation module. Our study reveals that IκBβ has essential functions within the Rel-NFκB generation module, specifically for the RelA:RelA homodimer, which controls a subset of NFκB target genes. Our findings revise the current dogma of the three classical, functionally related IκB proteins by distinguishing between a positive 'licensing' factor (IκBβ) that contributes to determining the available NFκB dimer repertoire in a cell's steady state, and negative feedback regulators (IκBα and -ɛ) that determine the duration and dynamics of the cellular response to an inflammatory stimulus.
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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.