ReviewScience signaling2023
The NF-κB multidimer system model: A knowledge base to explore diverse biological contexts.
Review in Science signaling, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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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Who cites it
18 citing papers in PubMed.
- Dysregulated NF-κB dynamics impair proteostasis and drive premature differentiation in aging B cell development.Cell press blue · 2026Article
- Elevated TNF-α level is correlated with NF-κB/p65 activation in patients with sporadic colorectal cancer.Molecular and clinical oncology · 2026Article
- NF-κB signaling as a critical inflammatory node in pulmonary arterial hypertension: from vascular remodeling to right heart failure.Frontiers in immunology · 2026Review
- Computational modelling of aggressive B-cell lymphoma.Biochemical Society transactions · 2025Review
- Systems biology-enabled targeting of NF-κΒ and BCL2 overcomes microenvironment-mediated BH3-mimetic resistance in DLBCL.Cell death & disease · 2025Article
- Synergy and antagonism in the integration of BCR and CD40 signals that control B-cell population expansion.Molecular systems biology · 2025Article
- Poxvirus K3 Orthologs Regulate NF-κB-Dependent Inflammatory Responses by Targeting the PKR-eIF2α Axis in Multiple Species.Vaccines · 2025Article
- Advances in the study of CCT3 in malignant tumors: A review.Medicine · 2025Review
- High-expression of BCL10 inhibits cell-mediated immunity within the tumor immune microenvironment.Frontiers in immunology · 2025Article
- NF-κB: master regulator of cellular responses in health and disease.Immunity & inflammation · 2025Review
- Not just for lymphoid cells: the role of the noncanonical NF-κB signaling pathway in early and late myelopoiesis with a focus on hypereosinophilic disorders.Journal of leukocyte biology · 2024Review
- Direct observation correlates NFκB cRel in B cells with activating and terminating their proliferative program.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Systems modeling of oncogenic G-protein and GPCR signaling reveals unexpected differences in downstream pathway activation.NPJ systems biology and applications · 2024Article
- Patient-specific computational models predict prognosis in B cell lymphoma by quantifying pro-proliferative and anti-apoptotic signatures from genetic sequencing data.Blood cancer journal · 2024Article
- Schisandrin A Alleviates Spatial Learning and Memory Impairment in Diabetic Rats by Inhibiting Inflammatory Response and Through Modulation of the PI3K/AKT Pathway.Molecular neurobiology · 2024Article
- The NF-ĸB p50 subunit generated by KPC1-mediated ubiquitination and limited proteasomal processing, suppresses tumor growth.Cancer cell international · 2023Review
- NF-κB fingerprinting reveals heterogeneous NF-κB composition in diffuse large B-cell lymphoma.Frontiers in oncology · 2023Article
- The noncanonical NFκB pathway: Regulatory mechanisms in health and disease.WIREs mechanisms of diseaseReview
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The nuclear factor κB (NF-κB) system is critical for various biological functions in numerous cell types, including the inflammatory response, cell proliferation, survival, differentiation, and pathogenic responses. Each cell type is characterized by a subset of 15 NF-κB dimers whose activity is regulated in a stimulus-responsive manner. Numerous studies have produced different mathematical models that account for cell type-specific NF-κB activities. However, whereas the concentrations or abundances of NF-κB subunits may differ between cell types, the biochemical interactions that constitute the NF-κB signaling system do not. Here, we synthesized a consensus mathematical model of the NF-κB multidimer system, which could account for the cell type-specific repertoires of NF-κB dimers and their cell type-specific activation and cross-talk. Our review demonstrates that these distinct cell type-specific properties of NF-κB signaling can be explained largely as emergent effects of the cell type-specific expression of NF-κB monomers. The consensus systems model represents a knowledge base that may be used to gain insights into the control and function of NF-κB in diverse physiological and pathological scenarios and that describes a path for generating similar regulatory knowledge bases for other pleiotropic signaling systems.
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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.