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- W4324133386 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." @default.
- W4324133386 created "2023-03-15" @default.
- W4324133386 creator A5004947772 @default.
- W4324133386 creator A5016433624 @default.
- W4324133386 creator A5019648671 @default.
- W4324133386 creator A5044717518 @default.
- W4324133386 creator A5047177237 @default.
- W4324133386 date "2023-03-14" @default.
- W4324133386 modified "2023-09-29" @default.
- W4324133386 title "The NF-κB multidimer system model: A knowledge base to explore diverse biological contexts" @default.
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- W4324133386 doi "https://doi.org/10.1126/scisignal.abo2838" @default.
- W4324133386 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36917644" @default.
- W4324133386 hasPublicationYear "2023" @default.