{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNFKB1, which encodes key subunits of the NF‑κB family (notably p105 and its processed p50 form), functions as a master transcriptional regulator in inflammation and immune responses. It integrates diverse extracellular cues – for example, signals from cytokine and pattern recognition receptors – to control the transcription of genes mediating proinflammatory cytokine production, inflammasome priming, and cell survival. Its activity is finely tuned by upstream kinases (such as IKK), post‐translational modifications, and interactions with corepressors or coactivators, ensuring that inflammatory signals are appropriately amplified or restrained."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the context of cancer, NFKB1‐dependent NF‑κB signaling exerts a complex duality. In some settings—such as in aggressive lymphomas, multiple myeloma and certain breast cancers—aberrant activation (or mutations in upstream regulators that modulate NFKB1 activity) contributes to enhanced cell survival, proliferation, metastasis, and resistance to apoptotic signals. 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These mechanisms allow NF‑κB to dynamically shift between activator and repressor states in response to different stimuli, such as reactive oxygen species, DNA damage, and cytokine engagement, thereby ensuring precise control over cell fate decisions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "35", "end_ref": "40"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional studies extend the functional landscape of NFKB1 by linking its activity to diverse biological processes such as tissue regeneration, synaptic plasticity and maintenance of immune tolerance. 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