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The entry "NF-κB, TNF-α" refers to a critical signaling axis in inflammation. TNF-α (Tumor necrosis factor alpha) is a pro-inflammatory cytokine that activates the NF-κB (Nuclear factor kappa-light-chain-enhancer of activated B cells) transcription factor pathway. NF-κB is a family of transcription factors that regulate gene expression in response to various stimuli, including TNF-α. Both are key regulators of immune response, inflammation, cell survival, and apoptosis. Dysregulated activity of this axis is implicated in numerous diseases including cancer, autoimmune, and inflammatory conditions. While both NF-κB and TNF-α are canonical therapeutic targets individually, their combined designation as a single molecular entity is incorrect, as they are distinct but interacting components of a signaling pathway.
This represents the targeting of two interconnected components of inflammatory signaling. Mechanisms include inhibition of the IκB kinase (IKK) complex, preventing IκB degradation, blocking NF-κB nuclear translocation, and inhibition of NF-κB DNA binding; as well as neutralization or blockade of the TNF-α cytokine by inhibiting its binding to TNF receptors (TNFR1/TNFR2).
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