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Proposed model of α7nAChR mediated prolonged regulation of TNF in macrophages. Activation of α7nAChR promotes activity of adenylyl cyclase 6, which increases production of cAMP. Increased intracellular levels of cAMP promotes phosphorylation of CREB, which enhances expression of c-FOS, c-FOS, in turn, is involved in NFκB mediated inhibition of TNF transcription. In this way, α7nAChR activation can inhibit endotoxin-induced TNF production.
