Evidences p(FPLX:NFkappaB) to p(HGNC:TNF)

Then the stimulation of RAGE is able to activate the mitogen-activated protein kinase signaling cascades which converge in IκB kinase complex to phosphorylate IκB, thereby release and activate NF-κB, thus trigger NF-κB dependent gene transcription including IL-1β and TNF-α, which in turn induce the translocation of NF-κB to the nucleus [50].

Our data clearly demonstrate that NSAIDs inhibit TNF-a-induced BACE1 transcription via its NF-kB cis-acting elements.

It inhibited the activation of NF-B in TNF- induced HepG2 cells [193].

Nuclear local- ization of NF-κB in differentiated neuron progenitor cells (NPCs) is in- creasing following exposure to IL-1β and TNF-α, strong inducers of the NF-κB pathway with increase in the phosphorylation of IKK and p65 while decrease in the level of IκB [32].

NSAIDs inhibit BACE1 tran- scriptional activation induced by strong NF-κB activator TNF-α.

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