Transcription factors of the NF-κB family are inducible proteins that regulate expression of genes involved in inflammation, immune response and cell survival [15]–[17]. These factors are homo- or heterodimers of p65 (Rel A), p50 and other proteins of the NF-κB family. The p65/p50 heterodimer (NF-κB) generally activates gene transcription while the p50 homodimer represses it [18], [19]. In most cell types, NF-κB is sequestered in the cytoplasm in a complex with inhibitor IκB proteins. Nuclear translocation of NF-κB is induced by multiple extracellular stimuli that trigger activation of an IκB kinase (IKK) complex, which phosphorylates the IκBs leading to their ubiquitination and proteasomal degradation. The released NF-κB migrates to the nucleus to act as a transcription factor. The IKK complex contains the two kinases IKKα and IKKβ and the regulatory subunit NEMO/IKKγ, and functions as integrator of signals regulating NF-κB activity. Transactivating capacity is also regulated in the cell nuclei through phosphorylation of p65 and p50 by IKKβ and other kinases [20]–[22]. In the brain, the p65 and p50 NF-κB subunits are abundantly expressed in neurons and glia, and a
