**2.1 The canonical pathway**

The canonical pathway is provoked by the pro-inflammatory cytokines, ligands of varied immune receptors and involves the rapid and transient activation of IκB kinase [22]. NF-κB activity at sites of inflammation is associated with activation of the canonical pathway and RelA- or cRel-containing complexes [23]. In the pathway, NF-κB/Rel proteins are tethered which are inhibited by IκB proteins. Pro inflammatory cytokines, lipopolysaccrahaide, growth factors and antigen receptors activate the IKK complex (IKKβ, IKKα and NEMO) [24]. The complex then phosphorylates IκB proteins which lead to ubiquitination and proteasomal degradation, freeing NF-κB/Rel complex. Active NF-κB/Rel complex is further activated by post transcriptional modifications and translocate to the nucleus, where either alone or in combination with other transcription factors including AP-1, Ets and STAT and induce target gene expression [25].
