Figure 3.

Canonical and alternative NF-κB signaling pathways. Canonical pathway is triggered by toll-like receptors (TLRs), pro-inflammatory cytokines such as IL1 and TNFα receptor, and CD40. It relies on inducible degradation of IκBs, particularly IκBα, leading to nuclear translocation of various NF-κB complexes, predominantly the p50/RelA dimer. Non-canonical NF-κB pathway relies on phosphorylation-induced p100 processing, which is triggered by signals from a subset of tumor necrosis factor α (TNFα) receptor (TNFR) members. This pathway is dependent on NF-κB-inducing kinase (NIK) and IκB kinase (IKK)α and mediates the activation of RelB/p52 complexes. Proteins potentially mutated in MCL are highlighted with a yellow star.