Figure 8

A schematic describing altered dynamic control of NFκB in diseased cells. A model depicting the proposed autoregulatory loop underlying protracted NFκB response to TNF in myeloma. Left, pro-inflammatory cytokines transiently induce NFκB activity, which is composed of RelA:p50 dimer, in healthy cells. Right, genetic aberrations in myeloma deplete p100 to provoke the autoregulatory circuitry in generating protracted RelB:p50/NF-κB response to canonical TNF signals.