Final answer:
NF-κB activates gene expression by dissociating from the inhibitor IκB when it is phosphorylated by PKC, allowing NF-κB to enter the nucleus and bind to DNA, promoting transcription.
Step-by-step explanation:
The classic NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) is a heterodimeric transcription factor made up of p50 and RelA (p65) subunits. It plays a critical role in regulating gene expression involved in various biological processes like inflammation and cell survival. NF-κB is normally held inactive in the cytoplasm by an inhibitor protein known as IκB (inhibitor of kappa B). When cells receive external stimuli, the signaling cascade leads to the activation of an enzyme known as Protein Kinase C (PKC). PKC then phosphorylates IκB, which results in its degradation and the release of NF-κB. Once freed, NF-κB translocates to the nucleus where it binds to specific DNA sequences and promotes the transcription of target genes which are crucial for cellular response to stress, such as the production of pro-inflammatory cytokines.
Thus, the pivotal mechanism by which NF-κB induces gene expression is through the phosphorylation of IκB, leading to the dissociation of the NF-κB/IκB complex. This enables NF-κB to enter the nucleus and stimulate transcription, which plays a central role in the cellular metabolism and response to environmental stresses.