What is the Origin of Nuclear Factor-Kappa B (NF-κB)?

NF-κB was first identified in B-cells as a factor binding to the kappa light chain enhancer of immunoglobulins, hence the "Kappa B" designation. Subsequent research revealed its ubiquitous presence and its pivotal role as a rapid-response transcription factor in nearly all cell types. The recognition of its constitutive activation in chronic disease states cemented its status as a critical target in molecular medicine and longevity research. This discovery was foundational to understanding the molecular basis of inflammation.

What is the Mechanism of Nuclear Factor-Kappa B (NF-κB)?

Under normal, resting conditions, NF-κB is sequestered in the cytoplasm, bound to an inhibitory protein called IκB. Upon cellular stimulation by inflammatory cytokines, stress signals, or hormonal cues, IκB is phosphorylated and degraded, allowing the now-free NF-κB dimer to translocate into the cell nucleus. Once in the nucleus, NF-κB binds to specific DNA sequences, initiating the transcription of pro-inflammatory genes, including those for interleukins and tumor necrosis factor-alpha (TNF-α), thereby perpetuating the inflammatory cascade.

Nuclear Factor-Kappa B (NF-κB) ∞ Area

Nuclear Factor-Kappa B (NF-κB)

Meaning

Nuclear Factor-Kappa B (NF-κB) is a protein complex that functions as a crucial transcription factor, playing a central role in regulating the expression of genes involved in inflammation, immunity, and cell survival. As a master regulator of the inflammatory response, its chronic activation is a key molecular driver in numerous age-related diseases and conditions of hormonal imbalance. Clinically, NF-κB activity is a significant biomarker for assessing systemic inflammatory load and biological aging. Controlling this factor is paramount for longevity.