What is NFkB pathway?
Nuclear factor kappa B (NF-κB) is an ancient protein transcription factor (Salminen et al., 2008) and considered a regulator of innate immunity (Baltimore, 2009). The NF-κB signaling pathway links pathogenic signals and cellular danger signals thus organizing cellular resistance to invading pathogens.
Why does NF-kB travel into the nucleus?
In most cells, NF-kB is present as a latent, inactive, IkB-bound complex in the cytoplasm. When a cell receives any of a multitude of extracellular signals (see INDUCERS link), NF-kB rapidly enters the nucleus and activates gene expression (see TARGET GENES link).
How is NF-kB activated?
The primary mechanism for canonical NF-κB activation is the inducible degradation of IκBα triggered through its site-specific phosphorylation by a multi-subunit IκB kinase (IKK) complex. IKK is composed of two catalytic subunits, IKKα and IKKβ, and a regulatory subunit named NF-κB essential modulator (NEMO) or IKKγ.
What genes does NFkB regulate?
NF-κB is a key transcription factor of M1 macrophages and is required for induction of a large number of inflammatory genes, including those encoding TNF-α, IL-1β, IL-6, IL-12p40 and cyclooxygenase-2.
Do all cells have NFkB?
NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, heavy metals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens. NF-κB plays a key role in regulating the immune response to infection.
What is p65 protein?
RELA, also known as p65, is a REL-associated protein involved in NF-κB heterodimer formation, nuclear translocation and activation. RELA has also been shown to modulate immune responses, and activation of RELA is positively associated with multiple types of cancer.
What cytokines does NF-kB activate?
As described above, NF-κB promotes Th17 differentiation both indirectly through induction of inflammatory cytokines, IL-1, IL-6 and IL-23, in innate immune cells and directly regulates Th17 lineage transcription factors in T cells.