The classic "canonical" NF-κB complex is a heterodimer of p50 and RelA. While in an inactivated state, NFKB is located in the cytosol complexed with the inhibitory protein IκB alpha. Through the intermediacy of integral membrane receptors, a variety of extracellular signals can activate the enzyme IκB kinase (IKK). IKK, in turn, phosphorylates the IκB alfa protein, which results in ubiquitination, dissociation of IκB alfa from NFKB, and eventual degradation of IκB alfa by the proteasome. The activated NFKB is then translocated into the nucleus, where it binds to specific sequences of DNA called response elements (RE). The DNA/NFKB complex then recruits proteins such as coactivators and RNA polymerase, which transcribe downstream DNA into mRNA. In turn, mRNA is translated into protein, resulting in cell function changes.
Results could be: Inflammation, inhibition of apoptosis, metastasis, angiogenesis
NFKB Signaling / NFKB Pathway is involved in immune processes in
Activation of NFKB signaling was necessary for TMAO to induce inflammatory gene expression in both of these relevant cell types as well as endothelial cell adhesion of leukocytes
Acute TMAO injection at physiological levels was sufficient to induce the same inflammatory markers and activate the well-known mitogen-activated protein kinase, and NFKB signaling cascade
Activated NF-κB is frequently detected in various inflammatory diseases and tumors
NF-κB has received extensive attention as a key regulator of inflammation and carcinogenesis
NFKB Signaling is necessary for IL-1 Expression
see also:
B Cells & NFKB Signaling / NFKB Pathway
Dendritic Cells (DCs) & NFKB Signaling / NFKB Pathway
Large Granular Lymphocytes / NK-cells & NFKB Signaling / NFKB Pathway
Macrophages (CD68s) & NFKB Signaling / NFKB Pathway
Neutrophils / Neutrophilic Granulocytes & NFKB Signaling / NFKB Pathway
NFKB / TLR4 signal transduction pathway
T cells & NFKB Signaling / NFKB Pathway