How does NFkB cause inflammation?
NF-κB target inflammation not only directly by increasing the production of inflammatory cytokines, chemokines and adhesion molecules, but also regulating the cell proliferation, apoptosis, morphogenesis and differentiation.
How does NFkB get activated?
Activation of the NF-κB is initiated by the signal-induced degradation of IκB proteins. This occurs primarily via activation of a kinase called the IκB kinase (IKK).
What is NFkB inflammation?
Nuclear factor-κB (NF-κB), a transcription factor that is essential for inflammatory responses, is one of the most important molecules linking chronic inflammation to cancer, and its activity is tightly regulated by several mechanisms.
How does Nfkb cause apoptosis?
39 In addition, NF-kB has been shown to play a role in apoptosis mediated by engagement of PPARa and PPARg in both TNFa stimulated and in unstimulated differentiated macrophages. 40 NF-kB has also been found to protect ras transformed tumor cells from apoptosis induced by chemotherapy.
What is the role of nuclear factor kappa B?
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.
Where are TADS located in nuclear factor kappa B?
Three of these proteins (RelA, RelB, and c-REL) also encode a transactivation domain (TADs) in their carboxy-terminal region.
What happens to the NF-κB protein in the nucleus?
The activated NF-κB is then translocated into the nucleus where it binds to specific sequences of DNA called response elements (RE). The DNA/NF-κB complex then recruits other proteins such as coactivators and RNA polymerase, which transcribe downstream DNA into mRNA.
What is the selectivity of the NF-κB response?
The selectivity of the NF-κB response is based on several factors ( Sen and Smale, 2010) including dimer composition, timing, and cell type. NF-κB’s influence on cell survival is also complex and can be neuroprotective or proinflammatory, depending on cell type, developmental stage, and pathological state ( Qin et al., 2007 ).