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NF-κB and interleukin 1 alpha mutually induce each other in senescent cells in a positive feedback loop causing the production of senescence-associated secretory phenotype (SASP) factors. [93] NF-κB and the NAD-degrading enzyme CD38 also mutually induce each other. [94] NF-κB is a central component of the cellular response to damage. [95]
NFKBIE is able to inhibit NF-κB-directed transactivation via cytoplasmic retention of REL proteins. [6] NFKB1 or NFKB2 is bound to REL, RELA, or RELB to form the NF-κB transcription factor complex. The NF-κB complex is inhibited by I-kappa-B proteins (NFKBIA or NFKBIB), which inactivate NF-kappa-B by trapping it in the cytoplasm.
NF-κB has been detected in numerous cell types that express cytokines, chemokines, growth factors, cell adhesion molecules, and some acute phase proteins in health and in various disease states. NF-κB is activated by a wide variety of stimuli such as cytokines, oxidant-free radicals, inhaled particles, ultraviolet irradiation, and bacterial ...
The 105 kD protein is a Rel protein-specific transcription inhibitor and the 50 kD protein is a DNA binding subunit of the NF-kappaB protein complex. NF-κB is a transcription factor that is activated by various intra- and extra-cellular stimuli such as cytokines, oxidant-free radicals, ultraviolet irradiation, and bacterial or viral products ...
It was reported that NFKBID interacts with p50, which is a subunit of NF-κB, p52, p65, RelB, and c-Rel. NFKBID binds these proteins only in the nucleus, except for p50, which can be bound both in the cytoplasm and in the nucleus [ 11 ] [ 12 ] Researchers suggest that apart from this, NFKBID can also interact with homo- and heterodimers ...
Activated IKK-β phosphorylates a protein called the inhibitor of NF-κB, IκB , which binds NF-κB to inhibit its function. Phosphorylated IκB is degraded via the ubiquitination pathway, freeing NF-κB, and allowing its entry into the nucleus of the cell where it activates various genes involved in inflammation and other immune responses.
IκBα inhibits NF-κB by masking the nuclear localization signals (NLS) of NF-κB proteins and keeping them sequestered in an inactive state in the cytoplasm. [5] In addition, IκBα blocks the ability of NF-κB transcription factors to bind to DNA, which is required for NF-κB's proper functioning.
Notably, the NBD peptide targets the inflammation induced NF-κB activation pathway sparing the protective functions of basal NF-κB activity allowing for greater therapeutic value and fewer undesired side effects. The NBD peptide was designed by identifying the amino acid binding sequence on IKK-α and IKK-β to which NEMO binds. [12]