NF-kappaB

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NF-κB

a transcription factor that regulates cytokine gene transcription. NF-κB is a target of glucocorticoid action.

NF-kappaB

A pleiotropic transcription factor present in most cell types, which is involved in many biological processes such as inflammation, immunity, differentiation, cell growth, tumourigenesis and apoptosis. It forms a homo- or heterodimeric complex with Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52, binding the kappa-B sites in the DNA of their target genes. Individual dimers have distinct preferences for different kappa-B sites, binding with distinct affinity and specificity; different dimer combinations act as transcriptional activators or repressors.

NF-kappaB is controlled by various mechanisms of post-translational modification and subcellular compartmentalisation, as well as by interactions with other cofactors or co-repressors. NF-kappaB complexes are held in the cytoplasm in an inactive state, complexed with members of the NF-kappaB inhibitor (I-kappa-B) family. In conventional activation, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators and subsequently degraded, liberating the active NF-kappaB complex, which translocates to the nucleus.
References in periodicals archive ?
Not enough NF-kB increases the risk of serious infections.
CaMKII[delta]C is suggested to act as a link between inflammation and CH by regulating NF-kB. The results of the present study showed that although CaMKII[delta]B silencing was sufficient to prevent HSP60-induced cardiomyocyte hypertrophy, it did not decrease inflammatory cytokine IL-6 and TNF-[alpha] levels.
However, treatment over time with sodium salicylate, an ingredient in aspirin, repressed NF-KB signals and related age-induced chronic inflammation, increasing the number and bone-healing contribution of skeletal stem cells.
Collect the colonic tissue specimen and determine contents of colonic mucosal tissue TLR4/9 and NF-kB of each group of rats through the immunohistochemistry and Western blot after the treatment.
Cocoa consumption reduces NF-KB activation in peripheral blood mononuclear cells in humans.
Dentro del proceso inflamatorio, el factor NF-kB participa en la respuesta inmunitaria, tanto en el desarrollo, formacion, progresion y apoptosis de diversos tumores.
Indirubin inhibits LPS-induced inflammation via TLR4 abrogation mediated by the NF-kB and MAPK signaling pathways.
When a person is exposed to a stressful event, their sympathetic nervous system (SNS) -- the system responsible for the 'fight-or-flight' response -- is triggered, in turn increasing production of a molecule called nuclear factor kappa B (NF-kB) which regulates how our genes are expressed.
Los resultados experimentales del uso de bloqueadores de la Ang II (Losartan: bloqueo de AT1) y de la inflamacion en general (pirrolidin-ditiocarbamato [PDTC]: bloqueo de NF-kB) en animales infectados, disminuyo el tiempo de sobrevida y la produccion de citocinas (IL1a, MCP-1, IL-10) en los homogenizados de cerebro/cerebelo.
The concentration of TNF-a, IL-1b and IL-6 was significantly higher, and there was enhanced expression of the inflammatory genes TLR4, MyD88, TRAF-6, NF-KB, IL-1b and IL-6 in the uteri of TG goats.
The tumor necrosis factor alfa (TNF[alpha]) is one of the most important proinflammatory cytokines involved in this process, and its transcription depends on the activation of the transcription factor known as nuclear factor kB (NF-kB) [1].