nuclear factor-kappaB

(redirected from nuclear factor-kB)

nuclear factor-κB

an evolutionarily conserved eukaryotic transcription factor system that contributes to the mounting of an effective immune response but also plays an important role in many other cellular processes. NF-κB and its regulators are linked to signal transduction pathways as well as transcriptional activation events that mediate critical stages of cell proliferation, development, and apoptosis.

nu·cle·ar fac·tor-κB

(nū'klē-ăr fak'tŏr)
A transcription factor associated with cytokine production.
References in periodicals archive ?
It does so by activating the cell signal pathways of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and by decreasing activity of the Nuclear Factor-KB (NF-KB), which are the two key transcription factors that regulate cellular responses to oxidative stress and inflammation, respectively.
Kelly Cordoro, a pediatric dermatologist at the University of California, San Francisco, described crisaborole as an anti-inflammatory agent that modifies inflammation by inhibiting the degradation of cAMP by PDE-4, resulting in downstream modification of nuclear factor-kB and T-cell signaling pathways.
Cordoro described this compound as an anti-inflammatory agent that modifies inflammation by inhibiting the degradation of cAMP by PDE4, resulting in downstream modification of nuclear factor-kB and T-cell signaling pathways.
Human aortic endothelial cells (HAECs) were stimulated by angiotensin II (Ang II, 100 nmol/L) with or without pretreatment of valsartan (100 nmol/L), and relative expression of cyclooxygenase-2 (COX-2) and thromboxane B [sub]2 (TXB [sub]2 ) and both p38 mitogen-activated protein kinase (p38MAPK) and nuclear factor-kB (NF-kB) activities were assessed.
Expression of receptor activator of nuclear factor-KB ligand by B cells in response to oral bacteria.
Keywords: Urtica dioica (stinging nettle) Accelerated solvent extraction (ASE) Anti-inflammatory Rheumatoid arthritis Osteoarthritis Nuclear factor-kB
Progression of alcoholic liver disease is associated with oxidative stress involving activation of transcription factor nuclear factor-kB (NF-kB), which further regulates production of inflammatory cytokines.
1992) and blocks nuclear factor-KB (NF-kB) activation (Saadane et al.
EGCG has been shown to modulate multiple signal transduction pathways which play key roles in tumorigenesis, including those mediated by PI3K, MAPKs, STAT-3, Smad2/3 and nuclear factor-KB [2].
Previous data have shown that IL-10 has multifaceted antiinflammatory effects and inhibits many cellular process that could play an important role in plaque progression and rupture, or thrombosis, including inhibition of the prototypic proinflammatory transcription nuclear factor-KB, leading to suppression of cytokine production (22), inhibition of matrix-degrading metalloproteinases (23), reduction in tissue factor expression (24), inhibition of apoptosis of macrophages and monocytes after infection (25), and promotion of the phenotypic switch of lymphocytes into the Th2 phenotype (26).
The possible exceptions to this are osteoprotegrin (OPG) and receptor activator of nuclear factor-kB ligand (RANKL).

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