NFkB nuclear factor kappa

Fig. 2 Possible mechanisms by which nanoparticles cause toxicity inside cells. GSH glutathione, GSSG glutathione disulfide, MDA malondialdehyde, NFkB nuclear factor kappa B, Nrf2 nuclear factor-erythroid 2-related factor 2, ROS reactive oxygen species...

Another study by Potter et al. looked at genotypes in the TLR (toll-like receptor) and NFkB (nuclear factor kappa B, a transcription factor) pathways to predict response to anti-TNF therapy in RA. A total of 187 SNPs in these pathways were studied in 909 patients with RA. Twelve SNPs in nine genes showed a nominal association with treatment response in patients on anti-TNF therapy [122],... 

NEMO kinase (regulatory subunit IKKy), NFkB (nuclear factor kappa B lymphoma) essential modulator, inhibitor of kappa kinase gamma (IKKy). Protein kinase C-interacting protein p62/sequestosome-l, is activated by interleukin IL-IP in sequence, it activates of nuclear factor NFkB in TNFa-stimulated cells (Zotti T et al Mol Immunol 2014 58 27-31). NEMO promotes vFFlP (Fas-associated death domain-like interleukin-1-converting enzyme inhibitory protein) expression by Kaposi sarcoma associated herpesvirus (KSHV) (Tolani B et al J Virol 2014 March 26 PMID 24672029). 

NFkB Nuclear factor kappa-light-chain-enhancer of activated B-cells... 

Inhibition of leucocyte adhesion to endothelium. By acting on the gene transcription factor called nuclear factor kappa B (NFkB), NO limits the expression by endothelial cells of monocyte chemotactic protein-1 (MCP-1) and VCAM-1. As both MCP-1 and VCAM-1 are involved with pro-inflammatory responses, NO is in this manner an anti-inflammatory agent ... 

After damage or infection, monocytes and KCs in the area detect the damaged cells or infectious agent and respond with release of primary mediators such as TNFa, IL-1 and some IL-6. These cytokines activate the surrounding cells, that respond with a secondary, amplified release of cytokines. This second wave includes large amounts of IL-6, which induce the synthesis of acute phase proteins in hepatocytes and chemoattractants such as IL-8 and MCP-1. These events will then lead to the typical inflammatory reactions. Both IL-1 and TNFa activate the central regulatory protein of many reactions involved in immunity and inflammation, nuclear factor kappa B (NFkB). These cytokines cause dissociation of NFkB from its inhibitor IkB, which makes translocation of NFkB to the nucleus possible. In the nucleus active NFkB induces the transcription of the second wave cytokines (see also Chapter 7 for the molecular mechanisms of cytokine-mediated cell activation). 

A1 receptors inhibit whereas A2 receptors stimulate the production of cAMR Hyperpolarization via A1 receptors is attributed to opening of potassium channels. A1 receptors also elicit metabolic responses (18). Thus, these receptors stimulate translocation of the transcription factor, nuclear factor kappa B (NFkB), into the nucleus of neurons in the basal forebrain via the inositol triphosphate-Ca2+ pathway, and may stimulate further synthesis of A1 receptors. Adenosine also elicits c-fos expression in noncholinergic basal forebrain neurons (19). 

NFkB Inhibition of nuclear factor kappa B (NF-kB) activity... 

The molecular mechanism linking the inflammatory response to redox equilibria and modification of nitric oxide production will be explored in an animal model system of septic shock, a generalized inflammation induced by bacterial lipopolisaccharide (LPS). It is known that endotoxemia induces a complex interplay between the activation of nuclear transcription factors such as nuclear factor kappa B (NFkB) and a cascade-activation of various enzymatic activities, mostly mediators of the inflammatory response with particular attention to the variation of the inducible form of nitric oxide synthase (iNOS). 

A77 1726 inhibits dihydro-rate dehydrogenase, the rate-limiting enzyme in pyrimidine synthesis. It inhibits the proliferation of T and B cells, and probably acts via the production and action of interleukin-2. Besides its immunomodulatory action, A77 1726 also has an antiinflammatory action by inhibition of nuclear factor kappa B (NFkB), tumor necrosis factor alfa (TNF-a),... 

Inflammation is induced by the release of proinflammatory mediators from the cytosol of damaged or infected cells (Sect. 13.2.2). One of the first identified cytokines was an osteoclast activation factor later found to induce a multitude of other proinflammatory events, InterLeukin-1 (IL-1). A second was Tumor Necrosis Factor (TNF), more formally known as tumor necrosis factor-alpha, TNF-a (Sect. 13.2.2). The binding of these proteins to receptors on adjacent cells activates Nuclear Factor kappa B (NFkB), a protein in the leukocyte cytosol. The hgand-bound receptor indirectly phosphorylates an NFkB partner protein (Inhibitor of NFkB, IkB) in the cytosol. The phosphorylated IkB is targeted for destruction and its loss exposes a nuclear locahzation sequence on the NFkB protein which can now enter the nucleus where it induces the expression of important proteins, depending on the type of cell that is activated. ODAR is a Receptor Activator of Nuclear Factor kappa B (RANK), one of a large family of proinflammatory hgand receptors on leukocytes. 

Furthermore, adipose tissues were found to have some possible links between obesity and insulin resistance [89]. Obesity often causes insulin resistance, a decline in the ability of insulin to stimulate glucose uptake in the body leads to compensatory oversecretion of this hormone by the pancreatic cells and eventually, to cell exhaustion and development of type-2 diabetes mellitus [11,75]. Likewise in type-1 diabetes mellitus, the role of genetic factors has been studied to highlight the relation between inflammation, oxidant stress, and insulin insensitivity. Nuclear factor kappa B (NFkB) is a crucial transcription factor for response to oxidative stress and inflammation. Investigations about NFkB gene have shown its possible role in the susceptibility to type-1 diabetes by means of allelic differentiations, individuals with the AlO allele may be more likely to develop diabetes compared with those with the A14 allele [90]. 

In addition to mitochondria, other prosurvival signaling pathways such as nuclear factor kappa B (NFkB) and BCL-2 family proteins may also become targets for cancer therapy as CSCs generally have higher activities or expressions of these pathways. 

BMP, bone morphogenetic protein, acting as diflferentiation-inducer tumor suppressor. Click for BMP-induced osteosarcoma or rhabdomyosarcoma cell differentiation Geng S et al Mol Cancer Ther 2014 Apr 10 PMID 24723453 Wolf S et al Int J Oncol 2014 44 1727-35. In metastatic prostate cancer cells, their contact with bone marrow stromal cells induced BMP production resulting in tumor cell proliferation in androgen-liee media via protein kinase C/nuclear factor kappa B (NFkB (Lee GT et al Br J Cancer 2014 110 1634- ). 

TNK = TANK-binding kinase TANK = TRAF-family member-associated NFkB activator TRAP- (tumor necrosis factor receptor-associated factor-) associated nuclear factor kappa B activator STEAP, six transmembrane epithelial antigen, prostate. 

Nuclear factor kappa-B (NFkB), a redox-sensitive transcription factor regulating a battery of inflammatory genes, has been indicated to play a role in the development of numerous pathological states [189]. Activation of NFkB induces gene programs leading to transcription of factors that promote inflammation, such as leukocyte adhesion molecules, cytokines and chemokines [181]. 

The inhibition of nuclear factor kappa B (NFkB) translocation into the nucleus in activated macrophages with FR is effective for the suppression of the inflammatory reaction in rheumatoid arthritis (Morishita et al. 2004). NP-F could effectively deliver an NFkB decoy into the cytoplasm of activated macrophages via FR and was detected in the cytoplasm of activated murine macrophage-like RAW264.7 cells. NP-F also exhibited an inhibitory effect on the translocation of NFkB into the nucleus (Hattori et al. 2006). 

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