NF-KB transcription factor

Borgatti M., Breda L., Cortesi R., Nastruzzi C., Romanelli A., Saviano M., Bianchi N., Mischiatic C, Gambari R. Cationic liposomes as delivery systems for double-stranded PNA-DNA chimeras exhibiting decoy activity against NF-kB transcription factors. Biochem. Pharmacol. 2002 64 609-616. 

Romanelli A., Pedone C., Saviano M., Bianchi N., Borgatti M., Mischiati C., Gambari R. Molecular interactions between nuclear factor B (NF-kB) transcription factors and a PNADNA chimera mimicking NF-kB binding sites. Eur. J. Biochem. 2001 268 6066-6075. 

Stress signal For example, nrf-2, AP-1, NF-kB transcription factor translocation... 

A3 receptors have been associated with the PI3K/Akt pathway (Merighi et al. 2003). Active Akt causes a variety of biological effects, including suppression of apoptosis by phosphorylation and inactivation of several targets along pro-apoptotic pathways (Vivanco and Sawyers 2002). In particular, activated Akt is able to phos-phorylate a variety of downstream substrates, for example the pro-apoptotic molecule Bad, caspase-9, the forkhead family transcription factors, I-K (a kinase that regulates the NF-kB transcription factor) and Raf. 

NF-kB transcription factor found in all cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ulhaviolet irradiation, and bacterial or viral antigens. 

Transcription factors involved in AMP regulation are also responsible for the transcription of inflammatory and immunity genes in mammals, suggesting that the expression of these peptides is coordinated with the expression of other factors of innate immunity and acute inflammation [147,170,171]. IL-ip- and LPS/peptidoglycan-induced hBD-2 syntheses in monocytes and intestinal epithelial cells, respectively, require the NF-kB transcription factor [167,172-174], and the expression of hBD-2,3 by IL-22-induced keratinocytes depends on STAT3 [166]. Secretion of hBD-2 by keratinocytes stimulated by IL-ip or culture supernatants of Pseudomonas aeruginosa requires the activation of transcription factors NF-kB (p50-p65) and AP-1 (activator protein-... 

Role of NF-kB in the PPARa Activator MOA. Central to the PPARa activator MOA is NF-kB activation. NF-kB transcription factors play critical roles in cancer development and progression (Arsnra and Cavin 2005 Karin... 

Signal-Induced Degradation of a Cytosolic Inhibitor Protein Activates the NF-kB Transcription Factor... 

The examples in previous sections have demonstrated the importance of signal-induced phosphorylation in modulating the activity of many transcription factors. Another mechanism for regulating transcription factor activity in response to extracellular signals was revealed in studies with both mammalian cells and Drosophila. This mechanism, which involves phosphorylation and subsequent ubiquitin-mediated degradation of an Inhibitor protein, is exemplified by the NF-kB transcription factor. 

The NF-kB transcription factor regulates many genes that permit cells to respond to infection and Inflammation. 

The central features of the Toll-Dorsal pathway in flies, which are analogous to those of the mammalian NF-kB pathway discussed in Chapter 14, exist in mammals and probably in all animals. Dorsal is similar to the NF-kB transcription factor Cactus, to its inhibitor, I-kB and the Toll receptor, to the receptor for interleukin 1, which acts through Tube and Pelle equivalents to cause the phosphorylation of... 

Curcuminoids, a group of natural products originally isolated from the Indian spice turmeric, have been known to be potent antioxidant and antiinflammatory agents for many years. Curcuminoids reduce tissue factor (TF) gene expression through the inhibition of the AP-1 and NF-kB transcription factors and thus lead to the loss of angiogenesis initiation [61, 62]. 

Chen FE, Ghosh G Regulation of DNA binding by Rel/NF-kB transcription factors Structural views. Oncogene 1999 18 6845-6852. 

Pahl HL Activators and target genes of RoI/NF-kB transcription factors. Oncogene 1999 18 6853-6866. 

Yao, J., Mackman, N., Edgington, T.S., and Fan, S.-T. (1997) Lipopolysaccharide Induction of Tumor Necrosis Factor-a Promoter in Human Monoc5dic Cells Regulation by Egr-1, c-Jun, and NF-kB Transcription Factors, J. Biol. Chem. 272,17795-17801. 

Visekruna A, Volkov A, Steinhoff U. A key role Iot NF-kB transcription factor c-Rel in T-lymphoc54e-differentiation and effector functions. Clin Dev Immunol. 2012 2912 239368. doi 10.1155.2012/239368. 

Other mechanisms, apart from PPARy modulation, have been reported and proposed to explain the observed protective effects exerted by nitroalkenes. An important pro-inflammatory pathway regulated by NO2-FA is the translocation to the nucleus of the nuclear factor-kappa B (NF-kB) transcription factor (Cui et al. 2006 Rudolph et al. 2010). NF-kB remains inactive in the cytosol bounded to the IkB repressor both NO2-LA and NO2-OA modulate the release of the transcription factor by nitroalkylating the NF-KB-p65 protein subunit leading to a decrease on lipopoly-saccharide-induced secretion of pro-inflammatory cytokines in macrophages (e.g. IL-6, TNFa, MCP-1). Similar mechanisms were reported for the inhibition of the expression of the vascular cell adhesion molecule 1 (VCAM-1) as well as monocyte rolling and adhesion (Cui et al. 2006). 

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