Nuclear factor-xB

Bao Z, Guan S, Cheng C, Wu S, Wong SH, Kemeny DM, Leung BP, Wong WSF. (2009) A novel anti-inflammatory role for andrographolide in asthma via inhibition of the nuclear factor-xB pathway. Am J Respir Crit Care Med 179 657-665. 

What is nuclear factor-xB (NF-xB) Describe the status of NF-xB in normal brain cells. What are the possible signaling mechanisms for the activation of NF-kB How is the activation of NF-kB related to neuroin-flaimnatory diseases like MS and meningitis ... 

Dicoumarol is an artefactual coumarin formed by putrefaction of ensiled sweet clover and has been employed as an anticoagulant because it inhibits quinone reductase activity and, therefore, the function of vitamin K in the way of synthesising coagulation factors. Given that quinones are involved in redox systems affecting mitogenic kinase cascades, dicoumarol was studied for its interaction with some of these enzymes. In fact dicoumarol prevented the activation of SAPK and of nuclear factor-xB (NF-kB) [59]. 

M. E. Ritchie, Nuclear factor-xB is selectively and markedly activated in humans with unstable angina pectoris, Circulation 98, 1707-1713 (1998). 

The antimalarial drug artemisinin extenuates amyloidogenesis and neuroinflammation in APPswe/PSldE9 transgenic mice via inhibition of nuclear factor-xB and NLRP3 inflammasome activation [559],... 

Ligation of a death receptor does not necessarily lead to caspase-8 activation and death. TNFR1 can also activate nuclear factor-xB (NF-kB) in cells that are resistant to TNFR1 -mediated apoptosis. Inhibition of this transcription factor can thus sensitize the cells to this particular form of cell death [38]. 

S.W. Ryter, C.J. Gomer (1993). Nuclear factor xB binding activity in mouse L1210 following Photofrin Il-mediated photosensitization. Photochem. Photobiol, 58,753-756. 

Fig. 4.4 Involvement of Fas and NMDA receptors in apoptotic and necrotic cell death. Fas ligand (FasL) Fas receptor (Fas-R) IV-methyl-D-aspartate receptor (NMDA-R) phosphatidylcholine (PtdCho) cytosolic phospholipase A2 (CPLA2) arachidonic add (ARA) arginine (Arg) nitric oxide synthase (NOS) nitric oxide (NO) superoxide (O2) peroxynitrite (ONOO ) arachidonic add (ARA) lyso-phosphatidylcholine (lyso-PtdCho) platelet-activating factor (PAF) cytochrome c (Cytc) apoptosome complex with apoptosis-activating factor-1 (Apaf-1) and poly(ADP)ribose polymerase (PARP) secretory phospholipase (SPLA2) inducible nitric oxide synthase (iNOS) cyclooxygenase-2 (COX-2) matrix metalloproteinase (MMP) nuclear factor-kappa B (NF-kB) inhibitory form of nuclear factor kappa B (I-kB/NF-kB) nuclear factor xB-response element (NF-kB-RE) inhibitory subunit of NF-kB (I-kB) tumor necrosis factor-a (TNF-a) interleukin-ip (IL-ip) and interleukin-6 (IL-6)...

L. Rodriguez-Manas, and C. F. Sdnchez-Ferrer, Glycosylated human oxyhemoglobin activates nuclear factor-xB and activator protein-1 in cultured human aortic smooth muscle, Br. J. Pharmacol, 140 (2003) 681-690. 

Teng YN, Chuang PJ, Liu YW. Nuclear factor-xB (NF-kB) regulates the expression of human testis-enriched leucine-rich repeats and WD repeat domain containing 1 (LRWDl) gene. Int J Med Sci. 2012 14 625-39. 

Specific chemokines are induced during/after ischemia and their time-dependent induction seems in accordance with the temporal profile of infiltration of blood cells. It is likely that the expression of chemokines is induced by proinflammatory cytokines which are produced in the ischemic area. For example, TNF-a and IL-1(3 activate transcription factors such as nuclear factor xB [62] that regulate the transcription of chemokines indicating that these proinflammatory cytokines activate the production of chemokines. Indeed expression of CCL2 mRN A in monocytes and astrocytes is induced by cytokines like IL-1 3 and TNFa and TGFp [63-65]. Furthermore, expression of CXCLIO in the brain is induced by interferon-y [66] and presumably also by factors such as IL-1 3 and TNFa. Cytokines produced in the ischemic area may thus be involved in the regulation of chemokine expression during the ischemic process. 

Under diabetic conditions, oxidative stress and endoplasmic reticulum stress are induced in various tissues [173, 176, 177, 178, 179]. Moreover, the y9-cells have very low levels of antioxidative enzymes, becoming them more susceptible to the stress [172]. ROS can function as signaling molecules to activate a number of cellular stress-sensitive pathways that cause cellular damage, and are ultimately responsible for the late complications of diabetes. Evidence suggests that common stress-activated signaling pathways such as nuclear factor nuclear factor-xB (NF-kB) [180, 181, 182], p38 mitogen-activated protein kinase (MARK) [183], protein kinase C (PKC) [184], toll-like receptors (TLRs) [185, 186], and c-Jun N-terminal kinase (INK) [187 188] underlie the development of these diabetic complications. 

Jove, M Planavila, A Sanehez, RM Merlos, M Laguna, JC Vazquez-Carrera, M. Palmitate Induees Tumor Necrosis Factor-a Expression in C2C12 Skeletal Muscle Cells by a Mechanism Involving Protein Kinase C and Nuclear Factor-xB Activation. Endocrinol 2006 147(1) 552-61. 

Using primary passage-1 human tracheobronchial epithehal cell cultures and an immortalised human bronchial epithehal cell line, HBEl, Harper et al. (2001) observed that tumour necrosis factor-a enhanced nuclear factor-xB (NF-xB) transcriptional activity. TNF-a activation coincided with translocation of NF-xB p65 from the cytoplasm to the nucleus. Pre-treatment with N-acetylcysteine (1-10 mM) inhibited TNF-a-induced activation of NF-xB transcriptional activity and lL-8 promoter-mediated reporter gene expression. In contrast, elevated thioredoxin protein levels in cells enhanced TNF-a-dependent NF-xB transcriptional activity and IL-8 promoter activity. 

In a rat type II pneumocyte analogue, the L2 cell line, exposed for 6 h to a combination of interferon-y (2,000 U/ml) and tumour necrosis factor-a (500 U/ml), extracellular superoxide dismutase and inducible nitric oxide synthase transcription was upregulated (Brady et al. 1997). Transcription of both genes was linked by activation of the transcription factor nuclear factor-xB. 

Upon lipopolysaccharide stimulation (1 tg/ml), Prabhu et al. (2002) found significantly higher iNOS transcript and protein expression levels with an increase in NO production in selenium-deficient RAW 264.7 cells than in the Se-complemented cells. Electrophoretic mobility-shift assays, nuclear factor-xB-luciferase reporter assays and Western blot analyses indicated that the increased expression of iNOS in Se deficiency could be due to an increased activation and consequent nuclear localization of the redox-sensitive transcription factor NF-xB. 

Activation of nuclear factor-xB is necessary for the induction of both TNF-a and Mn superoxide dismutase mRNAs by LPS (White et al. 2000). Neither hypoxia (1 % O2,5 % CO2, and 94 % N2) nor di-phenylene iodonium (0.5 to 5 pM) had any effect on LPS activation of nuclear factor-xB in human monocytes (White and Tsan 2001). Treatment of human alveolar macrophages with LPS, polymeric-and secretory-IgA, but not 12-0-tetradecanoyl-phorbol-13-acetate, induced NF-xB activation through IxBa phosphorylation and subsequent proteolysis (Ouadrhiri et al. 2002). 

Quinolinic acid-induced degradation of IxB-a, the cytoplasmic binding protein of the nuclear factor xB is almost totally mediated by a caspase-3-dependent mechanism, while kainic acid-induced IxB-a degradation is only partially dependent on caspase-3 (Nakai et al. 2000). A free radical scavenger (OPC-14117 600 mg/kg raf, orally) attenuated the effects of quinolinic acid but not kainic acid on IxB-a degradation, suggesting that oxidative stress contributes to the quinolinic acid- but not to the kainic acid-induced degradation of IxB-a. 

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