Relevant bibliographies by topics / NF-kappa B pathway

Academic literature on the topic 'NF-kappa B pathway'

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Published: 11 March 2023

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Journal articles on the topic "NF-kappa B pathway"

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Johns, L. D., T. Sarr, and G. E. Ranges. "Inhibition of ceramide pathway does not affect ability of TNF-alpha to activate nuclear factor-kappa B." Journal of Immunology 152, no. 12 (June 15, 1994): 5877–82. http://dx.doi.org/10.4049/jimmunol.152.12.5877.

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Abstract TNF-alpha is a multifunctional cytokine that has been shown to activate a number of intracellular second messenger pathways. Recent studies demonstrate that the sphingomyelinase-ceramide pathway plays a potential role in the activation of nuclear factor-kappa B (NF-kappa B) by TNF-alpha. The following experiments both confirm that the addition of ceramide to cells can activate NF-kappa B and demonstrate that a 48-h pretreatment with phorbol 12-myristate (PMA) results in the loss of the ceramide-induced NF-kappa B response. In parallel experiments, in which SW480 cells were pretreated with PMA, TNF-alpha provided a signal resulting in the nuclear translocation of NF-kappa B that was similar to untreated cells. These data combined suggest that additional pathways exist that TNF-alpha can use for the activation of NF-kappa B. Supplementary data demonstrates that TNF-alpha, ceramide, and PMA activate a human cytomegalovirus-(HCMV) beta gal construct (promoter is responsive to NF-kappa B) that was stably transfected into the TNF receptor-bearing tumor cell line, SW480. PMA pretreatment of these cells resulted in a significant decrease in both the PMA and ceramide generated responses, 6% and 0% of controls, respectively. However, the response generated by TNF-alpha was not inhibited significantly (96% of control cells). This data suggests that although ceramide and 1,2-diacylglycerol (DAG) pathways may contribute to TNF-alpha activation of NF-kappa B, impedance of these pathways does not block TNF-alpha from activating NF-kappa B nor induction of the functional activation of the NF-kappa B responsive reporter construct, HCMV.
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Otieno, M. A., and M. W. Anders. "Cysteine S-conjugates activate transcription factor NF-kappa B in cultured renal epithelial cells." American Journal of Physiology-Renal Physiology 273, no. 1 (July 1, 1997): F136—F143. http://dx.doi.org/10.1152/ajprenal.1997.273.1.f136.

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Activation of NF-kappa B by the nephrotoxic and cytotoxic cysteine S-conjugate S-(1,2-dichlorovinyl)-L-cysteine (DCVC) was investigated in porcine kidney-derived LLC-PK1 cells. DCVC induced binding of nuclear proteins to an NF-kappa B consensus oligonucleotide from the immunoglobulin kappa-light chain enhancer region, as determined by electrophoretic mobility shift assays, and the activated proteins were identified as the p50/RelA heterodimeric complex of NF-kappa B. Transient transfection experiments with a kappa B-controlled luciferase reporter construct showed that the NF-kappa B complex activated by DCVC was transcriptionally active. NF-kappa B transactivation was blocked by inhibition of DCVC bioactivation with the cysteine conjugate beta-lyase inhibitor (aminooxy)acetic acid, by the antioxidants N,N'-diphenyl-p-phenylenediamine and N-acetyl-L-cysteine, and by the protein kinase inhibitor staurosporine. The cysteine S-conjugates S-(2-bromo-2-chloro-1,1-difluoroethyl)-L-cysteine and S-(2-chloro-1,1,2-trifluoroethyl)-L-cysteine also activated NF-kappa B in LLC-PK1 cells. These results demonstrate that the NF-kappa B pathway is present in LLC-PK1 cells and is induced by cysteine S-conjugates. Inhibition of DCVC-induced transactivation of NF-kappa B by staurosporine and by antioxidants indicate roles for protein kinases and oxidative stress in the NF-kappa B pathway.
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Berberich, I., G. L. Shu, and E. A. Clark. "Cross-linking CD40 on B cells rapidly activates nuclear factor-kappa B." Journal of Immunology 153, no. 10 (November 15, 1994): 4357–66. http://dx.doi.org/10.4049/jimmunol.153.10.4357.

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Abstract The B cell-associated surface molecule CD40 functions to regulate B cell responses. Cross-linking CD40 on B cells can lead to homotypic cell adhesion, IL-6 production, and, in combination with cytokines, to Ig isotype switching. Tyrosine kinase activity is increased shortly after engagement of this receptor. Little is known about how the very early events induced by CD40 cross-linking link to cellular responses. In this study, we demonstrate that nuclear factor (NF)-kappa B and NF-kappa B-like transcription factors are activated after cross-linking CD40 on resting human tonsillar B cells and on B cell lines. The activation is rapid and is mediated through a tyrosine kinase-dependent pathway. The complexes detected in electrophoretic mobility shift assays contain p50, p65 (RelA), c-Rel, and most likely other components. By using transient transfection assays, we found that cross-linking CD40 supports NF-kappa B-dependent gene expression. Our results define the NF-kappa B system as an intermediate event in CD40 signaling and suggest that the CD40 pathway can influence the expression of B cell-associated genes with NF-kappa B consensus sites.
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Lalmanach-Girard, A. C., T. C. Chiles, D. C. Parker, and T. L. Rothstein. "T cell-dependent induction of NF-kappa B in B cells." Journal of Experimental Medicine 177, no. 4 (April 1, 1993): 1215–19. http://dx.doi.org/10.1084/jem.177.4.1215.

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In comparison to B cell stimulation mediated by surface immunoglobulin (Ig) antigen receptor ligation, little is known about the intracellular events associated with T cell-dependent B cell responses. A model for the efferent phase of T cell-B cell interaction was used to examine the capacity of activated T cells to trigger nuclear expression of the trans-acting transcription factor, NF-kappa B, in B cells. Fixed, activated, but not fixed, resting Th2 cells were found to induce increased binding activity for a kappa B site-containing oligonucleotide in a time-dependent manner. This induction of NF-kappa B was eliminated by an antibody directed against a 39-kD cell interaction protein on activated T cells as well as by a soluble form of B cell CD40. Of particular relevance to intracellular signaling, NF-kappa B induction was not diminished by prior depletion of B cell protein kinase C (PKC) with phorbol myristate acetate. These results strongly suggest that T cell-dependent B cell stimulation is associated with NF-kappa B induction via p39-CD40 interaction and that this is brought about by non-PKC dependent signaling, in marked contrast to the previously documented requirement for PKC in sIg receptor-mediated stimulation. This suggest that NF-kappa B responds to more than one receptor-mediated intracellular signaling pathway in B cells and may be part of a "final common pathway" for B cell stimulation.
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Suzuki, Y. J., M. Mizuno, and L. Packer. "Signal transduction for nuclear factor-kappa B activation. Proposed location of antioxidant-inhibitable step." Journal of Immunology 153, no. 11 (December 1, 1994): 5008–15. http://dx.doi.org/10.4049/jimmunol.153.11.5008.

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Abstract Reactive oxygen species are thought to be messengers for nuclear factor (NF)-kappa B activation because its activation can be abrogated by antioxidants. However, this study identifies, for the first time, NF-kappa B activators that are insensitive to antioxidants. NF-kappa B activation that is induced by either calyculin A or okadaic acid (inhibitors of serine/threonine protein phosphatases 1 and 2A) is not blocked by N-acetylcysteine or dihydrolipoate in Jurkat and U937 cells. Nonetheless, these antioxidants block induction by TNF-alpha, lymphotoxin, and PMA. Unlike okadaic acid and calyculin A, neither TNF-alpha, lymphotoxin, nor PMA inhibited activities of phosphatases 1 and 2A. NF-kappa B activation induced by okadaic acid or calyculin A was not blocked by a myosin light chain kinase inhibitor, but was prevented by a protease inhibitor. The mitochondrial inhibitor, rotenone, also inhibited NF-kappa B activation by calyculin A; however, this inhibition was accompanied by a depletion of cellular ATP. These results suggest that 1) phosphatase inhibitors either target a component of signal transduction, which occurs downstream to an antioxidant-sensitive step or use distinct signaling pathways; 2) inhibition of phosphatases 1 and 2A is not a step in the pathway of TNF-alpha-, lymphotoxin-, or PMA-induced NF-kappa B activation; 3) myosin light chain kinase does not participate in NF-kappa B activation; and 4) activation of NF-kappa B by phosphatase inhibitors is controlled by proteases.
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Dominguez, I., L. Sanz, F. Arenzana-Seisdedos, M. T. Diaz-Meco, J. L. Virelizier, and J. Moscat. "Inhibition of protein kinase C zeta subspecies blocks the activation of an NF-kappa B-like activity in Xenopus laevis oocytes." Molecular and Cellular Biology 13, no. 2 (February 1993): 1290–95. http://dx.doi.org/10.1128/mcb.13.2.1290-1295.1993.

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Nuclear factor kappa B (NF-kappa B) plays a critical role in the regulation of a large variety of cellular genes. However, the mechanism whereby this nuclear factor is activated remains to be determined. In this report, we present evidence that in oocytes from Xenopus laevis, (i) ras p21- and phospholipase C (PLC)-mediated phosphatidylcholine (PC) hydrolysis activates NF-kappa B and (ii) protein kinase C zeta subspecies is involved in the activation of NF-kappa B in response to insulin/ras p21/PC-PLC. Thus, the microinjection of either ras p21 or PC-PLC, or the exposure of oocytes to insulin, promotes a significant translocation to the nucleus of an NF-kappa B-like activity. This effect is not observed when oocytes are incubated with phorbol myristate acetate or progesterone, both of which utilize a ras p21-independent pathway for oocyte activation. These data strongly suggest a critical role of the insulin/ras p21/PC-PLC/protein kinase C zeta pathway in the control of NF-kappa B activation.
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Dominguez, I., L. Sanz, F. Arenzana-Seisdedos, M. T. Diaz-Meco, J. L. Virelizier, and J. Moscat. "Inhibition of protein kinase C zeta subspecies blocks the activation of an NF-kappa B-like activity in Xenopus laevis oocytes." Molecular and Cellular Biology 13, no. 2 (February 1993): 1290–95. http://dx.doi.org/10.1128/mcb.13.2.1290.

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Nuclear factor kappa B (NF-kappa B) plays a critical role in the regulation of a large variety of cellular genes. However, the mechanism whereby this nuclear factor is activated remains to be determined. In this report, we present evidence that in oocytes from Xenopus laevis, (i) ras p21- and phospholipase C (PLC)-mediated phosphatidylcholine (PC) hydrolysis activates NF-kappa B and (ii) protein kinase C zeta subspecies is involved in the activation of NF-kappa B in response to insulin/ras p21/PC-PLC. Thus, the microinjection of either ras p21 or PC-PLC, or the exposure of oocytes to insulin, promotes a significant translocation to the nucleus of an NF-kappa B-like activity. This effect is not observed when oocytes are incubated with phorbol myristate acetate or progesterone, both of which utilize a ras p21-independent pathway for oocyte activation. These data strongly suggest a critical role of the insulin/ras p21/PC-PLC/protein kinase C zeta pathway in the control of NF-kappa B activation.
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Singh, Shareen, and Thakur Gurjeet Singh. "Role of Nuclear Factor Kappa B (NF-κB) Signalling in Neurodegenerative Diseases: An Mechanistic Approach." Current Neuropharmacology 18, no. 10 (November 4, 2020): 918–35. http://dx.doi.org/10.2174/1570159x18666200207120949.

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A transcriptional regulatory nuclear factor kappa B (NF-κB) protein is a modulator of cellular biological activity via binding to a promoter region in the nucleus and transcribing various protein genes. The recent research implicated the intensive role of nuclear factor kappa B (NF-κB) in diseases like autoimmune disorder, inflammatory, cardiovascular and neurodegenerative diseases. Therefore, targeting the nuclear factor kappa B (NF-κB) protein offers a new opportunity as a therapeutic approach. Activation of IκB kinase/NF-κB signaling pathway leads to the development of various pathological conditions in human beings, such as neurodegenerative, inflammatory disorders, autoimmune diseases, and cancer. Therefore, the transcriptional activity of IκB kinase/NF- κB is strongly regulated at various cascade pathways. The nuclear factor NF-kB pathway plays a major role in the expression of pro-inflammatory genes, including cytokines, chemokines, and adhesion molecules. In response to the diverse stimuli, the cytosolic sequestered NF-κB in an inactivated form by binding with an inhibitor molecule protein (IkB) gets phosphorylated and translocated into the nucleus further transcribing various genes necessary for modifying various cellular functions. The various researches confirmed the role of different family member proteins of NF-κB implicated in expressing various genes products and mediating various cellular cascades. MicroRNAs, as regulators of NF- κB microRNAs play important roles in the regulation of the inflammatory process. Therefore, the inhibitor of NF-κB and its family members plays a novel therapeutic target in preventing various diseases. Regulation of NF- κB signaling pathway may be a safe and effective treatment strategy for various disorders.
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Lin, K. I., S. H. Lee, R. Narayanan, J. M. Baraban, J. M. Hardwick, and R. R. Ratan. "Thiol agents and Bcl-2 identify an alphavirus-induced apoptotic pathway that requires activation of the transcription factor NF-kappa B." Journal of Cell Biology 131, no. 5 (December 1, 1995): 1149–61. http://dx.doi.org/10.1083/jcb.131.5.1149.

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Oxidative stress has been proposed as a common mediator of apoptotic death. To investigate further the role of oxidants in this process we have studied the effects of antioxidants on Sindbis virus (SV)-induced apoptosis in two cell lines, AT-3 (a prostate carcinoma line) and N18 (a neuroblastoma line). The thiol antioxidant, N-acetylcysteine (NAC), at concentrations above 30 mM, completely abrogates SV-induced apoptosis in AT-3 and N18 cells. The effects of NAC cannot be attributed to inhibition of viral entry or viral replication, changes in extracellular osmolarity or to increases in cellular glutathione levels, nor can they be mimicked by chelators of trace metals, inhibitors of lipid peroxidation or peroxide scavengers. In contrast, other thiol agents including pyrrolidine dithiocarbamate (PDTC, 75 microM) are protective. Because NAC and PDTC are among the most effective inhibitors of the transcription factor NF-kappa B, we examined SV's ability to activate NF-kappa B before the onset of morphologic or biochemical evidence of apoptosis. Within hours of infection, SV induced a robust increase in nuclear NF-kappa B activity in AT-3 and N18 cells; this activation was suppressible by NAC and PDTC. Over-expression of bcl-2 in AT-3 cells, which has been shown to inhibit SV-induced apoptosis, also inhibits SV-induced NF-kappa B activation. To determine if NF-kappa B activation is necessary for SV-induced apoptosis in these cells, we used double stranded oligonucleotides with consensus NF-kappa B sequences as transcription factor decoys (TFDs) to inhibit NF-kappa B binding to native DNA sites. Wild-type, but not mutant, TFDs inhibit SV-induced apoptosis in AT-3 cells. In contrast, TFD inhibition of NF-kappa B nuclear activity in N18 cells did not prevent SV-induced apoptosis. Taken together, these observations define a cell type-specific, transcription factor signaling pathway necessary for SV-induced apoptosis. Understanding the precise mechanism by which Bcl-2 and thiol agents inhibit SV-induced nuclear NF-kappa B activity in AT-3 cells may provide insights into the pluripotent antiapoptotic actions of these agents.
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Blackwell, T. S., T. R. Blackwell, E. P. Holden, B. W. Christman, and J. W. Christman. "In vivo antioxidant treatment suppresses nuclear factor-kappa B activation and neutrophilic lung inflammation." Journal of Immunology 157, no. 4 (August 15, 1996): 1630–37. http://dx.doi.org/10.4049/jimmunol.157.4.1630.

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Abstract We hypothesized that endotoxin injection in rats would stimulate in vivo nuclear factor-kappa B (NF-kappa B) activation in lung tissue and that antioxidant treatment before endotoxin injection would attenuate endotoxin-induced NF-kappa B activation, chemokine gene expression, and neutrophilic lung inflammation. We studied NF-kappa B activation in rat lung tissue following a single i.p. injection of endotoxin (6 mg/kg). After in vivo endotoxin treatment, lung NF-kappa B activation peaked at 2 h and temporally correlated with the expression of cytokine-induced neutrophil chemoattractant mRNA in lung tissue. Treatment with the antioxidant N-acetylcysteine (NAC) 1 h before endotoxin resulted in decreased lung NF-kappa B activation in a dose-dependent manner (from 200-1000 mg/kg) and diminished cytokine-induced neutrophil chemoattractant mRNA expression in lung tissue. Treatment with NAC significantly suppressed endotoxin-induced neutrophilic alveolitis. The average total lung lavage neutrophil count was 5.5 x 10(6) with endotoxin treatment vs 0.9 x 10(6) with NAC treatment before endotoxin. The NF-kappa B pathway represents an attractive therapeutic target for strategies to control neutrophilic inflammation and lung injury.
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Dissertations / Theses on the topic "NF-kappa B pathway"

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陳俊峯 and Chun-fung Anthony Chan. "Dysregulation of nuclear factor-kappa B (NF-KB) signaling pathway in hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31227156.

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Lupica, Joseph A. "Inhibition of the NF-kB signaling pathway and its effects on apoptosis and cancer." Cleveland, Ohio : Cleveland State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=csu1214235115.

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Thesis (Ph.D.)--Cleveland State University, 2008.
Abstract. Title from PDF t.p. (viewed on Oct. 6, 2008). Includes bibliographical references (p. 213-240). Available online via the OhioLINK ETD Center. Also available in print.
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Guo, Xiaoxia. "Nuclear Factor Kappa B Pathway and human cancer therapeutics." Thesis, University of Wolverhampton, 2009. http://hdl.handle.net/2436/88553.

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Cancer is one of the major causes of morbidity in the world. Although the overall survival of cancer has been significantly improved by chemotherapy in the last three decades, the success of cancer chemotherapy is still severely limited by the lack of selectivity of anti-cancer drugs to malignant cells leading to dose-limiting toxicity and the resistance of cancer cells to the conventional anti-cancer drugs. Gene-directed enzyme prodrug therapy (GDEPT) was designed to direct the anti-cancer drugs to specifically target the cancer cells by using cancer specific promoter to drive the expression of enzyme which can convert prodrug into anti-cancer drug specifically in cancer cells. However, this strategy is hindered by the lack of strong cancer specific promoters to specifically express drug-converting enzymes in cancer cells. In consequence, there is not enough anti-cancer drug activated inside the cancer cells. The first part of this study was to employ NF-κB binding sites as a novel enhancer system to improve the promoter activity of carcinoembryonic antigen (CEA) and human telomerase reverse transcriptase (hTERT) for GDEPT. In this system, the basal CEA promoter sequences were placed downstream of the 4 or 8 NF-κB DNA binding sites linked in tandem (κB4 or κB8). The system was designed to serve two particular purposes: to exploit the high levels of intratumoural NF-kB expression and keep the relative tumour specificity of the CEA and hTERT promoters. The results demonstrated that κB enhancer systems increased the transcriptional activity of CEA and hTERT promoter without compromising its cancer specificity. The fidelity of the κB4-CEA enhancer-promoter system was therefore improved by the increased transcriptional contrast between the cancer and normal cells. Moreover, in comparison with CEA promoter alone, κB-CEA enhancer-promoter system expressed human thymidine phosphorylase (TP) protein at significantly higher levels which were comparable to those expressed by CMV promoter. The κBCEA- TP system transfected cells demonstrated significantly higher sensitivity to 5'-Deoxy-5-Fluorouridine (5'-DFUR), a prodrug of 5-fluorouracil (5-FU). The second part of this study was involved in using NF-κB inhibitor as a chemosensitizer to sentizise the anti-cancer drug-induced chemoresistance cells to anti-cancer drugs. The results derived from this study manifested that the anti-alcoholism drug, Disulfiram (DS), and anti-inflammatory drug, triptolide (PG490), markedly enhanced the cytotoxicity of several conventional anti-cancer drugs in colon, lung and breast cancer cell lines. PG490 induced caspase-dependent cell death accompanied by a significant decrease in Bcl-2 levels. PG490 induced the expression of p53 and down-regulated p21 expression. This study indicated that some clinically used non-cancerchemotherapeutic drugs may be developed as chemosensitizers for cancer chemotherapy
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Sunami, Yoshiaki. "Molecular analysis of the non-canonical NF-kappaB pathway." Université Louis Pasteur (Strasbourg) (1971-2008), 2006. http://www.theses.fr/2006STR13177.

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On a montré ici que les voies canonique/non-canonique de NF-B ne sont pas indépendantes et qu’un rôle principal de la voie canonique est l’activation des acteurs de la voie non-canonique. La traduction est requise et la stimulation par LPS régule positivement un éventuel intermédiaire dans la signalisation par LPS/CD40 qui supporte l'activation de la voie non-canonique. De plus, la voie non-canonique est constitutivement activée dans les cellules de HL, impliquant la phosphorylation persistante de p100. L'activation transitoire et constitutive de la voie non-canonique implique l'incorporation de p100 et p52 dans un complexe « megadalton ». TAP a permis d’identifier des partenaires interagissant avec p100. EDD (une molécule identifiée) induit le processing de p100 par co-expression. La formation du complexe de TRAF3 (autre facteur identifié) avec p100 est médiée par NIK et requiert son activité kinase. L'expression de NIK favorise le recrutement de TRAF3/p100 au signalosome p100
It is shown here that the canonical/non-canonical NF-B pathways are not independent and a master regulatory role of the canonical pathway is to upregulate activators of the non-canonical pathway. The data further implicate a translation requirement and that LPS stimulation upregulates a potential intermediate in LPS/CD40 signaling which supports activation of the non-canonical pathway. Further, the non-canonical pathway is constitutively activated in HL cells, involving persistent p100 phosphorylation. It was found that transient and constitutive activation of the non-canonical pathway involves incorporation of p100 and p52 into a megadalton complex. TAP was employed to identify novel p100 interacting partners. EDD (an identified molecule) induces processing of p100 upon co-expression. The complex formation of TRAF3 (another p100 interactor) with p100 is mediated by NIK and requires its kinase activity. The expression of NIK promotes recruitment of TRAF3/p100 to the p100 signalosome
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Torrie, Lindsay J. "Characterisation of the lipopolysaccharide stimulated NF#kappa#B signal transduction pathway in rat aortic smooth muscle cell." Thesis, University of Strathclyde, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249146.

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Konieczkowski, David Joseph. "Systematic approaches to overcoming limitations of MAPK pathway inhibition in melanoma." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11094.

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Metastatic melanoma is an aggressive, incurable cancer with historically few therapeutic options. The discovery that 60% of melanomas harbor the oncogenic BRAF_V600E mutation, which constitutively activates the MAPK pathway, has provided a promising new therapeutic axis. Although MAPK pathway inhibitor therapy has shown striking clinical results in BRAF_V600-mutant melanoma, this approach faces three limitations. First, 10-20% of BRAF_V600-mutant melanomas never achieve meaningful response to MAPK pathway inhibitor therapy (intrinsic resistance). Second, among BRAF_V600-mutant melanomas initially responding to MAPK pathway inhibitor therapy, relapse is universal (acquired resistance). Third, approximately 40% of melanomas lack BRAF_V600 mutations and so are not currently candidates for MAPK pathway inhibitor therapy. We sought to address each of these problems: by characterizing the phenomenon of intrinsic MAPK pathway inhibitor resistance, by finding ways to perturb mechanisms of acquired MAPK pathway inhibitor resistance, and by identifying novel dependencies in melanoma outside of the MAPK pathway. Intriguingly, the NF-kappa B pathway emerged as a common theme across these investigations. In particular, we establish that MAPK pathway inhibitor sensitive and resistant melanomas display distinct transcriptional signatures. Unlike most BRAF_V600-mutant melanomas, which highly express the melanocytic lineage transcription factor MITF, MAPK pathway inhibitor resistant lines display low MITF expression but high levels of NF-kappa B signaling. These divergent transcriptional states, which arise in melanocytes from aberrant MAPK pathway activation by BRAF_V600E, remain plastic and mutually antagonistic in established melanomas. Together, these results characterize a dichotomy between MITF and NF-kappa B cellular states as a determinant of intrinsic sensitivity versus resistance to MAPK pathway inhibitors in BRAF_V600-mutant melanoma. In separate investigations, we have shown that, NFKB1 p105, a member of the NF-kappa B family, intimately regulates levels of COT, a known effector of resistance to MAPK pathway inhibitors. Moreover, we have used shRNA screening to nominate particular nodes within the NF-kappa B pathway, including MYD88 and IRF3, as candidate melanoma lineage-specific dependencies. Cumulatively, although these studies use diverse approaches to investigate the limitations of MAPK pathway inhibitor therapy in melanoma, they converge in nominating the NF-kappa B pathway as a previously underappreciated feature of melanoma biology and suggest the relevance of this pathway for future investigation.
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Bu, De-xiu. "The nuclear factor k[kappa]B signal transduction pathway : its role in atherogenesis and intimal hyperplasia /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-615-8/.

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Cai, Chunhui, and 蔡春晖. "TAK1 promotes ovarian cancer aggressiveness through activation of NF-kB pathway." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193410.

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Ovarian cancer is one of the most deadly female malignancies. Despite advances in the treatment of ovarian cancer for the past decade, the cure rate of this disease is moderately improved. Emerging evidence suggests the molecular personalized therapeutic approach become popular for human cancer treatment. The nuclear factor-kappa B (NF-κB) signaling pathway has been shown to play multiple roles in cancer progression such as anti-apoptosis, cell cycle, angiogenesis and metastasis. This study attempted to characterize the functional roles of transforming growth factor (TGF)-β-activating kinase 1 (TAK1) in the activation of NF-κB signaling. Importantly, this study provided evidence showing the significance of TAK1-NF-κB signaling axis in ovarian cancer aggressiveness during omental metastasis. Using quantitative RT-PCR and immunohistochemical analyses, TAK1 was frequently up-regulated and was significantly associated with high-grade (P=0.001), lymph node and distant metastasis (P=0.025), as well as a tendency toward advanced stage ovarian cancers (P=0.08). Functionally, enforced expression of TAK1 could augment cell proliferation, colony formation, anchorage-independent growth ability and migration/invasion in ovarian cancer cells. Conversely, repression of TAK1 expression by genetically or pharmaceutical approach abrogated these tumorigenic capacities including tumor growth in vivo. Furthermore, co-treatment of (5Z) -7-Oxozeaenol could sensitize ovarian cancer cells to cisplatin-induced cell apoptosis, indicating TAK1 is also involved in chemoresistance. Mechanistically, using Western blotting and NF-κB -reporter luciferase analyses, the elevation of TAK1 phosphorylation at Ser412 but not Thr184/187 was found to associate with the activation of NF-κB in ovarian cancer cells solely. A series of functional studies with genetic and pharmaceutical alterations revealed that the increased TAK1 Ser412 phosphorylation was required for exerting the ovarian cancer cell oncogenesis. Omental metastasis is the common phenomenon observed in most of advanced-stage ovarian cancer. Using omentum conditioned medium (OCM), the findings of this study showed that the omentum tissue was able to secrete numerous factors including chemokines such as GRO-α and IL8 in activating TAK1-NF-κB signaling cascade, which thereby induced increased oncogenic capacities in cell growth, migration and invasion. Taken together, this study suggests that TAK1-NF-κB signaling axis is indispensable for promoting oncogenesis of ovarian cancer and targeting this pathway may be a promising personalized cancer therapeutic approach in ovarian cancer.
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Shaikh, Raziya Banu. "Light related TNF cytokines and the NF-[kappa]B pathway in development and function of mucosal and NK T cells /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2003. http://wwwlib.umi.com/cr/ucsd/fullcit?p3091315.

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Cude, Kelly J. "Activation of a novel ERK5-NF-kappaB pathway is required for G2/M progression in the cell cycle /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/5003.

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Books on the topic "NF-kappa B pathway"

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Hajra, Leena. The NF-[kappa]B signal transduction pathway in aortic endothelial cells is primed for activation in regions predisposed to atherosclerotic lesion formation. Ottawa: National Library of Canada, 2000.

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Book chapters on the topic "NF-kappa B pathway"

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Okamoto, Takashi, Shinsaku Sakurada, Yang Jian-Ping, and Naoko Takahashi. "Redox Regulation of the Nuclear Factor Kappa B (NF-κB) Signaling Pathway and Disease Control." In Oxygen Homeostasis and Its Dynamics, 438–49. Tokyo: Springer Japan, 1998. http://dx.doi.org/10.1007/978-4-431-68476-3_55.

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Klaidman, Lori. "Phytochemicals as Modulators of Signaling in Inflammation." In Extracellular and Intracellular Signaling, 230–46. The Royal Society of Chemistry, 2011. http://dx.doi.org/10.1039/bk9781849733434-00230.

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Inflammatory pathways are involved in numerous chronic conditions such as arthritis, autoimmune disorders, heart disease, neurodegeneration, cancer, diabetes and obesity. Inflammation is mediated primarily by NF-κB (nuclear factor kappa-light chain-enhancer of activated B cells) in cells. NF-κB is part of a signal transduction pathway activated by surface cell receptors, stimulated by ligands such as cytokines in immune cells. This triggers the translocation of activated NF-κB into the nucleus. NF-κB then binds to DNA response elements and promotes the transcription of inflammatory proteins. During chronic conditions, gene products of NF-κB activation tend to amplify injury to bystander tissues, resulting in further localized injury. Many phytochemicals can limit this excessive cellular damage by blocking translocation of NF-κB into the nucleus. Many natural products also exert indirect control over NF-κB, such as through peroxisome proliferator activated receptor-γ (PPARγ) and liver X receptor (LXR). PPARγ and LXR are transcription factors that control lipid and cholesterol metabolism. However, the activation of PPARγ and LXR also promotes a simultaneous repression of NF-κB pathways and, hence, attenuates inflammation. A well-known class of drugs that act as gonists of PPARγ are the thiazolidinediones, used in diabetes. However, many agonists of PPARγ and LXR also consist of natural products. Thus, it may be possible to inhibit NF-κB pathways directly or stimulate PPARγ and LXR induced repression of inflammatory pathways using phytochemicals in physio-logic doses from moderate dietary intake.
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Shivshankar M., Gunjegaonkar, Joshi Amol A., Wankhede Sagar B., Siraskar Balasaheb D., Merekar Abhijit N., and Shinde Sachin D. "Potential Defensive Involvement of Methyl Jasmonate in Oxidative Stress and Its Related Molecular Mechanisms." In Plant Hormones - Recent Advances, New Perspectives and Applications [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102783.

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Jasmonic acid (JA), cytokinins (CK), gibberellins (GA), abscisic acid (ABA), ethylene (ET), and salicylic acid (SA) are potent plant stress hormones (phytohormones/PTH). Methyl jasmonate (MeJA), a volatile ester of JA, is derived from the petals of Jasminum grandiflorum (jasmine). The MeJA has been meticulously confirmed for its food, agricultural, and therapeutic uses in the treatment of a range of serious illnesses. Several scientific articles have studied and reported on the role of free radicals in the development of life-threatening clinical illnesses. The inflammatory signaling pathway is triggered by a weak or interfering endogenous antioxidant system, or the elaborated production of free radicals, which causes damage to key cellular components. The current chapter focused on and demonstrated MeJA’s multifunctional role in antioxidant and anti-inflammatory signaling mechanisms such as inhibition of NF-B (nuclear factor kappa-light-chain-enhancer of activated B cells), mitogen-activated protein kinase (MAPK or MAP kinase) pathway inhibition/down-regulation of pro-inflammatory mediators (IL, TNF-), cyclo-oxygenase (COX), and (LOX). The antioxidant effect of MeJA’s interaction with miRNA, transcription of nuclear factor erythroid 2-related 2 (Nfr2), activation of sirtuins (SIRTs), antioxidant and redox signaling pathway were also discussed in the chapter.
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Tiwari, Vinod, Ankit Uniyal, Vineeta Tiwari, Vaibhav Thakur, Mousmi Rani, and Akhilesh. "Delineating the Neuroinflammatory Crosstalk in Neurodegeneration and Probing the Near Future Therapeutics." In Traditional Medicine for Neuronal Health, 24–46. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815040197123010005.

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Neurodegenerative disorders are threatening mankind with significant health and economic burden. Neurodegeneration involves the deterioration of neurons in the central nervous system (CNS), resulting in decreased neuronal survival. Therefore, it is of utmost requirement to develop a promising pharmacological strategy to minimize or prevent the progression of the underlying disease pathogenesis. In neurodegenerative disease conditions, neurons and glial cells present in the specific brain regions are damaged and depraved, resulting in specified disease symptoms in the patients. Neuroinflammation plays a major role in the degeneration of neuronal cells by regulating the expression of interleukin-1 beta (IL-1β), IL-6, IL-8, IL-33, tumor necrosis factor-alpha (TNF-α), chemokines Cxcl3 (C-C motif) ligand 2 (CCL2), CXCL5, granulocyte-macrophage colony-stimulating factor (GM-CSF), glia maturation factor (GMF), substance P, reactive oxygen species (ROS), reactive nitrogen species (RNS), impaired tuning of immune cells and nuclear factor kappa-B (NF-κB). Considering this, it is very important to understand the in-depth role of neuroinflammation in the initiation and progression of various neurodegenerative diseases, including Alzheimer's Disease (AD), Parkinson's Disease (PD), Huntington's Disease (HD), as well as Multiple Sclerosis (MS). Recent shreds of evidence have suggested that using exogenous ligands to approach various biological molecules or cellular functioning that modulates the neuroinflammation, such as microglia response, P2X7 receptors, TLR receptors, oxidative stress, PPARγ, NF-κB signaling pathway, NLRP3 inflammasome, caspase-1 signaling pathway, and mitochondrial dysfunction, helps to combat neurodegeneration in a variety of diseases. Thus, targeting the neuroinflammatory drive could provide a beacon for the management of neurodegenerative diseases. Here, we have attempted to provide comprehensive literature suggesting the role of neuroinflammation in neurodegeneration and its implication in the development of near-future neurotherapeutics.
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"The PI3K/Akt-NF-kappa B Signaling Pathway and Hypoxia-induced Mitogenic Factor in Vascular Adhesion Molecule 1 Gene Expression." In Adhesion Molecules, 97–101. CRC Press, 2016. http://dx.doi.org/10.1201/9780429196393-16.

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Li, Dechun. "The PI3K/Akt-NF-kappa B Signaling Pathway and Hypoxia-induced Mitogenic Factor in Vascular Adhesion Molecule 1 Gene Expression." In Adhesion Molecules, 87–102. Science Publishers, 2010. http://dx.doi.org/10.1201/b10167-7.

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Tarı Selçuk, Kevser. "Epidemiology of Inflammation-Related Diseases." In Role of Nutrition in Providing Pro-/Anti-Inflammatory Balance, 24–44. IGI Global, 2020. http://dx.doi.org/10.4018/978-1-7998-3594-3.ch002.

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Inflammation, a vital defense mechanism for health, is defined as the immune system's response to harmful stimuli such as pathogens, damaged cells, toxic compounds or irradiation. Inflammation is usually examined in two groups: acute and chronic. Chronic inflammation instigates various kinds of diseases that cause premature mortality and morbidity such us cardiovascular diseases, cancer, diabetes mellitus (DM), asthma-chronic obstructive pulmonary disease (COPD), obesity, metabolic syndrome (METs), inflammatory bowel disease (IBD), rheumatoid arthritis (RA), multiple sclerosis (MS), osteoporosis, and neurological diseases via dysregulation of various signaling pathways such as nuclear factor kappa-B (NF-κB), signal transducer, activator of transcription 3 (STAT3), etc. These inflammation-related diseases are among the major causes of mortality and morbidity in almost every region of the world. Studies have shown that these diseases associated with inflammation have tended to increase worldwide.
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Conference papers on the topic "NF-kappa B pathway"

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Feng, Yu-xiong, Jiang-Sha Zhao, Shu-Qun Cheng, Yunfei Yuan, Xiao-fan Wang, and Dong Xie. "Abstract 4109: EphrinA2 promotes tumorigenicity through Rac1/Akt/NF-kappa B signaling pathway in liver cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4109.

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Yuan, Q., and X. Gao. "AB0072 Rational designed gold nanoparticle suppresses rankl-induced osteoclastogenesis in raw264.7 cells via NF-KAPPA B pathway and MAPK pathways." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.2087.

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Zhou, Rui, Hong Zhang, Chi Shing Cho, Sze Chuen Wong, Mei Tian, and Wing Chi Chan. "Abstract 1116: The role of ADAM9 and PI3K-dependent NF-kappa B pathway in promoting metastasis of triple-negative breast cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1116.

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Zhou, Rui, Hong Zhang, Chi Shing Cho, Sze Chuen Wong, Mei Tian, and Wing Chi Chan. "Abstract 1116: The role of ADAM9 and PI3K-dependent NF-kappa B pathway in promoting metastasis of triple-negative breast cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1116.

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Lee, Dongheon, Yufang Ding, Arul Jayaraman, and Joseph Sang-Il Kwon. "Integrative Approach to Extract the Single-cell Dynamics of LPS-induced $\text{NF}\kappa\mathrm{B}$ Signal Pathway through Flow Cytometry Measurements and Parameter Estimation." In 2018 Annual American Control Conference (ACC). IEEE, 2018. http://dx.doi.org/10.23919/acc.2018.8430917.

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Hinohara, Kunihiko, Michiko Murohashi, Masahiko Kuroda, Takayuki Isagawa, Shingo Tsuji, Seiichiro Kobayashi, Kazuo Umezawa, Arinobu Tojo, Hiroyuki Aburatani, and Noriko Gotoh. "Abstract 4218: Potential roles of NF-kappa B pathways in breast cancer-initiating cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4218.

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Tully, Jane E., James D. Nolin, Sidra M. Hoffman, Amy Guala, and Karolyn G. Lahue. "Coordinate Activation Of Classical And Alternative NF-kappa B Pathways In Lung Epithelial Cells Dictates The Strength And Nature Of Lipopolyssacharide-Induced Pro-Inflammatory Mediators." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1348.

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Reports on the topic "NF-kappa B pathway"

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Harper, Jeffrey. Regulation of NF (kappa) B-Dependent Cell Survival Signals Through the SCF (Slimb) Ubiquitin Ligase Pathway. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada395543.

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Harper, Jeffrey. Regulation of NF (kappa) B-dependent Cell Survival Signals Through the SCF (slimb) Ubiquitin Ligase Pathway. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396779.

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Harper, Jeffrey. Regulation of NF (kappa) B-Dependent Cell Survival Signals Through the SCF (Slimb) Ubiquitin Ligase Pathway. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada407554.

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