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Relevant bibliographies by topics / Via NF-κB

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Academic literature on the topic 'Via NF-κB'

Author: Grafiati

Published: 10 September 2021

Last updated: 12 February 2022

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Journal articles on the topic "Via NF-κB"

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Mattson, Mark P. "Insulating axons via NF-κB". Nature Neuroscience 6, № 2 (2003): 105–6. http://dx.doi.org/10.1038/nn0203-105.

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Yu, Liang, Abdalla J. Mohamed, Oscar E. Simonson та ін. "Proteasome-dependent autoregulation of Bruton tyrosine kinase (Btk) promoter via NF-κB". Blood 111, № 9 (2008): 4617–26. http://dx.doi.org/10.1182/blood-2007-10-121137.

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Abstract Bruton tyrosine kinase (Btk) is critical for B-cell development. Btk regulates a plethora of signaling proteins, among them nuclear factor-[κ]B (NF-κB). Activation of NF-κB is a hallmark of B cells, and NF-κB signaling is severely compromised in Btk deficiency. We here present strong evidence indicating that NF-κB is required for efficient transcription of the Btk gene. First, we found that proteasome blockers and inhibitors of NF-κB signaling suppress Btk transcription and intracellular expression. Similar to Btk, proteasome inhibitors also reduced the expression of other members of this family of kinases, Itk, Bmx, and Tec. Second, 2 functional NF-κB–binding sites were found in the Btk promoter. Moreover, in live mice, by hydrodynamic transfection, we show that bortezomib (a blocker of proteasomes and NF-κB signaling), as well as NF-κB binding sequence-oligonucleotide decoys block Btk transcription. We also demonstrate that Btk induces NF-κB activity in mice. Collectively, we show that Btk uses a positive autoregulatory feedback mechanism to stimulate transcription from its own promoter via NF-κB.

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Huang, Bo, Xiao-Dong Yang, Ming-Ming Zhou, Keiko Ozato та Lin-Feng Chen. "Brd4 Coactivates Transcriptional Activation of NF-κB via Specific Binding to Acetylated RelA". Molecular and Cellular Biology 29, № 5 (2008): 1375–87. http://dx.doi.org/10.1128/mcb.01365-08.

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ABSTRACT Acetylation of the RelA subunit of NF-κB, especially at lysine-310, is critical for the transcriptional activation of NF-κB and the expression of inflammatory genes. In this study, we demonstrate that bromodomains of Brd4 bind to acetylated lysine-310. Brd4 enhances transcriptional activation of NF-κB and the expression of a subset of NF-κB-responsive inflammatory genes in an acetylated lysine-310-dependent manner. Bromodomains of Brd4 and acetylated lysine-310 of RelA are both required for the mutual interaction and coactivation function of Brd4. Finally, we demonstrate that Brd4 further recruits CDK9 to phosphorylate C-terminal domain of RNA polymerase II and facilitate the transcription of NF-κB-dependent inflammatory genes. Our results identify Brd4 as a novel coactivator of NF-κB through specifically binding to acetylated lysine-310 of RelA. In addition, these studies reveal a mechanism by which acetylated RelA stimulates the transcriptional activity of NF-κB and the NF-κB-dependent inflammatory response.

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Chow, Jimmy Y. C., Makiko Ban, Helen L. Wu та ін. "TGF-β downregulates PTEN via activation of NF-κB in pancreatic cancer cells". American Journal of Physiology-Gastrointestinal and Liver Physiology 298, № 2 (2010): G275—G282. http://dx.doi.org/10.1152/ajpgi.00344.2009.

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TGF-β utilizes receptor-activated SMAD signaling to mediate growth suppression; however, non-SMAD signaling that modulates the TGF-β response in epithelial cells become apparent when the SMAD signaling is abrogated, a common occurrence in pancreatic cancers. Here, we examined whether TGF-β utilized NF-κB to downregulate PTEN, a gene that is rarely mutated in pancreatic cancers. SMAD4-null BxPc3 and CAPAN-1 pancreatic cancer cells were treated with TGF-β (10 ng/ml) and lysed, and cellular proteins were analyzed by Western blots using p-IκB, p65, and PTEN antibodies. PTEN promoter and NF-κB activities were assessed by PTEN-luc and p-NF-luc constructs, respectively. Dominant negative p-IκB-α-M (NF-κB superrepressor) was used to block activation of NF-κB. Cell motility was assessed by Boyden chamber migration assay. TGF-β induced IκB-α phosphorylation followed by NF-κB p65 subunit nuclear translocation and increased NF-κB activity. IκB-α-M blocked TGF-β-induced NF-κB activity, reversed downregulated PTEN promoter activity and PTEN expression, and prevented augmentation of cell motility induced by TGF-β. SMAD4 restoration, but not knockdown of SMAD2 and/or 3, reversed TGF-β-induced NF-κB activity. Thus TGF-β suppresses PTEN in pancreatic cancer cells through NF-κB activation and enhances cell motility and invasiveness in a SMAD4-independent manner that can be counteracted when TGF-β-SMAD signaling is restored. The TGF-β/NF-κB/PTEN cascade may be a critical pathway for pancreatic cancer cells to proliferate and metastasize.

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Hsu, Fei-Ting, Yu-Chang Liu, Tsu-Te Liu та Jeng-Jong Hwang. "Curcumin Sensitizes Hepatocellular Carcinoma Cells to Radiation via Suppression of Radiation-Induced NF-κB Activity". BioMed Research International 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/363671.

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The effects and possible underlying mechanism of curcumin combined with radiation in human hepatocellular carcinoma (HCC) cellsin vitrowere evaluated. The effects of curcumin, radiation, and combination of both on cell viability, apoptosis, NF-κB activation, and expressions of NF-κB downstream effector proteins were investigated with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), NF-κB reporter gene, mitochondrial membrane potential (MMP), electrophoretic mobility shift (EMSA), and Western blot assays in Huh7-NF-κB-luc2, Hep3B, and HepG2 cells. Effect of I kappa B alpha mutant (IκBαM) vector, a specific inhibitor of NF-κB activation, on radiation-induced loss of MMP was also evaluated. Results show that curcumin not only significantly enhances radiation-induced cytotoxicity and depletion of MMP but inhibits radiation-induced NF-κB activity and expressions of NF-κB downstream proteins in HCC cells. IκBαM vector also shows similar effects. In conclusion, we suggest that curcumin augments anticancer effects of radiation via the suppression of NF-κB activation.

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Shiota, Masaki, Akira Yokomizo, Ario Takeuchi та ін. "Protein kinase C regulates Twist1 expression via NF-κB in prostate cancer". Endocrine-Related Cancer 24, № 4 (2017): 171–80. http://dx.doi.org/10.1530/erc-16-0384.

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The progression of prostate cancer to metastatic and castration-resistant disease represents a critical step. We previously showed that protein kinase C (PKC) activation followed by Twist1 and androgen receptor (AR) induction played a critical role in castration resistance, but the precise molecular mechanism remains unknown. This study aimed to elucidate the relevant molecular mechanism, focusing on NF-κB transcription factor. We examined the activity of NF-κB after PKC inhibition, and the expression of Twist1 and AR after inhibition of NF-κB in human prostate cancer cells. We also investigated the status of PKC/NF-κB after inhibition of AR signaling in cells resistant to hormonal therapy. As a result, inhibition of PKC signaling using knockdown and small-molecule inhibition of PKC suppressed RelA activity, while blocking NF-κB suppressed Twist1 and AR expression. Conversely, inhibition of AR signaling by androgen depletion and the novel antiandrogen enzalutamide induced PKC and RelA activation, resulting in Twist1/AR induction at the transcript level. Moreover, inhibition of NF-κB signaling prevented enzalutamide-induced Twist1 and AR induction. Finally, NF-κB was activated in both castration-resistant and enzalutamide-resistant cells. In conclusion, NF-κB signaling was responsible for Twist1 upregulation by PKC in response to AR inhibition, resulting in aberrant activation of AR. NF-κB signaling thus appears to play a critical role in promoting both castration resistance and enzalutamide resistance in PKC/Twist1 signaling in prostate cancer.

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Zaidi, Adeel H., та Sunil K. Manna. "Profilin–PTEN interaction suppresses NF-κB activation via inhibition of IKK phosphorylation". Biochemical Journal 473, № 7 (2016): 859–72. http://dx.doi.org/10.1042/bj20150624.

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Profilin-mediated tumour suppression involving nuclear transcription factor κB (NF-κB) is unknown. Profilin interacts with protein phosphatase, phosphatase and tension homologue (PTEN) and stabilizes it. Sustained PTEN level inhibits phosphorylation of IκBα kinase (IKK) and subsequently, down-regulates NF-κB and enhances cell death. Profilin acts as tumor suppressor via NF-κB inhibition.

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Hou, Yu-Chen, Wan-Chun Chiu, Chiu-Li Yeh та Sung-Ling Yeh. "Glutamine modulates lipopolysaccharide-induced activation of NF-κB via the Akt/mTOR pathway in lung epithelial cells". American Journal of Physiology-Lung Cellular and Molecular Physiology 302, № 1 (2012): L174—L183. http://dx.doi.org/10.1152/ajplung.00066.2011.

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Lung epithelial cells are important barriers in the respiratory system that provoke inflammatory responses through nuclear factor (NF)-κB activation to prevent pathogens from invading the body. Lipopolysaccharide (LPS) is a common pathogen-associated stimulus that activates IκB kinase (IKK) to regulate NF-κB-mediated inflammation through modulating nuclear translocation and phosphorylation of NF-κB. Previously, it was shown that Akt and the mammalian target of rapamycin (mTOR) are involved in the phosphorylation of IKK to activate NF-κB. Herein, we demonstrate that glutamine (GLN) modulated LPS-induced activation of NF-κB through the Akt/mTOR/IKK pathway in BEAS-2B cells. BEAS-2B cells in submerged culture were placed in medium containing different concentrations of GLN (0, 0.5, 1, and 2.5 mM) with 1 μg/ml LPS. Results showed that GLN deprivation induced phosphorylation of Akt/mTOR/IKK signaling, increased levels of NF-κB nuclear translocation and phosphorylated NF-κB, and upregulated NF-κB-dependent transcriptional activity, which was suppressed by GLN administration. Expressions of NF-κB-targeted genes were also reduced by supplemental GLN. GLN administration improved cell viability, whereas 0.5 mM GLN had a greater extent of inhibition on the Akt/mTOR/IKK/NF-κB signaling cascade. The inhibitory effects of GLN on NF-κB activation were also observed in cells cultured under air-liquid interface condition. These results indicate that GLN deprivation increased LPS-induced NF-κB activation and transcriptional activity, which was reversed by GLN administration. The findings provide potential mechanisms of GLN's modulation of LPS-induced NF-κB activation in lung epithelial cells and imply that maintaining a physiological concentration of GLN is essential in preventing LPS-induced lung inflammation.

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D’Ignazio, Laura, Dilem Shakir, Michael Batie, H. Arno Muller та Sonia Rocha. "HIF-1β Positively Regulates NF-κB Activity via Direct Control of TRAF6". International Journal of Molecular Sciences 21, № 8 (2020): 3000. http://dx.doi.org/10.3390/ijms21083000.

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NF-κB signalling is crucial for cellular responses to inflammation but is also associated with the hypoxia response. NF-κB and hypoxia inducible factor (HIF) transcription factors possess an intense molecular crosstalk. Although it is known that HIF-1α modulates NF-κB transcriptional response, very little is understood regarding how HIF-1β contributes to NF-κB signalling. Here, we demonstrate that HIF-1β is required for full NF-κB activation in cells following canonical and non-canonical stimuli. We found that HIF-1β specifically controls TRAF6 expression in human cells but also in Drosophila melanogaster. HIF-1β binds to the TRAF6 gene and controls its expression independently of HIF-1α. Furthermore, exogenous TRAF6 expression is able to rescue all of the cellular phenotypes observed in the absence of HIF-1β. These results indicate that HIF-1β is an important regulator of NF-κB with consequences for homeostasis and human disease.

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Tas, Sander W., Margriet J. Vervoordeldonk, Najat Hajji та ін. "Noncanonical NF-κB signaling in dendritic cells is required for indoleamine 2,3-dioxygenase (IDO) induction and immune regulation". Blood 110, № 5 (2007): 1540–49. http://dx.doi.org/10.1182/blood-2006-11-056010.

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Abstract Ligation of CD40 on dendritic cells (DCs) induces early production of inflammatory mediators via canonical NF-κB signaling, as well as late expression of the anti-inflammatory enzyme indoleamine 2,3-dioxygenase (IDO) via unknown signal transduction. By selective blocking of either the canonical NF-κB pathway using the NEMO-binding domain peptide or the noncanonical NF-κB pathway by small interfering RNA, we demonstrate that IDO expression requires noncanonical NF-κB signaling. Also, noncanonical NF-κB signaling down-regulates proinflammatory cytokine production in DCs. In addition, selective activation of the noncanonical NF-κB pathway results in noninflammatory DCs that suppress T-cell activation and promote the development of T cells with regulatory properties. These findings reveal an important role of the noncanonical NF-κB pathway in the regulation of immunity.

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Dissertations / Theses on the topic "Via NF-κB"

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Akizuki, Mayumi. "Optineurin suppression causes neuronal cell death via NF-κB pathway". Kyoto University, 2014. http://hdl.handle.net/2433/188648.

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Shi, Tao. "La withaferin A inhibe la transcription du VIH-1 via le facteur de transcription NF-κB". Mémoire, Université de Sherbrooke, 2016. http://hdl.handle.net/11143/8333.

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L’infection par le VIH-1 est un problème majeur de la santé publique qui touche plus de 35 millions de personnes à l’échelle mondiale. La réplication du VIH-1 est déclenchée par l’activation du promoteur LTR, qui contient deux sites de liaison pour le facteur de transcription NF-κB. Ces sites de liaison sont hautement conservés dans le génome du VIH-1, illustrant ainsi l’importance de NF-κB dans l’activité transcriptionelle des gènes du VIH-1 et la production de nouvelles particules virales. La withaferin A (WA) est une substance bioactive extraite de la plante Withania somnifera, qui possède des propriétés pharmacologiques non négligeables dans la régulation de la réponse immunitaire. Des études récentes ont démontré que le potentiel anti-inflammatoire de la WA est dû principalement à l’inhibition de la voie de NF-κB. Le but de ce projet est de déterminer l’effet de la WA sur la réplication du VIH-1 dans les cellules T, qui sont les cibles principales du virus. Des essais de transfections transitoires de cellules T Jurkat E6.1 avec des plasmides contenant le promoteur du VIH-1 ayant différentes constructions de NF-κB, ont démontré que la WA peut réduire l’activité du promoteur d’une manière dépendante de NF-κB. Quant à la production de particules virales, des essais d’infection avec des virus pseudotypés démontrent que la WA diminue la production virale jusqu’à 90% dans des cellules T stimulées avec PMA/PHA et TNF-α, tandis que les mutants ayant des sites de liaison défective pour NF-κB ne sont pas affectés. Des essais de retardement sur gel ainsi que des immunobuvardages de type Western ont montré que la WA altère l’habilité de NF-κB à transloquer dans le noyau, ce qui se traduit par l’inhibition de la synthèse de l’IκB-α, protéine inhibitrice de NF-κB, phénomène sous contrôle étroite de ce facteur de transcription. Ces résultats suggèrent que la WA pourrait permettre une diminution de la réplication virale d’une manière dépendante de NF-κB et ainsi empêcher la propagation du virus aux cellules T chez les individus infectés.

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Endo, Yoko. "Expression of activation-induced cytidine deaminase in human hepatocytes via NF-κB signaling". Kyoto University, 2008. http://hdl.handle.net/2433/135829.

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Diel, Diego Gustavo. "Caracterização de genes do vírus do ectima contagioso envolvidos na regulação da via de sinalização do NF-κB". Universidade Federal de Santa Maria, 2010. http://repositorio.ufsm.br/handle/1/4054.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico
Orf virus (ORFV), the type member of the genus Parapoxvirus of the family Poxviridae, is the etiologic agent of orf or contagious ecthyma, a contagious and ubiquitous disease of sheep and goats. ORFV genome consists of a double stranded DNA molecule with approximately 138 Kb, and contains 131 putative genes. Among those, 15 are novel genes, unique to parapoxviruses, which lack homology to other known viral or cellular genes. In the present study we describe the functional characterization of three of these genes, ORFV024, ORFV002, and ORFV121. Results presented here demonstrate that the proteins encoded by these genes inhibit the activation of the nuclear factor-kappa B (NF-κB) signaling pathway. ORFV-encoded ORFV024 inhibits activation of the NF-κB signaling pathway in the cell cytoplasm by inhibiting phosphorylation of the IκB kinases, IKKα and IKKβ, consequently inhibiting the activation of the IKK complex. Deletion of ORFV024 from the ORFV genome had no significant effect on disease severity, progression or time to resolution in sheep, indicating that ORFV024 does not contribute to ORFV virulence. ORFV-encoded ORFV002 functions in the cell nucleus, where it interacts with the NF-κB subunit NF-κB-p65, inhibiting its acetylation, a p300-mediated modification of NF-κB-p65 which modulates its transcriptional activity. Similarly to ORFV024, deletion of ORFV002 from the ORFV genome had no significant effect on ORFV virulence and disease pathogenesis in sheep. ORFV-encoded ORFV121 functions in the cell cytoplasm, where it binds to and inhibits phosphorylation and nuclear translocation of NF-κB-p65. Deletion of ORFV121 from the ORFV genome resulted in a marked attenuated disease phenotype in sheep, indicating that ORFV121 is a determinant of virulence of ORFV in the natural host. These results indicate that ORFV, like other poxviruses, has evolved multiple strategies to modulate NF-κB, targeting different steps of the signaling pathway. Results obtained in the pathogenesis studies performed here suggest that multiple NF-κB inhibitors encoded by ORFV may exert complementary and/or redundant functions to effectively block host cell responses regulated by the NF-κB signaling pathway. Additionally, it is possible that ORFV-encoded NF-κB inhibitors modulate distinct cellular processes regulated by NF-κB in vivo. A better understanding of ORFV-host interactions may provide valuable insights for the development of improved vaccines against orf, or yet for the development of novel ORFV-based therapeutic agents and vaccine vectors with enhanced safety and efficacy, and a broader applicability.
O vírus da orf (ORFV), protótipo do gênero Parapoxvirus da família Poxviridae, é o agente etiológico da orf ou ectima contagioso, uma enfermidade contagiosa de distribuição mundial que afeta primariamente ovinos e caprinos. O genoma do ORFV consiste de uma molécula de DNA de fita dupla com aproximadamente 138 Kb, que contém presumidamente 131 genes. Dentre estes, 15 são genes novos, identificados apenas nos parapoxvírus e que não possuem homologia com outros genes de origem viral ou celular. O presente estudo descreve a caracterização funcional de três destes genes, ORFV024, ORFV002 e ORFV121. Os resultados apresentados no presente estudo demonstram que as proteínas codificadas pelos genes ORFV024, ORFV002 e ORFV121 inibem a ativação da via de sinalização do fator de transcrição nuclear-kappa B (NF-κB). O produto da ORFV024 bloqueia a ativação da via do NF-κB no citoplasma celular, inibindo a fosforilação das quinases IκB (IKK), IKKα e IKKβ e, consequentemente inibindo a ativação do complexo IKK. A deleção do gene ORFV024 do genoma do ORFV não alterou a severidade, a progressão, ou o tempo de resolução das lesões produzidas pelo ORFV em ovinos, indicando que o produto deste gene não contribui para a virulência do vírus. O gene ORFV002 codifica um inibidor do NF-κB que atua no núcleo das células. O produto do ORFV002 interage com a subunidade NF-κB-p65 do NF-κB, inibindo a sua acetilação, uma modificação pós-traducional do NF-κB-p65 mediada pela acetiltransferase p300 que regula a sua atividade transcripcional. Semelhante ao ORFV024, a deleção do gene ORFV002 do genoma do ORFV não afetou a virulência do vírus nem alterou a patogenia da enfermidade em ovinos. O produto do gene ORFV121 atua no citoplasma das células, onde esta proteína viral interage com o NF-κB-p65 inibindo sua fosforilação e translocação nuclear. A deleção do gene ORFV121 do genoma do ORFV reduziu significativamente a severidade, a progressão e o tempo de resolução da doença em ovinos, indicando que este produto viral constitui-se em um fator de virulência para o ORFV em seu hospedeiro natural. Estes resultados demonstram que, assim como outros poxvírus, o ORFV também desenvolveu múltiplas estratégias para modular a via de sinalização do NF-κB, codificando proteínas que atuam em diferentes eventos desta complexa via de sinalização intracelular. Os resultados obtidos nos estudos de patogenia sugerem que os inibidores do NF-κB codificados pelo ORFV desempenham funções complementares e/ou redundantes, provavelmente, para promover um bloqueio efficiente dos processos biológicos regulados pelo NF-κB. Além disso, estes produtos virais podem modular diferentes processos biológicos controlados pelo NF-κB in vivo. Um melhor entendimento das interações do ORFV com o seu hospedeiro pode favorecer o desenvolvimento de vacinas mais eficazes para o ectima contagioso, ou ainda, promover o desenvolvimento de vacinas vetoriais ou imunoterápicos, baseados no ORFV, mais eficazes e com uma maior espectro de aplicações.

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Evans, Sean M. "Orientia tsutsugamushi secretes two ankyrin repeat-containing effectors via a type 1 secretion system to inhibit host NF-κB function". VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4813.

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Scrub typhus is a potentially fatal infection that threatens one billion persons in the Asia-Pacific region and is caused by the obligate intracellular bacterium, Orientia tsutsugamushi. How this organism facilitates its intracellular survival and pathogenesis is poorly understood. Intracellular bacterial pathogens utilize the Type 1 (T1SS) or Type 4 secretion system (T4SS) to translocate ankyrin repeat-containing proteins (Anks) into the host cell to modulate host cell processes. The O. tsutsugamushi genome encodes one of the largest known bacterial Ank libraries as well as Type 1 and Type 4 secretion systems (T1SS and T4SS), which are expressed during infection. In silico analyses of the Anks’ C-termini revealed that they possess characteristics of T1SS secretion signals. Escherichia coli expressing a functional T1SS was able to secrete chimeric hemolysin proteins bearing the C-termini of 19 of 20 O. tsutsugamushi Anks. In addition to infecting endothelial cells, O. tsutsugamushi infects professional phagocytes. To better understand why these innate immune cells are unable to eliminate O. tsutsugamushi, we addressed the activity of host NF-κB proinflammatory transcription factor. Screening of O. tsutsugamushi infected cells at an MOI of 1 revealed inhibition of NF-κB nuclear accumulation as early as 8 hours in HeLa and bone-marrow derived macrophage cells. When stimulating infected cells with TNF-α, IκBα degradation still occurs, however NF-κB dependent gene transcription remains downregulated. Immunofluorescence microscopic analysis of TNF-α treated cells ectopically expressing all O. tsutsugamushi Anks revealed that two nuclear trafficking Anks, Ank1 and Ank6, result in a significant decrease in NF-κB nuclear accumulation. Additionally, these Anks also significantly inhibited NF-κB dependent gene transcription. Co-immunoprecipitation experiments revealed that both Anks interact with importin-β1, exportin-1, and the p65 NF-κB subunit. Treating cells with importazole significantly reduces the nuclear accumulation of Ank1 and Ank6. Finally, treating infected cells or cells ectopically expressing Ank1 or Ank6 with leptomycin B resulted in restoration of NF-κB nuclear accumulation. With these data, we propose that O. tsutsugamushi secretes Ank1 and Ank6 to initially interact with importin-β1, which permits their nuclear entry where they then interact with NF-κB and subsequently exportin-1 to prevent NF-κB nuclear accumulation.

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Iguchi, Mikiko. "Overexpression of a minimal domain of calpastatin suppresses IL-6 production and Th17 development via reduced NF-κB and increased STAT5 signals". Kyoto University, 2012. http://hdl.handle.net/2433/157430.

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Kanjo, Ghaidaa. "Influence de Toxoplasma Gondii dans la régulation d'UHRF1 via la voie NF-KB." Thesis, Strasbourg, 2014. http://www.theses.fr/2014STRAJ068/document.

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T. gondii interfère avec l'activation des voies de signalisation de NF-kB des cellules hôtes. Ainsi, lors de l’infection par T. gondii, 85% des gènes dépendant de NF-kB sont up-régulés. Un autre facteur de transcription dont l’expression est modulée par le parasite est UHRF1 (Ubiquitin-like,containing PHD and RING finger domains, 1). UHRF1, en se fixant sur le promoteur du gène de la cycline b, induit une répression épigénétique de ce dernier conduisant à un arrêt du cycle cellulaire des cellules infectées en phase G2 et à un arrêt de la prolifération parasitaire. L’analyse in silico du promoteur du gène uhrf1 a montré qu’il possédait 9 sites de fixation de NF-kB. Effectivement nous avons démontré que NF-kB interagit avec le promoteur du gène uhrf1 lors d’une infection par T. gondii. L’expression d’UHRF1 serait donc modulée par NF-kB dans les cellules infectées par T. gondii. Or NF-kB a une régulation différentielle en fonction de la nature de la souche infectante. Là encore, nous avons pu observer une régulation différentielle d’UHRF1 selon la nature de la souche infectante, pouvant être dues à la régulation souche dépendante de NF-kB. La détermination du rôle précis de l’activation d’UHRF1 dans les cellules infectées et l’identification du ou des facteurs parasitaires responsables pourraient permettre de mieux comprendre les mécanismes de persistance intracellulaire du parasite et de découvrir de nouveaux points d’impact thérapeutiques
T.gondii interferes with the activation of NF-kB signaling pathways. Thus, upon infection by T.gondii, 85% of genes NF-kB-dependent are up-regulated. Another transcription factor whose expression is modulated by the parasite is UHRF1 (Ubiquitin-like, Containing PHD and RINGfinger domains, 1). UHRF1, bind to the gene promoter of cyclin b and induces epigenetic repression of this gene leading to cell cycle arrest in G2 phase of infected cells and stop the proliferation in both infected cells and parasite. In silico analysis of the uhrf1 gene promoter has been shown to possess 9 binding sites of NF-kB. Our study showed that NF-kB actually interacts with the promoter of gene uhrf1 during infection with T. gondii. This suggests that the expression of UHRF1 is modulated by NF-kB in T. gondii-infected cells. In addition we observed differential regulation of UHRF1 depending on the nature of the infecting strain. These variations may also be due to already well-known differential regulation of NF-kB by different strains of T.gondii. Determining the precise role of UHRF1 activation in infected cells and the identification of the parasitic factor responsible of this activation would allow to a better understanding of the mechanisms of intracellular persistence of the parasite and allow to unravel new therapeutic trails

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Hiramitsu, Teruko. "Intercellular adhesion molecule-1 mediates the inhibitory effects of hyaluronan on interleukin-1β-induced matrix metalloproteinase production in rheumatoid synovial fibroblasts via down-regulation of NF-κB and p38". Kyoto University, 2006. http://hdl.handle.net/2433/135627.

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Kretz, Carole. "Induction du LTR de VIH-1 dans des conditions de stress cellulaire : rôles de NF-κB et de l'état redox intracellulaire". Lyon 1, 1997. http://www.theses.fr/1997LYO10076.

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L'infection par vih-1 est caractérisée par une phase de latence clinique particulièrement longue. La progression de la maladie jusqu'au stade sida nécessite une forte activation de la réplication virale. Parmi les stimuli induisant cette activation, on trouve des stress cellulaires tels que choc thermique, choc oxydant ou irradiation aux uv. L'action de ces agents s'exerce sur la transcription du provirus et, pour certains, (tnfalpha, peroxyde d'hydrogene) a été corrélée à l'activation du facteur de transcription cellulaire nf-kappa b, capable de se lier en deux sites, au ltr de vih-1. Ce travail de thèse s'attache à étudier l'influence d'un stress oxydant ou thermique sur le fonctionnement du ltr de vih-1 et de nf-kappa b. Il précise le rôle des radicaux libres oxygénés (rlo) dans l'activation de nf-kappa b par un choc oxydant. Ainsi, la diminution du taux de rlo intracellulaire par surexpression de la glutathion peroxydase ou de la protéine de stress hsp27 inhibe l'activation, par un stress oxydant, de nf-kappa b et les étapes de phosphorylation et de dégradation de sa sous-unité inhibitrice i kappa b-alpha. D'autre part, il décrit le mécanisme d'activation du ltr de vih-1 par le choc thermique ; ce mécanisme fait intervenir l'activation du facteur nf-kappa b. Cette stimulation de nf-kappa b est indépendante d'une dégradation de sa sous-unité inhibitrice i kappa b-alpha, mais dépend du potentiel redox cellulaire. Enfin, il met en évidence de nouveaux inducteurs du ltr de vih-1, que sont les analogues d'acides aminés. Ces composes exercent leur effet par l'intermédiaire d'une activation de nf-kappa b, concomitante d'une dégradation de i kappa b-alpha, mais sans étape de phosphorylation préalable de la sous-unité inhibitrice ; cette activation dépend, de plus, d'une variation de l'état redox intracellulaire. Ces résultats illustrent l'avantage sélectif que nf-kappa b confère au virus vih-1, dans des conditions de stress cellulaire.

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Pagan, Luana Urbano. "Influência do exercício físico no remodelamento cardíaco, estresse oxidativo e vias de sinalização das MAPK e do NF-κB de ratos espontaneamente hipertensos". Universidade Estadual Paulista (UNESP), 2018. http://hdl.handle.net/11449/153063.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Introdução: A sobrecarga de pressão causada pela hipertensão arterial sistêmica (HAS) pode gerar mudança na arquitetura do colágeno, favorecer a fibrose, bem como o desbalanço entre a produção de espécies reativas de oxigênio (ERO) e a capacidade antioxidante. Aumento das ERO pode gerar ativação de vias sinalizadoras como a do fator nuclear kappa B (NF-kB) e das proteínas quinases ativadas por mitógenos (MAPK). Alterações dessas vias contribuem para o processo de remodelamento cardíaco causado pela HAS. O exercício físico desempenha importante papel na atenuação dos fatores de risco cardiovascular como a HAS. Dessa forma, o objetivo desse estudo foi avaliar a influência do treinamento físico sobre o remodelamento cardíaco de ratos espontaneamente hipertensos (SHR) na fase que antecede o desenvolvimento de insuficiência cardíaca. Métodos: Foram constituídos quatro grupos experimentais de ratos: normotensos Wistar (W) sedentários (W-SED, n=27); W exercitados (W-EX, n=31); SHR sedentários (SHR-SED, n=27); e SHR exercitados (SHR-EX, n=32). A partir de 13 meses de idade, os animais dos grupos exercitados foram submetidos a protocolo de exercício em esteira, cinco dias por semana, durante quatro meses. A avaliação estrutural e funcional in vivo do coração foi realizada por ecocardiograma. A função miocárdica in vitro foi avaliada em preparações de músculo papilar isolado do ventrículo esquerdo (VE). Amostras de tecido do VE foram obtidas para análises bioquímicas, histológicas e moleculares. A avaliação do colágeno miocárdico total foi realizada pela histologia e por quantificação de hidroxiprolina. O tamanho dos miócitos foi medido em cortes histológicos do VE. A atividade das enzimas antioxidantes foi quantificada por espectrofotometria. A atividade da NADPH oxidase foi avaliada pela redução da lucigenina. A quantificação proteica dos colágenos I e III, lisil oxidase, vias MAPK e NF-kB, e inibidores teciduais 1 e 2 das metaloproteinases foi realizada por Western blot. A atividade das metaloproteinases foi realizada por zimografia. As comparações entre os grupos foram realizadas por análise de variância (ANOVA) complementada pelo teste de Bonferroni (distribuição normal), ou o teste de Kruskal-Wallis complementado pelo teste de Dunn (distribuição não normal). Resultados: A pressão arterial sistólica foi maior nos grupos SHR. Os grupos exercitados apresentaram maior capacidade física. Os sinais de insuficiência cardíaca foram maiores nos grupos hipertensos em relação aos controles, e o grupo SHR-EX apresentou menor prevalência de derrame pleural e taquipneia em comparação ao SHR-SED. O ecocardiograma mostrou reduções da espessura da parede do VE, espessura relativa do VE, diâmetro do átrio esquerdo e melhora do relaxamento no grupo SHR-EX vs. SHR-SED. O estudo da função miocárdica in vitro mostrou melhor performance no grupo SHR-EX (derivada positiva da tensão desenvolvida) vs. SHR-SED. O grupo SHR-EX mostrou maior atividade das enzimas antioxidantes em comparação SHR-SED. A produção de hidroperóxido de lipídeo, diâmetros dos miócitos, expressões proteicas da JNK fosforilada e da IkB total foram maiores nos grupos hipertensos. A quantificação de hidroxiprolina, malondialdeído, atividade da NADPH oxidase, expressões proteicas do colágeno III, lisil oxidase, TIMP-1, JNK total, p38 fosforilada, p65 fosforilada e total e IkB fosforilada não apresentaram diferença entre os grupos. A fração colágena intersticial, a atividade da MMP-2 e a expressão proteica da p38 total, ERK total e fosforilada foram maiores no SHR-SED em comparação com controle. O exercício causou redução da atividade da MMP-2 e da expressão da ERK fosforilada nos ratos hipertensos. Conclusão: O exercício físico em ratos espontaneamente hipertensos atenua o remodelamento cardíaco que está associado à melhora da tolerância ao esforço físico e redução da frequência de sinais de insuficiência cardíaca. Além disso, associa-se ao aumento da atividade das enzimas antioxidantes, diminuição da fosforilação da ERK e da atividade da MMP-2, e atenuação da expressão proteica da ERK total.
Introduction: The pressure overload caused by systemic arterial hypertension (SAH) may change the collagen architecture, induce fibrosis, as well as imbalance between the reactive oxygen species (ROS) production and antioxidant capacity. Increased ROS leads to activation of signaling pathways such as nuclear factor kappa B (NF-kB) and mitogen-activated protein kinases (MAPK). Alterations in these pathways contribute to cardiac remodeling process induced by SAH. Physical exercise plays an important role in mitigating cardiovascular risk factors such as hypertension. Therefore, the aim of this study was to evaluate the influence of physical training, started before clinical evidence of heart failure, on cardiac remodeling in spontaneously hypertensive rats (SHR). Methods: Four experimental groups were used: sedentary (W-SED n=27) and trained (W-EX, n=31) normotensive Wistar rats, and sedentary (SHR-SED, n=27) and exercised (SHR-EX, n=32) hypertensive rats. Rats of the exercise groups underwent a protocol of treadmill exercise five days a week, for four months; exercise started at 13 months of age. Echocardiogram was performed to evaluate in vivo cardiac structures and function. In vitro myocardial function was analyzed in left ventricular (LV) papillary muscle preparations. LV tissue samples were obtained for biochemical, histological, and molecular analysis. Total myocardial collagen was assessed by histology and hydroxyproline quantification. Cardiomyocyte size was measured in LV histological sections. Antioxidant enzymes activity was quantified by spectrophotometry. NADPH oxidase activity was analyzed by reduction of lucigenin. Protein expression of collagen I and III, lysyl oxidase, MAPK and NF-kB, and metalloproteinases tissue inhibitors 1 and 2 was quantified by Western blot. The activity of metalloproteinases was evaluated by zymography. Comparisons between groups were performed by two factors analysis of variance (ANOVA), complemented with the Bonferroni test (normal distribution), or Kruskal-Wallis complemented with Dunn test (non-normal distribution). Results: Systolic blood pressure was higher in the SHR groups. The exercised groups showed greater physical capacity. Prevalence of heart failure signs was higher in the hypertensive groups compared to controls, and the SHR-EX group showed lower prevalence of pleural effusion and tachypnea compared to SHR-SED. Echocardiogram showed lower LV wall thickness, LV relative wall thickness, left atrium diameter, and relaxation time in the SHR-EX group vs. SHR-SED. Myocardial functional study showed better performance in the SHR-EX group (positive derivative of the developed tension) vs. SHR-SED. The SHR-EX group showed higher antioxidant enzymes activity compared to SHR-SED. Lipid hydroperoxide production, myocyte diameters, and phosphorylated JNK and total IkB protein expression were higher in the hypertensive groups. Quantification of hydroxyproline, malondialdehyde, NADPH oxidase activity, and protein expression of collagen III, lysyl oxidase, TIMP-1, total JNK, phosphorylated p38, phosphorylated and total p65, and phosphorylated IkB did not differ between groups. The interstitial collagen fraction, MMP-2 activity, protein expression of total p38, and total and phosphorylated ERK were higher in the SHR-SED group compared to normotensive control. Physical exercise reduced the MMP-2 activity and the phosphorylated ERK expression in hypertensive rats. Conclusion: Physical exercise in spontaneously hypertensive rats attenuates cardiac remodeling associated with improved physical capacity and reduced prevalence of heart failure signs. In addition, it is associated with increased antioxidant enzymes activity, decreased ERK phosphorylation and MMP-2 activity, and attenuation of total ERK protein expression.
FAPESP: 2014/00747-1

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Book chapters on the topic "Via NF-κB"

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Mukherjee, Tapas, Yashika Ratra, Balaji Banoth, Alvina Deka, Smarajit Polley, and Soumen Basak. "A for Measuring the Activity of the Induced via the Noncanonical NF-κB Pathway." In Methods in Molecular Biology. Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1669-7_10.

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Baritaki, Stavroula, and Benjamin Bonavida. "Nitric Oxide Inhibits Tumor Cell Metastasis via Dysregulation of the NF-κB/Snail/RKIP Loop." In Nitric Oxide (NO) and Cancer. Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1432-3_11.

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Jackson, Shawn S., and Shigeki Miyamoto. "Dissecting NF-κB Signaling Induced by Genotoxic Agents via Genetic Complementation of NEMO-Deficient 1.3E2 Cells." In Methods in Molecular Biology. Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2422-6_11.

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Nishina, Hiroshi, Tomomi Watanabe, Kentaro Nakagawa, Shinya Ohata, Satoshi Asaka, and Toshiaki Katada. "SAPK/JNK Signaling Participates in Embryonic Hepatoblast Proliferation via a Pathway Different from NF-κB-Induced Anti-Apoptosis." In Stem Cell and Liver Regeneration. Springer Japan, 2004. http://dx.doi.org/10.1007/978-4-431-53971-1_1.

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Bonavida, Benjamin. "Sensitization of Immune-Resistant Tumor Cells to CTL-Mediated Apoptosis via Interference at the Dysregulated NF-κB/Snail/YY1/PI3K/RKIP/PTEN Resistant Loop." In Resistance to Targeted Anti-Cancer Therapeutics. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17807-3_9.

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Hafeez, Zubair Bin, Khalid Umar Fakhri, Md Zafaryab, and M. Moshahid Alam Rizvi. "Functional Mechanisms of Green Tea Polyphenols and Their Molecular Targets in Prevention of Multiple Cancers." In Handbook of Research on Advancements in Cancer Therapeutics. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-7998-6530-8.ch022.

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Cancer is portrayed as a group of disease characterized by alteration in the normal regulation of cell growth by the successive acquisition of genetic, somatic, and epigenetic alteration. Synthetic drugs are single targets while natural products are multi-targeted to prevent cancer. NF-κB is persistently active in a number of disease states, including cancer, and therefore has a critical role in cancer development and progression. It also provides a mechanistic link between inflammation and cancer and is a major controlling factor resistant to apoptosis in both pre-neoplastic and malignant cells. Importantly, NF-kB and the signaling pathways that mediate its activation have become attractive targets for the development of new chemopreventive and chemotherapeutic approaches. Natural antioxidants have been shown to possess chemopreventive and chemotherapeutic potential via targeting NF-κB signaling, among which tea polyphenols have been studied extensively. In this chapter, the authors summarize the regulation of NF-κB pathway by green tea polyphenols in different cancer types.

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Tarı Selçuk, Kevser. "Epidemiology of Inflammation-Related Diseases." In Role of Nutrition in Providing Pro-/Anti-Inflammatory Balance. 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 "Via NF-κB"

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McArdle, Alison, Karen McMenemy та Stuart Ferguson. "The study of hepatic NF-κB transcription dynamics via fluorescent image analysis". У 2008 8th IEEE International Conference on Bioinformatics and BioEngineering. IEEE, 2008. http://dx.doi.org/10.1109/bibe.2008.4696802.

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Qie, Shuo, Clarissa Chu, Weihua Li, Chenguang Wang, Mauricio Reginato та Nianli Sang. "Abstract 5143: ErbB2 activation up-regulates glutaminase 1 expression via NF-κB pathway". У Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5143.

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Hovde, Stacy, Theresa A. Lansdell, Lauren Azevedo, Jetze J. Tepe та Ronald W. Henry. "Abstract 2777: Suppression of multiple myeloma via non-canonical inhibition of NF-κB". У Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2777.

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Starkweather, Kara, Karen Hales та Dale Hales. "Abstract B45: Anti-inflammatory actions of DHA via inhibition of the NF-κB pathway". У Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research; September 13-16, 2019; Atlanta, GA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.ovca19-b45.

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Ostrander, Julie H., Brian J. Girard, Todd Knutson, Bethanie Kuker та Victoria Seewaldt. "Abstract P4-05-03: Cytoplasmic PELP1 promotes breast cancer initiation via NF-κB signaling". У Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.sabcs14-p4-05-03.

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Wei, Tong-You Wade, Pei-Yu Wu, Ting-Jung Wu та Ming-Daw Tsai. "Abstract 3133: NF-κB-dependent inflammatory responses offset sorafenib cytotoxicity in hepatocellular carcinoma via TIFA". У Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3133.

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Tokino, Takashi, Lisa Kashima, Minoru Toyota та Yasushi Sasaki. "Abstract 3070: CHFR, a potential tumor suppressor, downregulates interleukin-8 via inhibition of NF-κB". У 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.am10-3070.

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Chen, Ruei-Ching. "Abstract 5293: CCN3 increases motility of human chondrosarcoma via PI3K, AKT and NF-κB pathways". У 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.am10-5293.

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Cachia, David, Rachel Malley, William A. Vandergrift, Sunil Patel, Gabriel A. Rabinovich та Arabinda Das. "Abstract 3559: Galectin-1 upregulates CXCR4 in glioblastoma through upregulation of CXCR4 via NF-κB activation". У Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3559.

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Kong, X., K. Shen, J. Ji, T. Fu, J. Yang та Z. Gu. "AB0174 Tnf-Α modulates microglia activation via nf-Κb activity in systemic lupus erythematosus with depression". У Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.6698.

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