scholarly journals Clinical and Laboratory Medicine-Sci Forschen Full Text RESEARCH ARTICLE Exocrine Pancreatic Cell NF-κB/AP-1 Crosstalk Downstream of ERK MAPK

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Twait EC ◽  
Samuel I
Keyword(s):  
Transcription Factors ◽  
Transcriptional Activity ◽  
Nuclear Factor Kappa B ◽  
Laboratory Medicine ◽  
Nuclear Factor ◽  
Activator Protein 1 ◽  
Pancreatic Cell ◽  
Cooperative Interactions ◽  
Research Article ◽  
Pancreatic Cells

Aim: To test the hypothesis that cooperative interactions between transcription factors Nuclear Factor-kappa B (NF-κB) and Activator Protein-1 (AP1) augment transcriptional activity in exocrine pancreatic cells.

scholarly journals Relationship of toll-like receptors and nuclear transcription factors in asthma

2020 ◽  
pp. 125-133
Author(s):  
О.Ю. Кытикова ◽  
Т.П. Новгородцева ◽  
Ю.К. Денисенко ◽  
М.В. Антонюк ◽  
Т.А. Гвозденко
Keyword(s):  
Transcription Factors ◽  
Glucocorticoid Receptor ◽  
Chronic Inflammation ◽  
Nuclear Factor Kappa B ◽  
Peroxisome Proliferator ◽  
Nuclear Factor ◽  
Activator Protein 1 ◽  
Anti Inflammatory ◽  
Peroxisome Proliferator Activated Receptors ◽  
The Relationship

Бронхиальная астма (БА) является широко распространенным, хроническим, гетерогенным заболеванием. В течение последних нескольких лет клинические исследования предоставили новую информацию о фенотипировании, эндотипировании и вариантах лечения астмы. При всей эффективности традиционных методов лечения БА у ряда пациентов заболевание либо частично контролируется, либо не контролируется, несмотря на интенсивное, основанное на рекомендациях лечение. Данное состояние вопроса делает крайне актуальным дальнейшее изучение патогенеза хронического воспаления при БА для поиска и разработки новых терапевтических стратегий. Развитие и прогрессирование БА обусловлены активацией внутриклеточных сигнальных путей и генов воспаления в ответ на действие триггерных факторов. Внутриклеточными модуляторами воспалительной реакции на генном уровне являются ядерные транскрипционные факторы, к которым относят активирующий протеин-1 (activator protein-1, AP-1) и ядерный фактор каппа B (nuclear factor-kappa B, NF-kB), обладающие провоспалительной активностью. К внутриклеточным модуляторам относят также рецептор глюкокортикоидов (glucocorticoid receptor, GR) и рецепторы, активирующие пролиферацию пероксисом (peroxisome proliferator-activated receptors, PPARs) с противоспалительной активностью. Взаимоотношения между провоспалительными и противовоспалительными ядерными транскрипционными факторами являются предметом пристального изучения в настоящее время, так как последние могут служить мишенью для разработки стратегий управления активностью воспалительного процесса, в том числе при БА. Важную роль в сигнальных механизмах воспалительной реакции играют толл-подобные рецепторы (TLRs), инициирующие воспаление через активацию NF-kB и AP-1. В то же время, TLRs обладают способностью модулировать экспрессию PPARs и GR, противовоспалительный механизм действия которых осуществляется за счет подавления активности NF-kB и АР-1. В данном обзоре суммированы современные взгляды на структуру, функцию ядерных транскрипционных факторов и TLRs, а также их участие в патогенезе хронического воспаления при БА. Регуляция взаимоотношений между TLRs и ядерными транскрипционными факторами может быть важной терапевтической мишенью при БА. Bronchial asthma is a common, chronic and heterogeneous disease. During the last few years, clinical studies have provided new information about asthma phenotyping, endotyping, and therapeutic options. With all effectiveness of traditional asthma treatments, in a number of patients the disease is either controlled partially or not controlled, despite intensive, recommendation-based treatment. This makes further study of the pathogenesis of asthma-related chronic inflammation essential for developing new therapeutic strategies. The development and progression of asthma are caused by activation of intracellular signaling pathways and inflammation genes in response to action of trigger factors. Intracellular modulators of the inflammatory response at the gene level are nuclear transcription factors, which include proinflammatory activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kB). Intracellular modulators also include the glucocorticoid receptor (GR)) and peroxisome proliferator-activated receptors (PPARs), which have an anti-inflammatory activity. The relationship between pro- and anti-inflammatory nuclear transcription factors is presently under close investigation since it may represent a target for strategies of managing the inflammatory process, including in asthma. Toll-like receptors (TLRs) play an important role in the signaling mechanisms that initiate inflammation through activation of NF-kB and AP-1. At the same time, TLRs can modulate the expression of PPARs and GR, which have an anti-inflammatory action due to suppressing the activity of NF-kB and AP-1. This review summarizes current views on the structure and function of nuclear transcription factors and TLRs, as well as their participation in the pathogenesis of chronic inflammation in asthma. Regulation of the relationship between TLRs and nuclear transcription factors may be an important therapeutic target in asthma.

Activation of transcription factors activator protein-1 and nuclear factor-κB by 2,3,7,8-Tetrachlorodibenzo-p-dioxin

2000 ◽  
Vol 59 (8) ◽  
pp. 997-1005 ◽  
Author(s):  
Alvaro Puga ◽  
Sonya J Barnes ◽  
Ching-yi Chang ◽  
Huan Zhu ◽  
Kenneth P Nephew ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Activator Protein 1 ◽  
Activator Protein ◽  
Activation Of Transcription ◽  
Tetrachlorodibenzo P Dioxin

scholarly journals Neisseria gonorrhoeae Epithelial Cell Interaction Leads to the Activation of the Transcription Factors Nuclear Factor κB and Activator Protein 1 and the Induction of Inflammatory Cytokines

1997 ◽  
Vol 186 (2) ◽  
pp. 247-258 ◽  
Author(s):  
Michael Naumann ◽  
Silja Weßler ◽  
Cornelia Bartsch ◽  
Björn Wieland ◽  
Thomas F. Meyer
Keyword(s):  
Transcription Factors ◽  
Epithelial Cells ◽  
Neisseria Gonorrhoeae ◽  
Transcriptional Activation ◽  
Inflammatory Cytokine ◽  
Nuclear Factor ◽  
Activator Protein 1 ◽  
Messenger Rnas ◽  
Basic Leucine Zipper ◽  
Activator Protein

We have studied the effect of human bacterial pathogen Neisseria gonorrhoeae (Ngo) on the activation of nuclear factor (NF)-κB and the transcriptional activation of inflammatory cytokine genes upon infection of epithelial cells. During the course of infection, Ngo, the etiologic agent of gonorrhea, adheres to and penetrates mucosal epithelial cells. In vivo, localized gonococcal infections are often associated with a massive inflammatory response. We observed upregulation of several inflammatory cytokine messenger RNAs (mRNAs) and the release of the proteins in Ngo-infected epithelial cells. Moreover, infection with Ngo induced the formation of a NF-κB DNA–protein complex and, with a delay in time, the activation of activator protein 1, whereas basic leucine zipper transcription factors binding to the cAMP-responsive element or CAAT/enhancer-binding protein DNA-binding sites were not activated. In supershift assays using NF-κB–specific antibodies, we identified a NF-κB p50/p65 heterodimer. The NF-κB complex was formed within 10 min after infection and decreased 90 min after infection. Synthesis of tumor necrosis factor α and interluekin (IL)-1β occurred at later times and therefore did not account for NF-κB activation. An analysis of transiently transfected IL-6 promoter deletion constructs suggests that NF-κB plays a crucial role for the transcriptional activation of the IL-6 promoter upon Ngo infection. Inactivation of NF-κB conferred by the protease inhibitor N-tosyl-l-phenylalanine chloromethyl ketone inhibited mRNA upregulation of most, but not all, studied cyctokine genes. Activation of NF-κB and cytokine mRNA upregulation also occur in Ngo-infected epithelial cells that were treated with cytochalasin D, indicating an extracellular signaling induced before invasion.

scholarly journals Transcriptional activation of the chicken lysozyme gene by NF-κ Bp65 (RelA) and c-Rel, but not by NF-κ Bp50

1996 ◽  
Vol 313 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Loc VAN PHI
Keyword(s):  
Transcription Factors ◽  
Transcriptional Activation ◽  
Nuclear Factor Kappa B ◽  
Protein Complexes ◽  
Terminal Differentiation ◽  
Binding Activity ◽  
Nuclear Factor ◽  
Lysozyme Gene ◽  
Chloramphenicol Acetyltransferase Gene ◽  
Chicken Lysozyme

The lysozyme gene is expressed at a low level in myeloblasts and is progressively activated to constitutively high expression in mature macrophages. The binding activity of the newly defined NF-ĸB/Rel family of transcription factors increases during the terminal differentiation of macrophages. In this study, I show that NF-ĸB/Rel-like proteins bind to the nuclear factor kappa B (ĸB)-like sequence of the lysozyme promoter. These binding activities were induced by treatment of HD11 cells with lipopolysaccharide. Immunomobility shift assays show that c-Rel is possibly a factor in the complexes that bind to the ĸB-like sequence lysĸB. Binding activity to one of the protein complexes seems to be regulated by phosphorylation. In fact, overexpression of p65 and c-Rel stimulates expression of the chloramphenicol acetyltransferase gene controlled by the lysozyme promoter. Furthermore, co-transfection experiments reveal that the ĸB-like sequence within the lysozyme promoter mediates the transactivation by p65 and c-Rel. These results indicate that the p65 and c-Rel could be components of the protein complexes that bind to the ĸB-like sequence and this binding could contribute to the progressively activated expression of the lysozyme gene during the terminal differentiation of macrophages.

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