Activators and Target Genes of Rel/NF-кB Transcription Factors

Loop, Torsten; Pahl, Heike L.

doi:10.1007/978-94-010-0163-2_1

Cited by 2,788 publications

(7 citation statements)

References 470 publications

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“…In the astrocytes of the spinal cord, TLR4 activation leads to cascade amplification, which leads to the activation of NF κ B. Subsequently, an increase is seen in proinflammatory cytokines and stress response mediators, such as TNF- α , COX-2, and iNOS, all of which are related to CNS diseases [17–19]. In the microglia, the TLR4/NF κ B signaling pathway shows the same results.…”

Section: Discussionmentioning

confidence: 99%

“…TLR4 is a member of the toll-like receptor family, which is associated with a variety of pathological changes in central nervous system cells [16]. TLR4/NF κ B is the classic pathway of inflammatory response; many studies have found that TLR4 activation results in a cascade amplification effect, NF κ B activation, then an increase in the proinflammatory factor and stress reaction medium expression, such as TNF- α , cox-2, and iNOS, and these cytokines are involved in CNS diseases [17–19].…”

Section: Introductionmentioning

confidence: 99%

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Isoflurane Preconditioning Attenuates Brain Injury Induced by Electromagnetic Pulse via the TLR4/NFκB Signaling Pathway

Deng

Zhang³

et al. 2019

Oxidative Medicine and Cellular Longevity

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Electromagnetic pulse (EMP) is a unique type of electromagnetic radiation, and EMP exposure causes a series of biological effects. The nervous system is sensitive to EMP. We studied the neuroprotective effects of isoflurane preconditioning against EMP exposure and used hematoxylin-eosin staining (HE) to observe the effects of electromagnetic pulse and isoflurane preconditioning on neurons. Inflammatory cytokines were detected by enzyme-linked immunosorbent assay (ELISA). Western blotting was used to detect the expression of caspase-3, CD11b, TLR4, and NFκBp65. We found that after EMP exposure, the number of abnormal neurons had increased, and the expression of caspase-3, CD11b, TLR4, and NFκBp65 had also increased. Isoflurane preconditioning can reverse the above phenomenon. Moreover, we found that isoflurane preconditioning can reduce neuronal apoptosis and improve cognitive impairment induced by EMP. These findings indicate that isoflurane preconditioning can protect neurons in the cerebral cortex from EMP exposure, alleviate the inflammatory reaction and cell apoptosis, and improve cognitive impairment induced by EMP. These effects may occur through the downregulation of the TLR4/NFκB signaling pathway and the inhibition of microglial activation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Isoflurane Preconditioning Attenuates Brain Injury Induced by Electromagnetic Pulse via the TLR4/NFκB Signaling Pathway

Deng

Zhang³

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…Monocytes/macrophages also act as antigen-presenting cells, which play a key role in immune response. The activation of Toll-like receptor (TLR) and lipopolysaccharide (LPS) receptors on the surface of monocytes/macrophages leads to various proinflammatory cytokines such as TNF-α, NO, IL-1β, IL-6, and IL-12 which are responsible for mediation by the NF-κB signaling pathway [54,55].…”

Section: Inhibition Of Baff Expression and Autoantibody Generation [5...mentioning

confidence: 99%

New Insights into Artesunate as a Pleiotropic Regulator of Innate and Adaptive Immune Cells

Lin

Tang

Shi

et al. 2022

Journal of Immunology Research

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Artesunate, one of the derivatives of artemisinin (“qinghaosu” in Chinese), is known as an antimalarial drug with high efficiency and low toxicity. Of interest, emerging evidences suggest that artesunate also possesses an immunomodulatory effect during innate and adaptive immune responses in cell types and context-dependent manner. Although it shows promising application in many diseases, such as inflammatory diseases, hypersensitivity, autoimmune diseases, and cancers, little is known about underlying molecular. In this review, we summarize recent advances of how artesunate regulates innate and adaptive immune cells. In addition, its potential application in immune-related diseases is also highlighted.

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“…The transcription factors c-myc, the homeodomain transcription factors (HOXs), the proto-oncogene AP-1 Transcription Factor Subunit (JunB), p53, the E2F transcription factor 3 (E2F3a), Twist, the E74 like ETS transcription factor 3 (Elf3), and the chromatin modifiers Bmi1 and jmjD3. Traditionally, the mechanism that underlies the regulation of distinct sets of genes by NF-κB is attributed to its different dimers and the association with several families of transcription factors specific to each cell phenotype 160 .…”

Section: Nf-κb Links Inflammation With Cellular Plasticitymentioning

confidence: 99%

On the Origin of Carcinoma

Méndez¹

2021

Preprint

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The origin of cancer remains one of the most important enigmas in modern biology. The prevailing paradigm has failed to grasp a comprehensive view of the disease. Naturally, therapies developed under the current assumptions are inadequate and cancer is practically an incurable disease. Meanwhile, descriptive studies continuously extend the molecular complexity of cancer without an equivalent advancement in its understanding. Furthermore, they tend to accumulate inconsistencies inexplicable under the classical view. This paper presents a compelling theory of the origin of carcinomas. By hypothesis, a series of generic events in epithelial tissues promoted by cellular aging and inflammation enables the reactivation of developmental programs. The origin of carcinomas in vivo is described as the time-ordered cell state transitions undergone by epithelial cells in the hyperplasia due to replicative senescence and inflammation towards a mesenchymal undifferentiated endogenous cell state with cancerous behavior. In support of the theory, the molecular, cellular, and histopathological evidence is critically reviewed. A plausible model for the origin of carcinomas is presented to explain the mechanism underlying carcinogenesis from an evolutive and developmental perspective. The implications of the hypothesis in the current strategies for cancer prevention and treatment are discussed along with rational alternatives and some predictions for possible experimental validation.

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Activators and Target Genes of Rel/NF-кB Transcription Factors

Cited by 2,788 publications

References 470 publications

Isoflurane Preconditioning Attenuates Brain Injury Induced by Electromagnetic Pulse via the TLR4/NFκB Signaling Pathway

Isoflurane Preconditioning Attenuates Brain Injury Induced by Electromagnetic Pulse via the TLR4/NFκB Signaling Pathway

New Insights into Artesunate as a Pleiotropic Regulator of Innate and Adaptive Immune Cells

On the Origin of Carcinoma

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