TNF phase III signalling in tolerant cells is tightly controlled by A20 and CYLD.

@article{Bikker2017TNFPI,
  title={TNF phase III signalling in tolerant cells is tightly controlled by A20 and CYLD.},
  author={Rolf Bikker and Martin Christmann and Katharina Preu{\ss} and Bastian Welz and Judith Friesenhagen and Oliver Dittrich‐Breiholz and Ren{\'e} Huber and Korbinian Brand},
  journal={Cellular signalling},
  year={2017},
  volume={37},
  pages={
          123-135
        }
}
TNF Tolerance in Monocytes and Macrophages: Characteristics and Molecular Mechanisms
TLDR
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TLDR
The data demonstrate that activation of GSK3 – either pathophysiologically or pharmacologically induced – may destroy the finely balanced condition necessary for the termination of inflammation-associated signaling.
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TLDR
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A20 Orchestrates Inflammatory Response in the Oral Mucosa through Restraining NF-κB Activity
TLDR
It is reported that A20 regulates inflammatory responses to a keystone oral bacterium, Porphyromonas gingivalis, and restrains periodontal inflammation through its effect on NF-κB signaling and cytokine production.
Proteome and Phosphoproteome Analysis in TNF Long Term-Exposed Primary Human Monocytes
TLDR
The experiments demonstrate that both proteome and phosphoproteome analysis can be effectively applied to study protein/phosphorylation patterns of primary monocytes and provide new regulatory candidates and evidence for a complex network of specific but synergistically acting/cooperating mechanisms enabling the affected cells to resist sustained TNF exposure and resulting in the resolution of inflammation.
Sepsis: From Historical Aspects to Novel Vistas. Pathogenic and Therapeutic Considerations.
TLDR
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The inhibitory effect of the deubiquitinase cylindromatosis (CYLD) on inflammatory responses in human gingival fibroblasts.
TLDR
The results suggest that CYLD participates in periodontal inflammatory responses by negatively regulating LPS-induced NF-κB signalling and knocking down CYLD expression greatly enhanced the mRNA expression of proinflammatory cytokines in L PS- or TNF-α-stimulated HGFs.
Decrease of miR-19b-3p in Brain Microvascular Endothelial Cells Attenuates Meningitic Escherichia coli-Induced Neuroinflammation via TNFAIP3-Mediated NF-κB Inhibition
TLDR
In vivo and in vitro findings indicate a novel quenching mechanism of the host by attenuating miR-19b-3p/TNFAIP3/NF-κB signaling in BMECs in response to meningitic E. coli, thus preventing CNS from further neuroinflammatory damage.
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