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10.1016/j.neulet.2018.02.035

http://scihub22266oqcxt.onion/10.1016/j.neulet.2018.02.035
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29474875!ä!29474875

suck abstract from ncbi


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pmid29474875      Neurosci+Lett 2018 ; 672 (ä): 46-52
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  • Rig-I is involved in inflammation through the IPS-1/TRAF(6) pathway in astrocytes under chemical hypoxia #MMPMID29474875
  • Li L; Yang R; Feng M; Guo Y; Wang Y; Guo J; Lu X
  • Neurosci Lett 2018[Apr]; 672 (ä): 46-52 PMID29474875show ga
  • The retinoic acid-inducible gene I (RIG-I) is a crucial cytoplasmic pathogen recognition receptor involved in neuroinflammation in degenerative diseases. In the present study, in vitro human astrocytes were subjected to a chemical hypoxia model using cobalt chloride pretreatment. Chemical hypoxia induces the up-regulation of RIG-I in astrocytes and results in the expression of inflammatory cytokines IL-1beta, IL-6, and TNF-alpha in an NF-kappaB dependent manner. Elevated RIG-I modulates the interaction of interferon-beta promoter stimulator-1 (IPS-1) and TNF receptor-associated factor 6 (TRAF6) following chemical hypoxia. Inhibition of IPS-1 or TRAF6 suppresses RIG-I-induced NF-kappaB activation and inflammatory cytokines in response to chemical hypoxia. These data suggest that chemical hypoxia leads to RIG-I activation and the expression of inflammatory cytokines through the NF-kappaB pathway. Blocking IPS-1/TRAF6 pathway relieves RIG-I-induced neuroinflammation in astrocytes subjected to hypoxia.
  • |Adaptor Proteins, Signal Transducing/*metabolism[MESH]
  • |Astrocytes/drug effects/*metabolism[MESH]
  • |Cell Hypoxia/drug effects/*physiology[MESH]
  • |Cell Line, Tumor[MESH]
  • |Cobalt/pharmacology[MESH]
  • |DEAD Box Protein 58/*metabolism[MESH]
  • |Humans[MESH]
  • |Inflammation/metabolism[MESH]
  • |Receptors, Immunologic[MESH]
  • |Signal Transduction/drug effects[MESH]
  • |TNF Receptor-Associated Factor 6/*metabolism[MESH]


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