2012
DOI: 10.1038/aps.2011.200
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Role of G protein-coupled receptors in inflammation

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Cited by 153 publications
(131 citation statements)
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“…It should be noted in this context that activation of chemoattractant GPCRs, including the fMLF and C5a receptors, also promotes ROS production in neutrophils in a G i -dependent fashion (47). In these cells, ROS accumulation requires the activity of multiple signaling pathways including the activation of PI3 kinase and the small GTPase Rac (47).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…It should be noted in this context that activation of chemoattractant GPCRs, including the fMLF and C5a receptors, also promotes ROS production in neutrophils in a G i -dependent fashion (47). In these cells, ROS accumulation requires the activity of multiple signaling pathways including the activation of PI3 kinase and the small GTPase Rac (47).…”
Section: Discussionmentioning
confidence: 99%
“…In these cells, ROS accumulation requires the activity of multiple signaling pathways including the activation of PI3 kinase and the small GTPase Rac (47). It remains to be explored whether similar signaling cascades are involved in G i -mediated ROS production in hepatocytes.…”
Section: Discussionmentioning
confidence: 99%
“…Inflammatory mediators modulate GRKs signaling either by transcription regulation or its degradation. GRK2 act as mediator in the pathway that causes inflammatory pain (Sun and Richard, 2012). Thus, targeting GRKS by P. longum could be the reason of its anti-inflammatory properties.…”
Section: Module and Go Enrichment Analysis Of Human Pinmentioning
confidence: 99%
“…thrombomodulin (TM) (which binds thrombin) and endothelial protein C receptor (EPCR) [42]. It has been demonstrated that cell receptor occupancy is one of the critical factors determining the switch in the effects of thrombin from anticoagulant (TM/EPCR-mediated generation of activated protein C) to proinflammatory action, mediated through PAR-1 [43][44][45]. At the same time, the interplay of environmental inflammatory factors may direct the effects of FVIIc-TF signaling towards proinflammatory actions, depending on the availability of TF-inhibiting forces (TF pathway inhibitor [TFPI]) and cellular receptors that act in concert with FVIIc-TF, including PAR-2 [46].…”
Section: Coagulation and Thrombosismentioning
confidence: 99%