| http://purl.uniprot.org/citations/30720883 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/30720883 | http://www.w3.org/2000/01/rdf-schema#comment | "Circulating neutrophils are, by necessity, quiescent and relatively unresponsive to acute stimuli. In regions of inflammation, mediators can prime neutrophils to react to acute stimuli with stronger proinflammatory, pathogen-killing responses. In neutrophils G protein-coupled receptor (GPCR)-driven proinflammatory responses, such as reactive oxygen species (ROS) formation and accumulation of the key intracellular messenger phosphatidylinositol (3,4,5)-trisphosphate (PIP3 ), are highly dependent on PI3K-γ, a Ras-GTP, and Gβγ coincidence detector. In unprimed cells, the major GPCR-triggered activator of Ras is the Ras guanine nucleotide exchange factor (GEF), Ras guanine nucleotide releasing protein 4 (RasGRP4). Although priming is known to increase GPCR-PIP3 signaling, the mechanisms underlying this augmentation remain unclear. We used genetically modified mice to address the role of the 2 RasGEFs, RasGRP4 and son of sevenless (SOS)1/2, in neutrophil priming. We found that following GM-CSF/TNFα priming, RasGRP4 had only a minor role in the enhanced responses. In contrast, SOS1/2 acquired a substantial role in ROS formation, PIP3 accumulation, and ERK activation in primed cells. These results suggest that SOS1/2 signaling plays a key role in determining the responsiveness of neutrophils in regions of inflammation."xsd:string |
| http://purl.uniprot.org/citations/30720883 | http://purl.org/dc/terms/identifier | "doi:10.1002/jlb.2hi0918-359rr"xsd:string |
| http://purl.uniprot.org/citations/30720883 | http://purl.uniprot.org/core/author | "Davidson K."xsd:string |
| http://purl.uniprot.org/citations/30720883 | http://purl.uniprot.org/core/author | "Santos E."xsd:string |
| http://purl.uniprot.org/citations/30720883 | http://purl.uniprot.org/core/author | "Hawkins P.T."xsd:string |
| http://purl.uniprot.org/citations/30720883 | http://purl.uniprot.org/core/author | "Stephens L.R."xsd:string |
| http://purl.uniprot.org/citations/30720883 | http://purl.uniprot.org/core/author | "Suire S."xsd:string |
| http://purl.uniprot.org/citations/30720883 | http://purl.uniprot.org/core/author | "Segonds-Pichon A."xsd:string |
| http://purl.uniprot.org/citations/30720883 | http://purl.uniprot.org/core/author | "Baltanas F.C."xsd:string |
| http://purl.uniprot.org/citations/30720883 | http://purl.uniprot.org/core/date | "2019"xsd:gYear |
| http://purl.uniprot.org/citations/30720883 | http://purl.uniprot.org/core/name | "J Leukoc Biol"xsd:string |
| http://purl.uniprot.org/citations/30720883 | http://purl.uniprot.org/core/pages | "815-822"xsd:string |
| http://purl.uniprot.org/citations/30720883 | http://purl.uniprot.org/core/title | "Frontline Science: TNF-alpha and GM-CSF1 priming augments the role of SOS1/2 in driving activation of Ras, PI3K-gamma, and neutrophil proinflammatory responses."xsd:string |
| http://purl.uniprot.org/citations/30720883 | http://purl.uniprot.org/core/volume | "106"xsd:string |
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| http://purl.uniprot.org/uniprot/#_A0A0N4SVP1-mappedCitation-30720883 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/30720883 |
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| http://purl.uniprot.org/uniprot/#_A0A0N4SW33-mappedCitation-30720883 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/30720883 |
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| http://purl.uniprot.org/uniprot/#_A0A0N4SUQ3-mappedCitation-30720883 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/30720883 |