| http://purl.uniprot.org/citations/24086766 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24086766 | http://www.w3.org/2000/01/rdf-schema#comment | "High concentrations of reactive oxygen species (ROS) induce cellular damage, however at lower concentrations ROS act as intracellular second messengers. In this study, we demonstrate that serotonin (5-HT) transactivates the platelet-derived growth factor (PDGF) type β receptor as well as the TrkB receptor in neuronal cultures and SH-SY5Y cells, and that the transactivation of both receptors is ROS-dependent. Exogenous application of H₂O₂ induced the phosphorylation of these receptors in a dose-dependent fashion, similar to that observed with 5-HT. However the same concentrations of H₂O₂ failed to increase ERK1/2 phosphorylation. Yet, the NADPH oxidase inhibitors diphenyleneiodonium chloride and apocynin blocked both 5-HT-induced PDGFβ receptor phosphorylation and ERK1/2 phosphorylation. The increases in PDGFβ receptor and ERK1/2 phosphorylation were also dependent on protein kinase C activity, likely acting upstream of NADPH oxidase. Additionally, although the ROS scavenger N-acetyl-l-cysteine abrogated 5-HT-induced PDGFβ and TrkB receptor transactivation, it was unable to prevent 5-HT-induced ERK1/2 phosphorylation. Thus, the divergence point for 5-HT-induced receptor tyrosine kinase (RTK) transactivation and ERK1/2 phosphorylation occurs at the level of NADPH oxidase in this system. The ability of 5-HT to induce the production of ROS resulting in transactivation of both PDGFβ and TrkB receptors may suggest that instead of a single GPCR to single RTK pathway, a less selective, more global RTK response to GPCR activation is occurring."xsd:string |
| http://purl.uniprot.org/citations/24086766 | http://purl.org/dc/terms/identifier | "doi:10.1371/journal.pone.0077027"xsd:string |
| http://purl.uniprot.org/citations/24086766 | http://purl.uniprot.org/core/author | "Beazely M.A."xsd:string |
| http://purl.uniprot.org/citations/24086766 | http://purl.uniprot.org/core/author | "Heikkila J.J."xsd:string |
| http://purl.uniprot.org/citations/24086766 | http://purl.uniprot.org/core/author | "Kruk J.S."xsd:string |
| http://purl.uniprot.org/citations/24086766 | http://purl.uniprot.org/core/author | "Vasefi M.S."xsd:string |
| http://purl.uniprot.org/citations/24086766 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/24086766 | http://purl.uniprot.org/core/name | "PLoS One"xsd:string |
| http://purl.uniprot.org/citations/24086766 | http://purl.uniprot.org/core/pages | "e77027"xsd:string |
| http://purl.uniprot.org/citations/24086766 | http://purl.uniprot.org/core/title | "Reactive oxygen species are required for 5-HT-induced transactivation of neuronal platelet-derived growth factor and TrkB receptors, but not for ERK1/2 activation."xsd:string |
| http://purl.uniprot.org/citations/24086766 | http://purl.uniprot.org/core/volume | "8"xsd:string |
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