| http://purl.uniprot.org/citations/17651798 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17651798 | http://www.w3.org/2000/01/rdf-schema#comment | "In human neutrophils, the neuropeptide pituitary adenylate cyclase activating polypeptide (PACAP) acting via the G protein-coupled receptors vasoactive intestinal peptide/PACAP receptor 1 (VPAC-1) and formyl peptide receptor-like 1 (FPRL1) modulates Ca2+ and pro-inflammatory activities. We evaluated in human monocytes the importance of the Ca2+ signal and the participation of FPRL1 in PACAP-associated signaling pathways and pro-inflammatory activities. PACAP-evoked Ca2+ transient involved both Ca2+ influx and intracytoplasmic Ca2+ mobilisation. This was pertussis toxin, protein kinase A and adenylate cyclase dependent indicating the participation of Galphai and Galphas with mobilisation of both InsP3 sensitive and insensitive stores. Intra- or extracellular Ca2+ depletion resulted in the inhibition of PACAP-induced, Akt, ERK, p38 and NF-kappaB activations as well as a decrease in PACAP-associated reactive oxygen species (ROS) production and integrin CD11b membrane upregulation. The FPRL1 antagonist, Trp-Arg-Trp-Trp-Trp (WRW4), decreased PACAP-evoked Ca2+ signal, Akt, ERK phosphorylation, ROS and CD11b upregulation without affecting p38 phosphorylation. NF-kappaB inhibitors prevented PACAP-induced Ca2+ mobilisation. Monocytes pre-treatment with fMLP but not with LPS desensitised cells to the pro-inflammatory effects of PACAP. Thus, both intra- and extracellular Ca2+ play a role in controlling pro-inflammatory functions stimulated by PACAP which acts through a VPAC-1, FPRL1/Galphai/PI3K/ERK pathway and a VPAC-1/Galphas/PKA/p38 pathway to fully activate monocytes."xsd:string |
| http://purl.uniprot.org/citations/17651798 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.ceca.2007.05.017"xsd:string |
| http://purl.uniprot.org/citations/17651798 | http://purl.uniprot.org/core/author | "Sariban E."xsd:string |
| http://purl.uniprot.org/citations/17651798 | http://purl.uniprot.org/core/author | "Badran B."xsd:string |
| http://purl.uniprot.org/citations/17651798 | http://purl.uniprot.org/core/author | "El Zein N."xsd:string |
| http://purl.uniprot.org/citations/17651798 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/17651798 | http://purl.uniprot.org/core/name | "Cell Calcium"xsd:string |
| http://purl.uniprot.org/citations/17651798 | http://purl.uniprot.org/core/pages | "270-284"xsd:string |
| http://purl.uniprot.org/citations/17651798 | http://purl.uniprot.org/core/title | "The neuropeptide pituitary adenylate cyclase activating polypeptide modulates Ca2+ and pro-inflammatory functions in human monocytes through the G protein-coupled receptors VPAC-1 and formyl peptide receptor-like 1."xsd:string |
| http://purl.uniprot.org/citations/17651798 | http://purl.uniprot.org/core/volume | "43"xsd:string |
| http://purl.uniprot.org/citations/17651798 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17651798 |
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| http://purl.uniprot.org/uniprot/#_P25090-mappedCitation-17651798 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17651798 |
| http://purl.uniprot.org/uniprot/#_P32241-mappedCitation-17651798 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17651798 |
| http://purl.uniprot.org/uniprot/B4DNY6 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/17651798 |
| http://purl.uniprot.org/uniprot/P25090 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/17651798 |
| http://purl.uniprot.org/uniprot/P32241 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/17651798 |