| http://purl.uniprot.org/citations/16157310 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16157310 | http://www.w3.org/2000/01/rdf-schema#comment | "Selective antagonists for the adenosine A(3) receptor (A3AR), a member of the G protein-coupled receptors, have been indicated as potential drugs for anti-asthma or anti-inflammation. However, potent antagonists for the rodent A3AR have not been identified. To evaluate the pharmacological effects of human A3AR antagonists in mice, we here generated A3AR-humanized mice, in which the mouse A3AR gene was replaced by its human counterpart. The expression levels of human A3AR in the A3AR-humanized mice were equivalent to those of mouse A3AR in wild-type mice. Elevation of the intracellular Ca(2+) concentration induced by an A3AR agonist was observed in bone marrow-derived mast cells from the A3AR-humanized mice and this Ca(2+) mobilization was completely antagonized by a human A3AR antagonist. However, antigen-dependent degranulation was not potentiated by the A3AR agonist in the mast cells from A3AR-humanized mice. The agonist-stimulated human A3AR did not lead to the phosphorylation of either extracellular signal-regulated kinase 1/2 or protein kinase B in A3AR-humanized mice. The rate of human A3AR internalization in the mast cells was also markedly decreased compared with that of mouse A3AR in the mast cells. These results demonstrate that the human A3AR is insufficient to activate phosphoinositide 3-kinase gamma-dependent signaling pathways in mice, probably due to the uncoupling of member(s) of the G proteins, which are capable of activating phosphoinositide 3-kinase gamma, to the human A3AR, despite the mouse G protein(s) responsible for the Ca(2+) elevation are coupled with the human A3AR."xsd:string |
| http://purl.uniprot.org/citations/16157310 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.bcp.2005.08.003"xsd:string |
| http://purl.uniprot.org/citations/16157310 | http://purl.uniprot.org/core/author | "Inoue M."xsd:string |
| http://purl.uniprot.org/citations/16157310 | http://purl.uniprot.org/core/author | "Satoh M."xsd:string |
| http://purl.uniprot.org/citations/16157310 | http://purl.uniprot.org/core/author | "Ichimura M."xsd:string |
| http://purl.uniprot.org/citations/16157310 | http://purl.uniprot.org/core/author | "Yamano K."xsd:string |
| http://purl.uniprot.org/citations/16157310 | http://purl.uniprot.org/core/author | "Masaki S."xsd:string |
| http://purl.uniprot.org/citations/16157310 | http://purl.uniprot.org/core/author | "Saki M."xsd:string |
| http://purl.uniprot.org/citations/16157310 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
| http://purl.uniprot.org/citations/16157310 | http://purl.uniprot.org/core/name | "Biochem Pharmacol"xsd:string |
| http://purl.uniprot.org/citations/16157310 | http://purl.uniprot.org/core/pages | "1487-1496"xsd:string |
| http://purl.uniprot.org/citations/16157310 | http://purl.uniprot.org/core/title | "Human adenosine A(3) receptor leads to intracellular Ca(2+) mobilization but is insufficient to activate the signaling pathway via phosphoinositide 3-kinase gamma in mice."xsd:string |
| http://purl.uniprot.org/citations/16157310 | http://purl.uniprot.org/core/volume | "70"xsd:string |
| http://purl.uniprot.org/citations/16157310 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16157310 |
| http://purl.uniprot.org/citations/16157310 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/16157310 |
| http://purl.uniprot.org/uniprot/#_Q61618-mappedCitation-16157310 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16157310 |
| http://purl.uniprot.org/uniprot/Q61618 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/16157310 |