http://purl.uniprot.org/citations/17923674 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/17923674 | http://www.w3.org/2000/01/rdf-schema#comment | "Calcitonin gene-related peptide (CGRP) is thought to be a prominent neuropeptide in cardiovascular regulation and neuroimmune modulation. There are two isoforms of CGRP (alphaCGRP and betaCGRP), and the main CGRP receptors are probably composed of a calcitonin receptor-like receptor (CLR) and a receptor activity-modifying protein (RAMP)1. However, the physiological functions of CGRP that are mediated through the CLR/RAMP1 receptors remain to be clarified. For an improved understanding of the functions, we generated mice deficient in RAMP1, a specific subunit of CGRP receptors, by a conditional gene-targeting technique. The RAMP1-deficient mice (RAMP1(-/-)) exhibited high blood pressure, with no changes in heart rate. alphaCGRP was found to have a potent vascular relaxant activity compared with betaCGRP in the artery of the WT (RAMP1(+/+)) mice. The activities of both CGRP isoforms were remarkably suppressed in the arteries of the RAMP1(-/-) mice. The LPS-induced inflammatory responses of the RAMP1(-/-) mice revealed a transient and significant increase in the serum CGRP levels and high serum levels of proinflammatory cytokines compared with the RAMP1(+/+) mice. alphaCGRP and betaCGRP equally suppressed the production of TNF-alpha and IL-12 in bone marrow-derived dendritic cells stimulated with lipopolysaccharide. Their inhibitory effects were not observed in the bone marrow-derived dendritic cells of the RAMP1(-/-) mice. These results indicate that CGRP signaling through CLR/RAMP1 receptors plays a crucial role in the regulation of both blood pressure by vascular relaxation and proinflammatory cytokine production from dendritic cells."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.org/dc/terms/identifier | "doi:10.1073/pnas.0705974104"xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/author | "Hayashi T."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/author | "Kato T."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/author | "Ikawa M."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/author | "Okamoto H."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/author | "Yamamoto H."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/author | "Yamaguchi T."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/author | "Okabe M."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/author | "Kawasaki H."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/author | "Tsujikawa K."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/author | "Matsushita H."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/author | "Fukada S."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/author | "Hirayama M."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/author | "Yayama K."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/author | "Ogitani Y."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/author | "Shigeno T."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/author | "Takatori S."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/name | "Proc Natl Acad Sci U S A"xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/pages | "16702-16707"xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/title | "Hypertension and dysregulated proinflammatory cytokine production in receptor activity-modifying protein 1-deficient mice."xsd:string |
http://purl.uniprot.org/citations/17923674 | http://purl.uniprot.org/core/volume | "104"xsd:string |
http://purl.uniprot.org/citations/17923674 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17923674 |