| http://purl.uniprot.org/citations/17566078 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17566078 | http://www.w3.org/2000/01/rdf-schema#comment | "Guanylyl cyclase/natriuretic peptide receptor-A (GC-A/NPRA) signaling antagonizes the physiological effects mediated by the renin-angiotensin system (RAS). The objective of this study was to determine whether the targeted-disruption of Npr1 gene (coding for GC-A/NPRA) leads to the activation of cardiac RAS genes involved on the hypertrophic remodeling process. The Npr1 gene-knockout (Npr1(-/-)) mice showed 30-35 mmHg higher systolic blood pressure (SBP) and a 63% greater heart weight-to-body weight (HW/BW) ratio compared with wild-type (Npr1(+/+)) mice. The mRNA levels of both angiotensin-converting enzyme and angiotensin II type 1a receptor were increased by three- and fourfold, respectively, in Npr1(-/-) null mutant mice hearts compared with the wild-type Npr1(+/+) mice hearts. In parallel, the expression levels of interleukin-6 and tumor necrosis factor-alpha were increased by four-to fivefold, in Npr1(-/-) mice hearts compared with control animals. The NF-kappaB binding activity in nuclear extracts of Npr1(-/-) mice hearts was increased by fourfold compared with wild-type Npr1(+/+) mice hearts. Treatments with captopril or hydralazine equally attenuated SBP; however, only captopril significantly decreased the HW/BW ratio and suppressed cytokine gene expression in Npr1(-/-) mice hearts. The ventricular cGMP level was reduced by almost sixfold in Npr1(-/-) mice compared with wild-type control mice. The results of the present study indicate that disruption of NPRA/cGMP signaling leads to the augmented expression of cardiac RAS pathways that promote the development of cardiac hypertrophy and remodeling."xsd:string |
| http://purl.uniprot.org/citations/17566078 | http://purl.org/dc/terms/identifier | "doi:10.1152/physiolgenomics.00079.2007"xsd:string |
| http://purl.uniprot.org/citations/17566078 | http://purl.uniprot.org/core/author | "Zhao D."xsd:string |
| http://purl.uniprot.org/citations/17566078 | http://purl.uniprot.org/core/author | "Pandey K.N."xsd:string |
| http://purl.uniprot.org/citations/17566078 | http://purl.uniprot.org/core/author | "Vellaichamy E."xsd:string |
| http://purl.uniprot.org/citations/17566078 | http://purl.uniprot.org/core/author | "Somanna N."xsd:string |
| http://purl.uniprot.org/citations/17566078 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17566078 | http://purl.uniprot.org/core/name | "Physiol Genomics"xsd:string |
| http://purl.uniprot.org/citations/17566078 | http://purl.uniprot.org/core/pages | "193-202"xsd:string |
| http://purl.uniprot.org/citations/17566078 | http://purl.uniprot.org/core/title | "Genetic disruption of guanylyl cyclase/natriuretic peptide receptor-A upregulates ACE and AT1 receptor gene expression and signaling: role in cardiac hypertrophy."xsd:string |
| http://purl.uniprot.org/citations/17566078 | http://purl.uniprot.org/core/volume | "31"xsd:string |
| http://purl.uniprot.org/citations/17566078 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17566078 |
| http://purl.uniprot.org/citations/17566078 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/17566078 |
| http://purl.uniprot.org/uniprot/#_F6W125-mappedCitation-17566078 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17566078 |
| http://purl.uniprot.org/uniprot/#_F6QCP8-mappedCitation-17566078 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17566078 |
| http://purl.uniprot.org/uniprot/#_Q2TAY4-mappedCitation-17566078 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17566078 |
| http://purl.uniprot.org/uniprot/#_Q3UY30-mappedCitation-17566078 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17566078 |
| http://purl.uniprot.org/uniprot/#_Q3TU20-mappedCitation-17566078 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17566078 |
| http://purl.uniprot.org/uniprot/#_P09470-mappedCitation-17566078 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17566078 |
| http://purl.uniprot.org/uniprot/#_P18293-mappedCitation-17566078 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17566078 |
| http://purl.uniprot.org/uniprot/#_Q5XK22-mappedCitation-17566078 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17566078 |
| http://purl.uniprot.org/uniprot/#_Q91X04-mappedCitation-17566078 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17566078 |
| http://purl.uniprot.org/uniprot/#_Q3U3Q7-mappedCitation-17566078 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17566078 |
| http://purl.uniprot.org/uniprot/#_Q7TSV8-mappedCitation-17566078 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/17566078 |