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http://purl.uniprot.org/citations/11116112http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11116112http://www.w3.org/2000/01/rdf-schema#comment"In polygenetic disorders, such as ischemic heart disease, the investigation of gene-gene interactions rather than determination of single gene effects is crucial to better understand the contribution of genetic factors. The 825T allele of the G-protein ss(3)-subunit gene (GNB3) associated with enhanced G-protein signaling is a candidate to interact with the angiotensin-converting enzyme (ACE) deletion/insertion (D/I) polymorphism to increase the risk for myocardial infarction (MI). The ACE D:/I variant affects the renin-angiotensin system hormones that activate G-protein-coupled receptors. Genotyping at the ACE and GNB3 loci was performed on 585 patients with coronary artery disease with (n=270) or without (n=315) previous MI. Logistic regression analysis demonstrated a significant interaction between the ACE D: allele and the GNB3 825T allele (P<0.001). The odds ratio for MI, associated with the 825T allele, was not increased in the presence of the ACE II genotype (OR 0.5; P=0.09) but was significantly higher in 825T allele carriers with the ACE DI genotype (OR 1.9; P=0.01) and further increased in individuals with the ACE DD genotype (OR 2.4; P=0.02). The highest odds ratio was found in homozygous 825T allele carriers with the ACE DD genotype (OR 7.5; P=0.006). Our data suggest a significant interaction of the GNB3 825T allele with the ACE D allele in MI. These hypothesis-generating data may justify larger prospective studies."xsd:string
http://purl.uniprot.org/citations/11116112http://purl.org/dc/terms/identifier"doi:10.1161/01.hyp.36.6.986"xsd:string
http://purl.uniprot.org/citations/11116112http://purl.uniprot.org/core/author"Siffert W."xsd:string
http://purl.uniprot.org/citations/11116112http://purl.uniprot.org/core/author"Erbel R."xsd:string
http://purl.uniprot.org/citations/11116112http://purl.uniprot.org/core/author"Husing J."xsd:string
http://purl.uniprot.org/citations/11116112http://purl.uniprot.org/core/author"Naber C.K."xsd:string
http://purl.uniprot.org/citations/11116112http://purl.uniprot.org/core/author"Wolfhard U."xsd:string
http://purl.uniprot.org/citations/11116112http://purl.uniprot.org/core/date"2000"xsd:gYear
http://purl.uniprot.org/citations/11116112http://purl.uniprot.org/core/name"Hypertension"xsd:string
http://purl.uniprot.org/citations/11116112http://purl.uniprot.org/core/pages"986-989"xsd:string
http://purl.uniprot.org/citations/11116112http://purl.uniprot.org/core/title"Interaction of the ACE D allele and the GNB3 825T allele in myocardial infarction."xsd:string
http://purl.uniprot.org/citations/11116112http://purl.uniprot.org/core/volume"36"xsd:string
http://purl.uniprot.org/citations/11116112http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/11116112
http://purl.uniprot.org/citations/11116112http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/11116112
http://purl.uniprot.org/uniprot/#_E9PCP0-mappedCitation-11116112http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/11116112
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http://purl.uniprot.org/uniprot/#_P16520-mappedCitation-11116112http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/11116112
http://purl.uniprot.org/uniprot/#_Q59G26-mappedCitation-11116112http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/11116112
http://purl.uniprot.org/uniprot/#_Q8IWZ9-mappedCitation-11116112http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/11116112
http://purl.uniprot.org/uniprot/A0A6Q8PF84http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/11116112
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