Interaction of the ACE D Allele and the GNB3 825T Allele in Myocardial Infarction
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 β3-subunit gene (GNB3) associated with enhanced...
Gespeichert in:
| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2000-12, Vol.36 (6), p.986-989 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 989 |
|---|---|
| container_issue | 6 |
| container_start_page | 986 |
| container_title | Hypertension (Dallas, Tex. 1979) |
| container_volume | 36 |
| creator | Naber, Christoph K Hüsing, Johannes Wolfhard, Ulrich Erbel, Raimund Siffert, Winfried |
| description | 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 β3-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 |
| doi_str_mv | 10.1161/01.HYP.36.6.986 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_205298728</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>66037654</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4443-dbcc8459a21f0fb5223235065b16188b48a54007d2fac13d5274be2ac36411bc3</originalsourceid><addsrcrecordid>eNpFkEtPxCAURonR6PhYuzNE161cXqXLcXxN4jPRRFeEUpqpYqvQifHfyzijsoAbOPfj5iC0DyQHkHBMIL98vsuZzGVeKrmGRiAoz7iQbB2NCJQ8KwGettB2jC-EAOe82ERbAItuoCN0P-0GF4wd2r7DfYOHmcPjyRk-xWPvnXfYdPXP5cXNCcOKioffh7bD11-9NaFujcfTrjHhJ2UXbTTGR7e3OnfQ4_nZw-Qyu7q9mE7GV5lNQ7CsrqxVXJSGQkOaSlDKKBNEiipNplTFlRGckKKmjbHAakELXjlqLJMcoLJsBx0uc99D_zF3cdAv_Tx06UtNiaClKqhK0PESsqGPMbhGv4f2zYQvDUQvHGgCOhnUTGqpk8HUcbCKnVdvrv7nV8oScLQCTLTGN8F0to1_nBIFYSJRfEl99j4Jjq9-_umCnjnjh5kmaXEqVUZTAYstWxSMfQM8WoPX</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>205298728</pqid></control><display><type>article</type><title>Interaction of the ACE D Allele and the GNB3 825T Allele in Myocardial Infarction</title><source>MEDLINE</source><source>American Heart Association Journals</source><source>Journals@Ovid Complete</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Naber, Christoph K ; Hüsing, Johannes ; Wolfhard, Ulrich ; Erbel, Raimund ; Siffert, Winfried</creator><creatorcontrib>Naber, Christoph K ; Hüsing, Johannes ; Wolfhard, Ulrich ; Erbel, Raimund ; Siffert, Winfried</creatorcontrib><description>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 β3-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.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.HYP.36.6.986</identifier><identifier>PMID: 11116112</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Aged ; Alleles ; Angiography ; Biological and medical sciences ; Cardiology. Vascular system ; Coronary Disease - genetics ; Coronary heart disease ; Female ; Gene Deletion ; Genotype ; Heart ; Heterotrimeric GTP-Binding Proteins - genetics ; Heterotrimeric GTP-Binding Proteins - metabolism ; Humans ; Male ; Medical sciences ; Middle Aged ; Myocardial Infarction - genetics ; Peptidyl-Dipeptidase A - genetics ; Peptidyl-Dipeptidase A - metabolism ; Risk Factors</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2000-12, Vol.36 (6), p.986-989</ispartof><rights>2000 American Heart Association, Inc.</rights><rights>2001 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Dec 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4443-dbcc8459a21f0fb5223235065b16188b48a54007d2fac13d5274be2ac36411bc3</citedby><cites>FETCH-LOGICAL-c4443-dbcc8459a21f0fb5223235065b16188b48a54007d2fac13d5274be2ac36411bc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=857035$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11116112$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Naber, Christoph K</creatorcontrib><creatorcontrib>Hüsing, Johannes</creatorcontrib><creatorcontrib>Wolfhard, Ulrich</creatorcontrib><creatorcontrib>Erbel, Raimund</creatorcontrib><creatorcontrib>Siffert, Winfried</creatorcontrib><title>Interaction of the ACE D Allele and the GNB3 825T Allele in Myocardial Infarction</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>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 β3-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.</description><subject>Aged</subject><subject>Alleles</subject><subject>Angiography</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Coronary Disease - genetics</subject><subject>Coronary heart disease</subject><subject>Female</subject><subject>Gene Deletion</subject><subject>Genotype</subject><subject>Heart</subject><subject>Heterotrimeric GTP-Binding Proteins - genetics</subject><subject>Heterotrimeric GTP-Binding Proteins - metabolism</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - genetics</subject><subject>Peptidyl-Dipeptidase A - genetics</subject><subject>Peptidyl-Dipeptidase A - metabolism</subject><subject>Risk Factors</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkEtPxCAURonR6PhYuzNE161cXqXLcXxN4jPRRFeEUpqpYqvQifHfyzijsoAbOPfj5iC0DyQHkHBMIL98vsuZzGVeKrmGRiAoz7iQbB2NCJQ8KwGettB2jC-EAOe82ERbAItuoCN0P-0GF4wd2r7DfYOHmcPjyRk-xWPvnXfYdPXP5cXNCcOKioffh7bD11-9NaFujcfTrjHhJ2UXbTTGR7e3OnfQ4_nZw-Qyu7q9mE7GV5lNQ7CsrqxVXJSGQkOaSlDKKBNEiipNplTFlRGckKKmjbHAakELXjlqLJMcoLJsBx0uc99D_zF3cdAv_Tx06UtNiaClKqhK0PESsqGPMbhGv4f2zYQvDUQvHGgCOhnUTGqpk8HUcbCKnVdvrv7nV8oScLQCTLTGN8F0to1_nBIFYSJRfEl99j4Jjq9-_umCnjnjh5kmaXEqVUZTAYstWxSMfQM8WoPX</recordid><startdate>200012</startdate><enddate>200012</enddate><creator>Naber, Christoph K</creator><creator>Hüsing, Johannes</creator><creator>Wolfhard, Ulrich</creator><creator>Erbel, Raimund</creator><creator>Siffert, Winfried</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope></search><sort><creationdate>200012</creationdate><title>Interaction of the ACE D Allele and the GNB3 825T Allele in Myocardial Infarction</title><author>Naber, Christoph K ; Hüsing, Johannes ; Wolfhard, Ulrich ; Erbel, Raimund ; Siffert, Winfried</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4443-dbcc8459a21f0fb5223235065b16188b48a54007d2fac13d5274be2ac36411bc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Aged</topic><topic>Alleles</topic><topic>Angiography</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Coronary Disease - genetics</topic><topic>Coronary heart disease</topic><topic>Female</topic><topic>Gene Deletion</topic><topic>Genotype</topic><topic>Heart</topic><topic>Heterotrimeric GTP-Binding Proteins - genetics</topic><topic>Heterotrimeric GTP-Binding Proteins - metabolism</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myocardial Infarction - genetics</topic><topic>Peptidyl-Dipeptidase A - genetics</topic><topic>Peptidyl-Dipeptidase A - metabolism</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Naber, Christoph K</creatorcontrib><creatorcontrib>Hüsing, Johannes</creatorcontrib><creatorcontrib>Wolfhard, Ulrich</creatorcontrib><creatorcontrib>Erbel, Raimund</creatorcontrib><creatorcontrib>Siffert, Winfried</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Naber, Christoph K</au><au>Hüsing, Johannes</au><au>Wolfhard, Ulrich</au><au>Erbel, Raimund</au><au>Siffert, Winfried</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interaction of the ACE D Allele and the GNB3 825T Allele in Myocardial Infarction</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2000-12</date><risdate>2000</risdate><volume>36</volume><issue>6</issue><spage>986</spage><epage>989</epage><pages>986-989</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>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 β3-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.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>11116112</pmid><doi>10.1161/01.HYP.36.6.986</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0194-911X |
| ispartof | Hypertension (Dallas, Tex. 1979), 2000-12, Vol.36 (6), p.986-989 |
| issn | 0194-911X 1524-4563 |
| language | eng |
| recordid | cdi_proquest_journals_205298728 |
| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Aged Alleles Angiography Biological and medical sciences Cardiology. Vascular system Coronary Disease - genetics Coronary heart disease Female Gene Deletion Genotype Heart Heterotrimeric GTP-Binding Proteins - genetics Heterotrimeric GTP-Binding Proteins - metabolism Humans Male Medical sciences Middle Aged Myocardial Infarction - genetics Peptidyl-Dipeptidase A - genetics Peptidyl-Dipeptidase A - metabolism Risk Factors |
| title | Interaction of the ACE D Allele and the GNB3 825T Allele in Myocardial Infarction |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-22T10%3A22%3A23IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Interaction%20of%20the%20ACE%20D%20Allele%20and%20the%20GNB3%20825T%20Allele%20in%20Myocardial%20Infarction&rft.jtitle=Hypertension%20(Dallas,%20Tex.%201979)&rft.au=Naber,%20Christoph%20K&rft.date=2000-12&rft.volume=36&rft.issue=6&rft.spage=986&rft.epage=989&rft.pages=986-989&rft.issn=0194-911X&rft.eissn=1524-4563&rft.coden=HPRTDN&rft_id=info:doi/10.1161/01.HYP.36.6.986&rft_dat=%3Cproquest_cross%3E66037654%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=205298728&rft_id=info:pmid/11116112&rfr_iscdi=true |