Sequence Analysis of Six Blood Pressure Candidate Regions in 4,178 Individuals: The Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Targeted Sequencing Study
Genome-wide association studies (GWAS) identified multiple loci for blood pressure (BP) and hypertension. Six genes--ATP2B1, CACNB2, CYP17A1, JAG1, PLEKHA7, and SH2B3--were evaluated for sequence variation with large effects on systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pre...
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| Published in: | PloS one Vol. 9; no. 10; p. e109155 |
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| Main Authors: | , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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02.10.2014
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| ISSN: | 1932-6203, 1932-6203 |
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| Abstract | Genome-wide association studies (GWAS) identified multiple loci for blood pressure (BP) and hypertension. Six genes--ATP2B1, CACNB2, CYP17A1, JAG1, PLEKHA7, and SH2B3--were evaluated for sequence variation with large effects on systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), and mean arterial pressure (MAP).
Targeted genomic sequence was determined in 4,178 European ancestry participants from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. Common variants (≥50 minor allele copies) were evaluated individually and rare variants (minor allele frequency, MAF≤1%) were aggregated by locus. 464 common variants were identified across the 6 genes. An upstream CYP17A1 variant, rs11191416 (MAF = 0.09), was the most significant association for SBP (P = 0.0005); however the association was attenuated (P = 0.0469) after conditioning on the GWAS index single nucleotide polymorphism (SNP). A PLEKHA7 intronic variant was the strongest DBP association (rs12806040, MAF = 0.007, P = 0.0006) and was not in LD (r² = 0.01) with the GWAS SNP. A CACNB2 intronic SNP, rs1571787, was the most significant association with PP (MAF = 0.27, P = 0.0003), but was not independent from the GWAS SNP (r² = 0.34). Three variants (rs6163 and rs743572 in the CYP17A1 region and rs112467382 in PLEKHA7) were associated with BP traits (P<0.001). Rare variation, aggregately assessed in the 6 regions, was not significantly associated with BP measures.
Six targeted gene regions, previously identified by GWAS, did not harbor novel variation with large effects on BP in this sample. |
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| AbstractList | BackgroundGenome-wide association studies (GWAS) identified multiple loci for blood pressure (BP) and hypertension. Six genes--ATP2B1, CACNB2, CYP17A1, JAG1, PLEKHA7, and SH2B3--were evaluated for sequence variation with large effects on systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), and mean arterial pressure (MAP).Methods and resultsTargeted genomic sequence was determined in 4,178 European ancestry participants from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. Common variants (≥50 minor allele copies) were evaluated individually and rare variants (minor allele frequency, MAF≤1%) were aggregated by locus. 464 common variants were identified across the 6 genes. An upstream CYP17A1 variant, rs11191416 (MAF = 0.09), was the most significant association for SBP (P = 0.0005); however the association was attenuated (P = 0.0469) after conditioning on the GWAS index single nucleotide polymorphism (SNP). A PLEKHA7 intronic variant was the strongest DBP association (rs12806040, MAF = 0.007, P = 0.0006) and was not in LD (r² = 0.01) with the GWAS SNP. A CACNB2 intronic SNP, rs1571787, was the most significant association with PP (MAF = 0.27, P = 0.0003), but was not independent from the GWAS SNP (r² = 0.34). Three variants (rs6163 and rs743572 in the CYP17A1 region and rs112467382 in PLEKHA7) were associated with BP traits (P<0.001). Rare variation, aggregately assessed in the 6 regions, was not significantly associated with BP measures.ConclusionSix targeted gene regions, previously identified by GWAS, did not harbor novel variation with large effects on BP in this sample. Genome-wide association studies (GWAS) identified multiple loci for blood pressure (BP) and hypertension. Six genes - ATP2B1, CACNB2, CYP17A1, JAG1, PLEKHA7, and SH2B3 - were evaluated for sequence variation with large effects on systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), and mean arterial pressure (MAP). Targeted genomic sequence was determined in 4,178 European ancestry participants from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. Common variants ([greater than or equal to]50 minor allele copies) were evaluated individually and rare variants (minor allele frequency, MAF[less than or equal to]1%) were aggregated by locus. 464 common variants were identified across the 6 genes. An upstream CYP17A1 variant, rs11191416 (MAF = 0.09), was the most significant association for SBP (P = 0.0005); however the association was attenuated (P = 0.0469) after conditioning on the GWAS index single nucleotide polymorphism (SNP). A PLEKHA7 intronic variant was the strongest DBP association (rs12806040, MAF = 0.007, P = 0.0006) and was not in LD (r.sup.2 = 0.01) with the GWAS SNP. A CACNB2 intronic SNP, rs1571787, was the most significant association with PP (MAF = 0.27, P = 0.0003), but was not independent from the GWAS SNP (r.sup.2 = 0.34). Three variants (rs6163 and rs743572 in the CYP17A1 region and rs112467382 in PLEKHA7) were associated with BP traits (P<0.001). Rare variation, aggregately assessed in the 6 regions, was not significantly associated with BP measures. Six targeted gene regions, previously identified by GWAS, did not harbor novel variation with large effects on BP in this sample. Background Genome-wide association studies (GWAS) identified multiple loci for blood pressure (BP) and hypertension. Six genes – ATP2B1, CACNB2, CYP17A1, JAG1, PLEKHA7, and SH2B3 – were evaluated for sequence variation with large effects on systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), and mean arterial pressure (MAP). Methods and Results Targeted genomic sequence was determined in 4,178 European ancestry participants from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. Common variants (≥50 minor allele copies) were evaluated individually and rare variants (minor allele frequency, MAF≤1%) were aggregated by locus. 464 common variants were identified across the 6 genes. An upstream CYP17A1 variant, rs11191416 (MAF = 0.09), was the most significant association for SBP (P = 0.0005); however the association was attenuated (P = 0.0469) after conditioning on the GWAS index single nucleotide polymorphism (SNP). A PLEKHA7 intronic variant was the strongest DBP association (rs12806040, MAF = 0.007, P = 0.0006) and was not in LD (r2 = 0.01) with the GWAS SNP. A CACNB2 intronic SNP, rs1571787, was the most significant association with PP (MAF = 0.27, P = 0.0003), but was not independent from the GWAS SNP (r2 = 0.34). Three variants (rs6163 and rs743572 in the CYP17A1 region and rs112467382 in PLEKHA7) were associated with BP traits (P<0.001). Rare variation, aggregately assessed in the 6 regions, was not significantly associated with BP measures. Conclusion Six targeted gene regions, previously identified by GWAS, did not harbor novel variation with large effects on BP in this sample. Genome-wide association studies (GWAS) identified multiple loci for blood pressure (BP) and hypertension. Six genes--ATP2B1, CACNB2, CYP17A1, JAG1, PLEKHA7, and SH2B3--were evaluated for sequence variation with large effects on systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), and mean arterial pressure (MAP).BACKGROUNDGenome-wide association studies (GWAS) identified multiple loci for blood pressure (BP) and hypertension. Six genes--ATP2B1, CACNB2, CYP17A1, JAG1, PLEKHA7, and SH2B3--were evaluated for sequence variation with large effects on systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), and mean arterial pressure (MAP).Targeted genomic sequence was determined in 4,178 European ancestry participants from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. Common variants (≥50 minor allele copies) were evaluated individually and rare variants (minor allele frequency, MAF≤1%) were aggregated by locus. 464 common variants were identified across the 6 genes. An upstream CYP17A1 variant, rs11191416 (MAF = 0.09), was the most significant association for SBP (P = 0.0005); however the association was attenuated (P = 0.0469) after conditioning on the GWAS index single nucleotide polymorphism (SNP). A PLEKHA7 intronic variant was the strongest DBP association (rs12806040, MAF = 0.007, P = 0.0006) and was not in LD (r² = 0.01) with the GWAS SNP. A CACNB2 intronic SNP, rs1571787, was the most significant association with PP (MAF = 0.27, P = 0.0003), but was not independent from the GWAS SNP (r² = 0.34). Three variants (rs6163 and rs743572 in the CYP17A1 region and rs112467382 in PLEKHA7) were associated with BP traits (P<0.001). Rare variation, aggregately assessed in the 6 regions, was not significantly associated with BP measures.METHODS AND RESULTSTargeted genomic sequence was determined in 4,178 European ancestry participants from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. Common variants (≥50 minor allele copies) were evaluated individually and rare variants (minor allele frequency, MAF≤1%) were aggregated by locus. 464 common variants were identified across the 6 genes. An upstream CYP17A1 variant, rs11191416 (MAF = 0.09), was the most significant association for SBP (P = 0.0005); however the association was attenuated (P = 0.0469) after conditioning on the GWAS index single nucleotide polymorphism (SNP). A PLEKHA7 intronic variant was the strongest DBP association (rs12806040, MAF = 0.007, P = 0.0006) and was not in LD (r² = 0.01) with the GWAS SNP. A CACNB2 intronic SNP, rs1571787, was the most significant association with PP (MAF = 0.27, P = 0.0003), but was not independent from the GWAS SNP (r² = 0.34). Three variants (rs6163 and rs743572 in the CYP17A1 region and rs112467382 in PLEKHA7) were associated with BP traits (P<0.001). Rare variation, aggregately assessed in the 6 regions, was not significantly associated with BP measures.Six targeted gene regions, previously identified by GWAS, did not harbor novel variation with large effects on BP in this sample.CONCLUSIONSix targeted gene regions, previously identified by GWAS, did not harbor novel variation with large effects on BP in this sample. Background Genome-wide association studies (GWAS) identified multiple loci for blood pressure (BP) and hypertension. Six genes - ATP2B1, CACNB2, CYP17A1, JAG1, PLEKHA7, and SH2B3 - were evaluated for sequence variation with large effects on systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), and mean arterial pressure (MAP). Methods and Results Targeted genomic sequence was determined in 4,178 European ancestry participants from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. Common variants ([greater than or equal to]50 minor allele copies) were evaluated individually and rare variants (minor allele frequency, MAF[less than or equal to]1%) were aggregated by locus. 464 common variants were identified across the 6 genes. An upstream CYP17A1 variant, rs11191416 (MAF = 0.09), was the most significant association for SBP (P = 0.0005); however the association was attenuated (P = 0.0469) after conditioning on the GWAS index single nucleotide polymorphism (SNP). A PLEKHA7 intronic variant was the strongest DBP association (rs12806040, MAF = 0.007, P = 0.0006) and was not in LD (r.sup.2 = 0.01) with the GWAS SNP. A CACNB2 intronic SNP, rs1571787, was the most significant association with PP (MAF = 0.27, P = 0.0003), but was not independent from the GWAS SNP (r.sup.2 = 0.34). Three variants (rs6163 and rs743572 in the CYP17A1 region and rs112467382 in PLEKHA7) were associated with BP traits (P<0.001). Rare variation, aggregately assessed in the 6 regions, was not significantly associated with BP measures. Conclusion Six targeted gene regions, previously identified by GWAS, did not harbor novel variation with large effects on BP in this sample. Background Genome-wide association studies (GWAS) identified multiple loci for blood pressure (BP) and hypertension. Six genes – ATP2B1 , CACNB2 , CYP17A1 , JAG1 , PLEKHA7 , and SH2B3 – were evaluated for sequence variation with large effects on systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), and mean arterial pressure (MAP). Methods and Results Targeted genomic sequence was determined in 4,178 European ancestry participants from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. Common variants (≥50 minor allele copies) were evaluated individually and rare variants (minor allele frequency, MAF≤1%) were aggregated by locus. 464 common variants were identified across the 6 genes. An upstream CYP17A1 variant, rs11191416 (MAF = 0.09), was the most significant association for SBP (P = 0.0005); however the association was attenuated (P = 0.0469) after conditioning on the GWAS index single nucleotide polymorphism (SNP). A PLEKHA7 intronic variant was the strongest DBP association (rs12806040, MAF = 0.007, P = 0.0006) and was not in LD (r 2 = 0.01) with the GWAS SNP. A CACNB2 intronic SNP, rs1571787, was the most significant association with PP (MAF = 0.27, P = 0.0003), but was not independent from the GWAS SNP (r 2 = 0.34). Three variants (rs6163 and rs743572 in the CYP17A1 region and rs112467382 in PLEKHA7 ) were associated with BP traits (P<0.001). Rare variation, aggregately assessed in the 6 regions, was not significantly associated with BP measures. Conclusion Six targeted gene regions, previously identified by GWAS, did not harbor novel variation with large effects on BP in this sample. Genome-wide association studies (GWAS) identified multiple loci for blood pressure (BP) and hypertension. Six genes--ATP2B1, CACNB2, CYP17A1, JAG1, PLEKHA7, and SH2B3--were evaluated for sequence variation with large effects on systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), and mean arterial pressure (MAP). Targeted genomic sequence was determined in 4,178 European ancestry participants from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. Common variants (≥50 minor allele copies) were evaluated individually and rare variants (minor allele frequency, MAF≤1%) were aggregated by locus. 464 common variants were identified across the 6 genes. An upstream CYP17A1 variant, rs11191416 (MAF = 0.09), was the most significant association for SBP (P = 0.0005); however the association was attenuated (P = 0.0469) after conditioning on the GWAS index single nucleotide polymorphism (SNP). A PLEKHA7 intronic variant was the strongest DBP association (rs12806040, MAF = 0.007, P = 0.0006) and was not in LD (r² = 0.01) with the GWAS SNP. A CACNB2 intronic SNP, rs1571787, was the most significant association with PP (MAF = 0.27, P = 0.0003), but was not independent from the GWAS SNP (r² = 0.34). Three variants (rs6163 and rs743572 in the CYP17A1 region and rs112467382 in PLEKHA7) were associated with BP traits (P<0.001). Rare variation, aggregately assessed in the 6 regions, was not significantly associated with BP measures. Six targeted gene regions, previously identified by GWAS, did not harbor novel variation with large effects on BP in this sample. |
| Audience | Academic |
| Author | Boerwinkle, Eric Rice, Kenneth Gibbs, Richard A. Morrison, Alanna C. Hwang, Shih-Jen Levy, Daniel Bis, Joshua C. Psaty, Bruce M. Ehret, Georg B. Chakravarti, Aravinda Muzny, Donna Lumley, Thomas |
| AuthorAffiliation | 4 Department of Health Services, University of Washington, Seattle, Washington, United States of America 9 Center for Complex Disease Genomics, Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America 6 The Population Sciences Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, United States of America 11 Group Health Research Institute, Group Health Cooperative, Seattle, Washington, United States of America 2 Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, Washington, United States of America 5 The Framingham Heart Study, Framingham, Massachusetts, United States of America 1 University of Texas Health Science Center at Houston, Houston, Texas, United States of America 7 Department of Specialties of Medicine, Geneva University Hospitals, Geneva, Switzerland 3 Department of Epidemiology, University of Washington, Seattle, Washington, |
| AuthorAffiliation_xml | – name: 11 Group Health Research Institute, Group Health Cooperative, Seattle, Washington, United States of America – name: 1 University of Texas Health Science Center at Houston, Houston, Texas, United States of America – name: 2 Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, Washington, United States of America – name: 3 Department of Epidemiology, University of Washington, Seattle, Washington, United States of America – name: Sapienza University of Rome, Italy – name: 5 The Framingham Heart Study, Framingham, Massachusetts, United States of America – name: 7 Department of Specialties of Medicine, Geneva University Hospitals, Geneva, Switzerland – name: 10 Human Genome Sequencing Center, Baylor College of Medicine, Houston, Texas, United States of America – name: 8 Department of Statistics, University of Auckland, Auckland, New Zealand – name: 9 Center for Complex Disease Genomics, Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America – name: 4 Department of Health Services, University of Washington, Seattle, Washington, United States of America – name: 6 The Population Sciences Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, United States of America |
| Author_xml | – sequence: 1 givenname: Alanna C. surname: Morrison fullname: Morrison, Alanna C. – sequence: 2 givenname: Joshua C. surname: Bis fullname: Bis, Joshua C. – sequence: 3 givenname: Shih-Jen surname: Hwang fullname: Hwang, Shih-Jen – sequence: 4 givenname: Georg B. surname: Ehret fullname: Ehret, Georg B. – sequence: 5 givenname: Thomas surname: Lumley fullname: Lumley, Thomas – sequence: 6 givenname: Kenneth surname: Rice fullname: Rice, Kenneth – sequence: 7 givenname: Donna surname: Muzny fullname: Muzny, Donna – sequence: 8 givenname: Richard A. surname: Gibbs fullname: Gibbs, Richard A. – sequence: 9 givenname: Eric surname: Boerwinkle fullname: Boerwinkle, Eric – sequence: 10 givenname: Bruce M. surname: Psaty fullname: Psaty, Bruce M. – sequence: 11 givenname: Aravinda surname: Chakravarti fullname: Chakravarti, Aravinda – sequence: 12 givenname: Daniel surname: Levy fullname: Levy, Daniel |
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| DOI | 10.1371/journal.pone.0109155 |
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| DocumentTitleAlternate | Sequencing of 6 Blood Pressure Candidate Regions |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 ObjectType-Undefined-3 Competing Interests: The authors have read the journal's policy and an author of this manuscript has the following competing interests: Dr. Psaty serves on the DSMB for a clinical trial of a device funded by the manufacturer (Zoll LifeCor), and on the Steering Committee for the Yale Open-Data Access Project funded by Medtronic. Dr. Psaty, co-author, has indicated a potential competing interest for the purpose of transparency, but this disclosure does not alter the authors' adherence to PLOS ONE policies on sharing data and materials. Conceived and designed the experiments: RAG EB BMP AC DL. Performed the experiments: DM RAG. Analyzed the data: ACM JCB SJH. Contributed reagents/materials/analysis tools: TL KR. Wrote the paper: ACM JCB SJH GBE. Determined the regions for targeted sequencing: GBE. ACM, JB, and SJH are joint first authors on this work. |
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| References_xml | – volume: 8 start-page: e1000294 year: 2010 ident: ref16 article-title: Rare variants create synthetic genome-wide associations publication-title: PLoS Biol doi: 10.1371/journal.pbio.1000294 – volume: 129 start-page: 687 year: 1989 ident: ref8 article-title: The Atherosclerosis Risk in Communities (ARIC) study: Design and objectives publication-title: Am J Epidemiol doi: 10.1093/oxfordjournals.aje.a115184 – volume: 43 start-page: 1005 year: 2011 ident: ref5 article-title: Genome-wide association study identifies six new loci influencing pulse pressure and mean arterial pressure publication-title: Nat Genet doi: 10.1038/ng.922 – volume: 90 start-page: 4362 year: 2005 ident: ref6 article-title: 17alpha-hydroxylase/17,20-lyase deficiency caused by a novel homozygous mutation (y27stop) in the cytochrome CYP17 gene publication-title: J Clin Endocrin Metab doi: 10.1210/jc.2005-0136 – volume: 4 start-page: 518 year: 1975 ident: ref11 article-title: The Framingham Offspring Study. Design and preliminary data publication-title: Prev Med doi: 10.1016/0091-7435(75)90037-7 – volume: 26 start-page: 2190 year: 2010 ident: ref15 article-title: Metal: Fast and efficient meta-analysis of genomewide association scans publication-title: Bioinf doi: 10.1093/bioinformatics/btq340 – volume: 2 start-page: 73 year: 2009 ident: ref7 article-title: Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium: Design of prospective meta-analyses of genome-wide association studies from 5 cohorts publication-title: Circ Cardiov Genet doi: 10.1161/CIRCGENETICS.108.829747 – volume: 7 start-page: 335 year: 2014 ident: ref14 article-title: Strategies to Design and Analyze Targeted Sequencing Data: the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Targeted Sequencing Study publication-title: Circ Cardiov Genet doi: 10.1161/CIRCGENETICS.113.000350 – volume: 365 start-page: 217 year: 2005 ident: ref2 article-title: Global burden of hypertension: Analysis of worldwide data publication-title: Lancet doi: 10.1016/S0140-6736(05)70151-3 – volume: 18 start-page: 935 year: 2005 ident: ref13 article-title: A summary of the effects of antihypertensive medications on measured blood pressure publication-title: Am J Hypertens doi: 10.1016/j.amjhyper.2005.01.011 – volume: 478 start-page: 103 year: 2011 ident: ref4 article-title: Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk publication-title: Nature doi: 10.1038/nature10405 – volume: 41 start-page: 677 year: 2009 ident: ref3 article-title: Genome-wide association study of blood pressure and hypertension publication-title: Nat Genet doi: 10.1038/ng.384 – volume: 17 start-page: 5 year: 1974 ident: ref1 article-title: Role of blood pressure in cardiovascular morbidity and mortality publication-title: Prog Cardiov Dis doi: 10.1016/0033-0620(74)90034-6 – volume: 1 start-page: 263 year: 1991 ident: ref9 article-title: The Cardiovascular Health Study: Design and rationale publication-title: Ann Epidemiol doi: 10.1016/1047-2797(91)90005-W – volume: 41 start-page: 279 year: 1951 ident: ref10 article-title: Epidemiological approaches to heart disease: The Framingham Study publication-title: Am J Pub Hlth Nat Hlth doi: 10.2105/AJPH.41.3.279 – volume: 7 start-page: 332 year: 2014 ident: ref17 article-title: Following-up genome-wide association study signals: lessons learned from the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium Targeted Sequencing Study publication-title: Circ Cardiovasc Genet doi: 10.1161/CIRCGENETICS.113.000078 – volume: 24 start-page: 2911 year: 2005 ident: ref12 article-title: Adjusting for treatment effects in studies of quantitative traits: Antihypertensive therapy and systolic blood pressure publication-title: Stat Med doi: 10.1002/sim.2165 |
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| Snippet | Genome-wide association studies (GWAS) identified multiple loci for blood pressure (BP) and hypertension. Six genes--ATP2B1, CACNB2, CYP17A1, JAG1, PLEKHA7,... Background Genome-wide association studies (GWAS) identified multiple loci for blood pressure (BP) and hypertension. Six genes - ATP2B1, CACNB2, CYP17A1, JAG1,... Genome-wide association studies (GWAS) identified multiple loci for blood pressure (BP) and hypertension. Six genes - ATP2B1, CACNB2, CYP17A1, JAG1, PLEKHA7,... Background Genome-wide association studies (GWAS) identified multiple loci for blood pressure (BP) and hypertension. Six genes – ATP2B1, CACNB2, CYP17A1, JAG1,... BackgroundGenome-wide association studies (GWAS) identified multiple loci for blood pressure (BP) and hypertension. Six genes--ATP2B1, CACNB2, CYP17A1, JAG1,... Background Genome-wide association studies (GWAS) identified multiple loci for blood pressure (BP) and hypertension. Six genes – ATP2B1 , CACNB2 , CYP17A1 ,... |
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| SubjectTerms | Aging Aging - genetics Alleles Atherosclerosis Biology and Life Sciences Blood Blood pressure Blood Pressure - genetics Cardiovascular disease Cohort Studies Consortia Cytochrome Epidemiology Gene frequency Gene sequencing Genes Genetic research Genome-wide association studies Genomes Genomics Heart Heart - physiology Humans Hydroxylases Hypertension Loci Medical research Medicine Medicine and Health Sciences Polymorphism Pressure effects Sequence Analysis Single-nucleotide polymorphism Studies Variation |
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| Title | Sequence Analysis of Six Blood Pressure Candidate Regions in 4,178 Individuals: The Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Targeted Sequencing Study |
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