Mapping the Genetic Architecture of Gene Expression in Human Liver
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{"title"=>"Mapping the genetic architecture of gene expression in human liver", "type"=>"journal", "authors"=>[{"first_name"=>"Eric E.", "last_name"=>"Schadt", "scopus_author_id"=>"6701604029"}, {"first_name"=>"Cliona", "last_name"=>"Molony", "scopus_author_id"=>"23987362300"}, {"first_name"=>"Eugene", "last_name"=>"Chudin", "scopus_author_id"=>"6603175835"}, {"first_name"=>"Ke", "last_name"=>"Hao", "scopus_author_id"=>"34770116300"}, {"first_name"=>"Xia", "last_name"=>"Yang", "scopus_author_id"=>"57190745663"}, {"first_name"=>"Pek Y.", "last_name"=>"Lum", "scopus_author_id"=>"7005247011"}, {"first_name"=>"Andrew", "last_name"=>"Kasarskis", "scopus_author_id"=>"7801322611"}, {"first_name"=>"Bin", "last_name"=>"Zhang", "scopus_author_id"=>"35301153100"}, {"first_name"=>"Susanna", "last_name"=>"Wang", "scopus_author_id"=>"8866317800"}, {"first_name"=>"Christine", "last_name"=>"Suver", "scopus_author_id"=>"24367502200"}, {"first_name"=>"Jun", "last_name"=>"Zhu", "scopus_author_id"=>"35286163000"}, {"first_name"=>"Joshua", "last_name"=>"Millstein", "scopus_author_id"=>"24367129900"}, {"first_name"=>"Solveig", "last_name"=>"Sieberts", "scopus_author_id"=>"6506705866"}, {"first_name"=>"John", "last_name"=>"Lamb", "scopus_author_id"=>"55124779200"}, {"first_name"=>"Debraj", "last_name"=>"GuhaThakurta", "scopus_author_id"=>"6603166273"}, {"first_name"=>"Jonathan", "last_name"=>"Derry", "scopus_author_id"=>"7003962699"}, {"first_name"=>"John D.", "last_name"=>"Storey", "scopus_author_id"=>"7102822940"}, {"first_name"=>"Iliana", "last_name"=>"Avila-Campillo", "scopus_author_id"=>"8872273100"}, {"first_name"=>"Mark J.", "last_name"=>"Kruger", "scopus_author_id"=>"24366849400"}, {"first_name"=>"Jason M.", "last_name"=>"Johnson", "scopus_author_id"=>"36089848400"}, {"first_name"=>"Carol A.", "last_name"=>"Rohl", "scopus_author_id"=>"6701511259"}, {"first_name"=>"Atila", "last_name"=>"Van Nas", "scopus_author_id"=>"8689319400"}, {"first_name"=>"Margarete", "last_name"=>"Mehrabian", "scopus_author_id"=>"7004155137"}, {"first_name"=>"Thomas A.", "last_name"=>"Drake", "scopus_author_id"=>"24760059600"}, {"first_name"=>"Aldons J.", "last_name"=>"Lusis", "scopus_author_id"=>"35463122100"}, {"first_name"=>"Ryan C.", "last_name"=>"Smith", "scopus_author_id"=>"57189650980"}, {"first_name"=>"F. Peter", "last_name"=>"Guengerich", "scopus_author_id"=>"7201536236"}, {"first_name"=>"Stephen C.", "last_name"=>"Strom", "scopus_author_id"=>"7102269420"}, {"first_name"=>"Erin", "last_name"=>"Schuetz", "scopus_author_id"=>"7005227768"}, {"first_name"=>"Thomas H.", "last_name"=>"Rushmore", "scopus_author_id"=>"7003426334"}, {"first_name"=>"Roger", "last_name"=>"Ulrich", "scopus_author_id"=>"7201561761"}], "year"=>2008, "source"=>"PLoS Biology", "identifiers"=>{"scopus"=>"2-s2.0-45149108420", "isbn"=>"1545-7885 (Electronic)\\n1544-9173 (Linking)", "doi"=>"10.1371/journal.pbio.0060107", "pui"=>"351824739", "sgr"=>"45149108420", "issn"=>"15449173", "pmid"=>"18462017"}, "id"=>"2cfd99ea-3afd-308d-b827-9f356e0d44bd", "abstract"=>"Genetic variants that are associated with common human diseases do not lead directly to disease, but instead act on intermediate, molecular phenotypes that in turn induce changes in higher-order disease traits. Therefore, identifying the molecular phenotypes that vary in response to changes in DNA and that also associate with changes in disease traits has the potential to provide the functional information required to not only identify and validate the susceptibility genes that are directly affected by changes in DNA, but also to understand the molecular networks in which such genes operate and how changes in these networks lead to changes in disease traits. Toward that end, we profiled more than 39,000 transcripts and we genotyped 782,476 unique single nucleotide polymorphisms (SNPs) in more than 400 human liver samples to characterize the genetic architecture of gene expression in the human liver, a metabolically active tissue that is important in a number of common human diseases, including obesity, diabetes, and atherosclerosis. This genome-wide association study of gene expression resulted in the detection of more than 6,000 associations between SNP genotypes and liver gene expression traits, where many of the corresponding genes identified have already been implicated in a number of human diseases. The utility of these data for elucidating the causes of common human diseases is demonstrated by integrating them with genotypic and expression data from other human and mouse populations. This provides much-needed functional support for the candidate susceptibility genes being identified at a growing number of genetic loci that have been identified as key drivers of disease from genome-wide association studies of disease. By using an integrative genomics approach, we highlight how the gene RPS26 and not ERBB3 is supported by our data as the most likely susceptibility gene for a novel type 1 diabetes locus recently identified in a large-scale, genome-wide association study. We also identify SORT1 and CELSR2 as candidate susceptibility genes for a locus recently associated with coronary artery disease and plasma low-density lipoprotein cholesterol levels in the process.", "link"=>"http://www.mendeley.com/research/mapping-genetic-architecture-gene-expression-human-liver-1", "reader_count"=>431, "reader_count_by_academic_status"=>{"Unspecified"=>7, "Professor > Associate Professor"=>39, "Researcher"=>139, "Student > Doctoral Student"=>14, "Student > Ph. D. Student"=>129, "Student > Postgraduate"=>13, "Student > Master"=>33, "Other"=>18, "Student > Bachelor"=>17, "Lecturer"=>2, "Lecturer > Senior Lecturer"=>1, "Professor"=>19}, "reader_count_by_user_role"=>{"Unspecified"=>7, "Professor > Associate Professor"=>39, "Researcher"=>139, "Student > Doctoral Student"=>14, "Student > Ph. D. Student"=>129, "Student > Postgraduate"=>13, "Student > Master"=>33, "Other"=>18, "Student > Bachelor"=>17, "Lecturer"=>2, "Lecturer > Senior Lecturer"=>1, "Professor"=>19}, "reader_count_by_subject_area"=>{"Unspecified"=>15, "Agricultural and Biological Sciences"=>258, "Arts and Humanities"=>3, "Veterinary Science and Veterinary Medicine"=>1, "Chemistry"=>1, "Computer Science"=>22, "Earth and Planetary Sciences"=>1, "Engineering"=>3, "Environmental Science"=>1, "Biochemistry, Genetics and Molecular Biology"=>40, "Mathematics"=>8, "Medicine and Dentistry"=>61, "Neuroscience"=>4, "Design"=>1, "Pharmacology, Toxicology and Pharmaceutical Science"=>1, "Sports and Recreations"=>1, "Physics and Astronomy"=>3, "Psychology"=>2, "Immunology and Microbiology"=>5}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>61}, "Sports and Recreations"=>{"Sports and Recreations"=>1}, "Physics and Astronomy"=>{"Physics and Astronomy"=>3}, "Psychology"=>{"Psychology"=>2}, "Mathematics"=>{"Mathematics"=>8}, "Unspecified"=>{"Unspecified"=>15}, "Environmental Science"=>{"Environmental Science"=>1}, "Pharmacology, Toxicology and Pharmaceutical Science"=>{"Pharmacology, Toxicology and Pharmaceutical Science"=>1}, "Arts and Humanities"=>{"Arts and Humanities"=>3}, "Design"=>{"Design"=>1}, "Engineering"=>{"Engineering"=>3}, "Chemistry"=>{"Chemistry"=>1}, "Neuroscience"=>{"Neuroscience"=>4}, "Earth and Planetary Sciences"=>{"Earth and Planetary Sciences"=>1}, "Immunology and Microbiology"=>{"Immunology and Microbiology"=>5}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>258}, "Computer Science"=>{"Computer Science"=>22}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>40}, "Veterinary Science and Veterinary Medicine"=>{"Veterinary Science and Veterinary Medicine"=>1}}, "reader_count_by_country"=>{"Republic of Singapore"=>1, "United States"=>38, "Japan"=>1, "United Kingdom"=>4, "Switzerland"=>2, "Portugal"=>1, "Spain"=>3, "New Zealand"=>1, "Canada"=>3, "Sweden"=>1, "Netherlands"=>1, "Korea (South)"=>1, "Belgium"=>2, "Norway"=>1, "Ireland"=>1, "China"=>1, "Denmark"=>1, "Brazil"=>2, "France"=>1, "Germany"=>5, "Indonesia"=>1}, "group_count"=>29}

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/459876", "https://ndownloader.figshare.com/files/459965", "https://ndownloader.figshare.com/files/459979", "https://ndownloader.figshare.com/files/459999", "https://ndownloader.figshare.com/files/460040", "https://ndownloader.figshare.com/files/460076", "https://ndownloader.figshare.com/files/460134"], "description"=>"<div><p>Genetic variants that are associated with common human diseases do not lead directly to disease, but instead act on intermediate, molecular phenotypes that in turn induce changes in higher-order disease traits. Therefore, identifying the molecular phenotypes that vary in response to changes in DNA and that also associate with changes in disease traits has the potential to provide the functional information required to not only identify and validate the susceptibility genes that are directly affected by changes in DNA, but also to understand the molecular networks in which such genes operate and how changes in these networks lead to changes in disease traits. Toward that end, we profiled more than 39,000 transcripts and we genotyped 782,476 unique single nucleotide polymorphisms (SNPs) in more than 400 human liver samples to characterize the genetic architecture of gene expression in the human liver, a metabolically active tissue that is important in a number of common human diseases, including obesity, diabetes, and atherosclerosis. This genome-wide association study of gene expression resulted in the detection of more than 6,000 associations between SNP genotypes and liver gene expression traits, where many of the corresponding genes identified have already been implicated in a number of human diseases. The utility of these data for elucidating the causes of common human diseases is demonstrated by integrating them with genotypic and expression data from other human and mouse populations. This provides much-needed functional support for the candidate susceptibility genes being identified at a growing number of genetic loci that have been identified as key drivers of disease from genome-wide association studies of disease. By using an integrative genomics approach, we highlight how the gene <em>RPS26</em> and not <em>ERBB3</em> is supported by our data as the most likely susceptibility gene for a novel type 1 diabetes locus recently identified in a large-scale, genome-wide association study. We also identify <em>SORT1</em> and <em>CELSR2</em> as candidate susceptibility genes for a locus recently associated with coronary artery disease and plasma low-density lipoprotein cholesterol levels in the process.</p> </div>", "links"=>[], "tags"=>[], "article_id"=>150600, "categories"=>["Biological Sciences", "Genetics", "Chemistry", "Medicine"], "users"=>["Eric E Schadt", "Cliona Molony", "Eugene Chudin", "Ke Hao", "Xia Yang", "Pek Y Lum", "Andrew Kasarskis", "Bin Zhang", "Susanna Wang", "Christine Suver", "Jun Zhu", "Joshua Millstein", "Solveig Sieberts", "John Lamb", "Debraj GuhaThakurta", "Jonathan Derry", "John D Storey", "Iliana Avila-Campillo", "Mark J Kruger", "Jason M Johnson", "Carol A Rohl", "Atila Van Nas", "Margarete Mehrabian", "Thomas A Drake", "Aldons J Lusis", "Ryan C Smith", "F. Peter Guengerich", "Stephen C Strom", "Erin Schuetz", "Thomas H Rushmore", "Roger Ulrich"], "doi"=>["https://dx.doi.org/10.1371/journal.pbio.0060107.sg001", "https://dx.doi.org/10.1371/journal.pbio.0060107.st001", "https://dx.doi.org/10.1371/journal.pbio.0060107.st002", "https://dx.doi.org/10.1371/journal.pbio.0060107.st003", "https://dx.doi.org/10.1371/journal.pbio.0060107.st004", "https://dx.doi.org/10.1371/journal.pbio.0060107.st005", "https://dx.doi.org/10.1371/journal.pbio.0060107.st006"], "stats"=>{"downloads"=>26, "page_views"=>18, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/Mapping_the_Genetic_Architecture_of_Gene_Expression_in_Human_Liver/150600", "title"=>"Mapping the Genetic Architecture of Gene Expression in Human Liver", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2008-05-06 00:10:00"}
  • {"files"=>["https://ndownloader.figshare.com/files/932805"], "description"=>"<div><p>(A) Mouse network for <i>Psrc1</i>, <i>Celsr2</i>, and <i>Sort1</i> derived from the liver, adipose, muscle, and brain gene expression data generated from the BXH/wt and BXC mouse crosses.</p>\n <p>(B) Human network for <i>PSRC1</i>, <i>CELSR2</i>, and <i>SORT1</i> derived from the HLC and from a previously published adipose and blood tissue cohort [<a href=\"http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0060107#pbio-0060107-b021\" target=\"_blank\">21</a>].</p></div>", "links"=>[], "tags"=>["networks", "derived", "probabilistic", "whole-gene"], "article_id"=>603215, "categories"=>["Biological Sciences", "Genetics", "Chemistry", "Medicine"], "users"=>["Eric E Schadt", "Cliona Molony", "Eugene Chudin", "Ke Hao", "Xia Yang", "Pek Y Lum", "Andrew Kasarskis", "Bin Zhang", "Susanna Wang", "Christine Suver", "Jun Zhu", "Joshua Millstein", "Solveig Sieberts", "John Lamb", "Debraj GuhaThakurta", "Jonathan Derry", "John D Storey", "Iliana Avila-Campillo", "Mark J Kruger", "Jason M Johnson", "Carol A Rohl", "Atila Van Nas", "Margarete Mehrabian", "Thomas A Drake", "Aldons J Lusis", "Ryan C Smith", "F. Peter Guengerich", "Stephen C Strom", "Erin Schuetz", "Thomas H Rushmore", "Roger Ulrich"], "doi"=>"https://dx.doi.org/10.1371/journal.pbio.0060107.g003", "stats"=>{"downloads"=>1, "page_views"=>6, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Local_Networks_for_PSRC1_CELSR2_and_SORT1_Derived_from_Causal_Probabilistic_Whole_Gene_Networks_in_Mouse_and_Human_/603215", "title"=>"Local Networks for <i>PSRC1</i>, <i>CELSR2</i>, and <i>SORT1</i> Derived from Causal, Probabilistic Whole-Gene Networks in Mouse and Human", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2008-05-06 00:53:35"}
  • {"files"=>["https://ndownloader.figshare.com/files/932414"], "description"=>"<div><p>(A) The <i>Rps26</i> subnetwork includes a number of known T1D associated genes (green nodes), and <i>RPS26</i> in this subnetwork is directly linked to <i>H2-Eb1</i>, a mouse ortholog of <i>HLA-DRB1</i>, a previously identified T1D susceptibility gene that is also strongly associated with a <i>cis</i> eSNP in the HLC (<a href=\"http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0060107#pbio-0060107-t002\" target=\"_blank\">Table 2</a>). The known T1D genes annotated by the Gene Ontology are significantly enriched in this subnetwork (<a href=\"http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0060107#pbio-0060107-t003\" target=\"_blank\">Table 3</a>).</p>\n <p>(B) The <i>Erbb3</i> subnetwork is not associated with any pathways known or predicted to be involved in T1D.</p></div>", "links"=>[], "tags"=>["networks", "derived", "probabilistic", "whole-gene", "constructed", "generated", "bxc"], "article_id"=>602811, "categories"=>["Biological Sciences", "Genetics", "Chemistry", "Medicine"], "users"=>["Eric E Schadt", "Cliona Molony", "Eugene Chudin", "Ke Hao", "Xia Yang", "Pek Y Lum", "Andrew Kasarskis", "Bin Zhang", "Susanna Wang", "Christine Suver", "Jun Zhu", "Joshua Millstein", "Solveig Sieberts", "John Lamb", "Debraj GuhaThakurta", "Jonathan Derry", "John D Storey", "Iliana Avila-Campillo", "Mark J Kruger", "Jason M Johnson", "Carol A Rohl", "Atila Van Nas", "Margarete Mehrabian", "Thomas A Drake", "Aldons J Lusis", "Ryan C Smith", "F. Peter Guengerich", "Stephen C Strom", "Erin Schuetz", "Thomas H Rushmore", "Roger Ulrich"], "doi"=>"https://dx.doi.org/10.1371/journal.pbio.0060107.g001", "stats"=>{"downloads"=>1, "page_views"=>6, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Local_Networks_for_Rps26_and_Erbb3_Derived_from_Causal_Probabilistic_Whole_Gene_Networks_Constructed_from_the_Liver_Adipose_Muscle_and_Brain_Gene_Expression_Data_Generated_from_the_BXH_wt_and_BXC_Mouse_Crosses_/602811", "title"=>"Local Networks for <i>Rps26</i> and <i>Erbb3</i> Derived from Causal, Probabilistic Whole-Gene Networks Constructed from the Liver, Adipose, Muscle, and Brain Gene Expression Data Generated from the BXH/wt and BXC Mouse Crosses", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2008-05-06 00:46:51"}
  • {"files"=>["https://ndownloader.figshare.com/files/932554"], "description"=>"<p>The CAD risk allele for SNP rs599839 was established in a previous WTCCC study [<a href=\"http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0060107#pbio-0060107-b016\" target=\"_blank\">16</a>] (lilac panel). In the HLC, this same SNP is strongly associated with <i>PSRC1</i>, <i>CELSR2</i>, and <i>SORT1</i> expression, with the CAD risk allele associated with lower relative expression (pink panel). In the BXH/wt cross designed to study metabolic traits that increase cardiovascular risk (green panel), all three of these expression traits were strongly correlated with plasma LDL cholesterol levels, a major CAD risk factor (scatter plots associated with the green panel). Given the association of these genes to plasma LDL-cholesterol levels, we examined whether rs599839 was associated with LDL cholesterol in a previously published GWAS [<a href=\"http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0060107#pbio-0060107-b035\" target=\"_blank\">35</a>] and found this SNP was significantly associated with LDL cholesterol levels, where the CAD risk allele was associated with higher LDL cholesterol levels in this cohort. Lower levels of <i>CELSR2</i> and <i>SORT1</i> expression were associated with the risk allele in humans, and with higher LDL cholesterol levels in mouse, making them ideal candidate susceptibility genes for the CAD and LDL cholesterol associations to this locus. On the other hand, lower levels of <i>PSRC1</i> expression were associated with the risk allele in humans, but with lower LDL cholesterol levels in mouse, suggesting that <i>PSRC1</i> is not the gene increasing CAD risk, but instead may be acting to protect against it.</p>", "links"=>[], "tags"=>["cad", "allele", "plasma", "ldl"], "article_id"=>602967, "categories"=>["Biological Sciences", "Genetics", "Chemistry", "Medicine"], "users"=>["Eric E Schadt", "Cliona Molony", "Eugene Chudin", "Ke Hao", "Xia Yang", "Pek Y Lum", "Andrew Kasarskis", "Bin Zhang", "Susanna Wang", "Christine Suver", "Jun Zhu", "Joshua Millstein", "Solveig Sieberts", "John Lamb", "Debraj GuhaThakurta", "Jonathan Derry", "John D Storey", "Iliana Avila-Campillo", "Mark J Kruger", "Jason M Johnson", "Carol A Rohl", "Atila Van Nas", "Margarete Mehrabian", "Thomas A Drake", "Aldons J Lusis", "Ryan C Smith", "F. Peter Guengerich", "Stephen C Strom", "Erin Schuetz", "Thomas H Rushmore", "Roger Ulrich"], "doi"=>"https://dx.doi.org/10.1371/journal.pbio.0060107.g002", "stats"=>{"downloads"=>2, "page_views"=>30, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_PSRC1_CELSR2_and_SORT1_Liver_Expression_Is_Associated_with_a_CAD_Risk_Allele_and_Plasma_LDL_Cholesterol_Levels_/602967", "title"=>"<i>PSRC1</i>, <i>CELSR2</i>, and <i>SORT1</i> Liver Expression Is Associated with a CAD Risk Allele and Plasma LDL Cholesterol Levels", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2008-05-06 00:49:27"}

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  • {"unique-ip"=>"23", "full-text"=>"19", "pdf"=>"5", "abstract"=>"0", "scanned-summary"=>"0", "scanned-page-browse"=>"0", "figure"=>"10", "supp-data"=>"1", "cited-by"=>"0", "year"=>"2018", "month"=>"3"}

Relative Metric

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