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  1. Article ; Online: Exact coalescent simulation of new haplotype data from existing reference haplotypes.

    Kang, Chul Joo / Marjoram, Paul

    Bioinformatics (Oxford, England)

    2012  Volume 28, Issue 6, Page(s) 838–844

    Abstract: Motivation: We introduce a coalescent-based method (RECOAL) for the simulation of new haplotype data from a reference population of haplotypes. A coalescent genealogy for the reference haplotype data is sampled from the appropriate posterior probability ...

    Abstract Motivation: We introduce a coalescent-based method (RECOAL) for the simulation of new haplotype data from a reference population of haplotypes. A coalescent genealogy for the reference haplotype data is sampled from the appropriate posterior probability distribution, then a coalescent genealogy is simulated which extends the sampled genealogy to include new haplotype data. The new haplotype data will, therefore, contain both some of the existing polymorphic sites and new polymorphisms added based on the structure of the simulated coalescent genealogy. This allows exact coalescent simulation of new haplotype data, compared with other methods which are more approximate in nature.
    Results: We demonstrate the performance of our method using a variety of data simulated under a coalescent model, before applying it to data from the 1000 Genomes project.
    MeSH term(s) Algorithms ; Computer Simulation ; Genome, Human ; Genome-Wide Association Study ; Haplotypes ; Humans ; Models, Genetic ; Population Groups ; Probability
    Language English
    Publishing date 2012-01-17
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1422668-6
    ISSN 1367-4811 ; 1367-4803
    ISSN (online) 1367-4811
    ISSN 1367-4803
    DOI 10.1093/bioinformatics/bts033
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  2. Article ; Online: A sample selection strategy for next-generation sequencing.

    Kang, Chul Joo / Marjoram, Paul

    Genetic epidemiology

    2012  Volume 36, Issue 7, Page(s) 696–709

    Abstract: Next-generation sequencing technology provides us with vast amounts of sequence data. It is efficient and cheaper than previous sequencing technologies, but deep resequencing of entire samples is still expensive. Therefore, sensible strategies for ... ...

    Abstract Next-generation sequencing technology provides us with vast amounts of sequence data. It is efficient and cheaper than previous sequencing technologies, but deep resequencing of entire samples is still expensive. Therefore, sensible strategies for choosing subsets of samples to sequence are required. Here we describe an algorithm for selection of a sub-sample of an existing sample if one has either of two possible goals in mind: maximizing the number of new polymorphic sites that are detected, or improving the efficiency with which the remaining unsequenced individuals can have their types imputed at newly discovered polymorphisms. We then describe a variation on our algorithm that is more focused on detecting rarer variants. We demonstrate the performance of our algorithm using simulated data and data from the 1000 Genomes Project.
    MeSH term(s) Algorithms ; Computer Simulation ; Diploidy ; Genetic Variation ; Genome, Human ; Genome-Wide Association Study ; Haplotypes ; High-Throughput Nucleotide Sequencing ; Human Genome Project ; Humans ; Models, Genetic ; Polymorphism, Single Nucleotide ; Sequence Analysis, DNA/methods
    Language English
    Publishing date 2012-08-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 605785-8
    ISSN 1098-2272 ; 0741-0395
    ISSN (online) 1098-2272
    ISSN 0741-0395
    DOI 10.1002/gepi.21664
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  3. Article ; Online: Author Correction: SVEP1 is an endogenous ligand for the orphan receptor PEAR1.

    Elenbaas, Jared S / Pudupakkam, Upasana / Ashworth, Katrina J / Kang, Chul Joo / Patel, Ved / Santana, Katherine / Jung, In-Hyuk / Lee, Paul C / Burks, Kendall H / Amrute, Junedh M / Mecham, Robert P / Halabi, Carmen M / Alisio, Arturo / Di Paola, Jorge / Stitziel, Nathan O

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 1511

    Language English
    Publishing date 2023-03-17
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-37005-x
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  4. Article ; Online: SVEP1 is an endogenous ligand for the orphan receptor PEAR1.

    Elenbaas, Jared S / Pudupakkam, Upasana / Ashworth, Katrina J / Kang, Chul Joo / Patel, Ved / Santana, Katherine / Jung, In-Hyuk / Lee, Paul C / Burks, Kendall H / Amrute, Junedh M / Mecham, Robert P / Halabi, Carmen M / Alisio, Arturo / Di Paola, Jorge / Stitziel, Nathan O

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 850

    Abstract: Sushi, von Willebrand factor type A, EGF and pentraxin domain containing 1 (SVEP1) is an extracellular matrix protein that causally promotes vascular disease and associates with platelet reactivity in humans. Here, using a human genomic and proteomic ... ...

    Abstract Sushi, von Willebrand factor type A, EGF and pentraxin domain containing 1 (SVEP1) is an extracellular matrix protein that causally promotes vascular disease and associates with platelet reactivity in humans. Here, using a human genomic and proteomic approach, we identify a high affinity, disease-relevant, and potentially targetable interaction between SVEP1 and the orphan receptor Platelet and Endothelial Aggregation Receptor 1 (PEAR1). This interaction promotes PEAR1 phosphorylation and disease associated AKT/mTOR signaling in vascular cells and platelets. Mice lacking SVEP1 have reduced platelet activation, and exogenous SVEP1 induces PEAR1-dependent activation of platelets. SVEP1 and PEAR1 causally and concordantly relate to platelet phenotypes and cardiovascular disease in humans, as determined by Mendelian Randomization. Targeting this receptor-ligand interaction may be a viable therapeutic strategy to treat or prevent cardiovascular and thrombotic disease.
    MeSH term(s) Humans ; Animals ; Mice ; Blood Platelets/metabolism ; Ligands ; Proteomics ; Receptors, Cell Surface/metabolism ; Platelet Aggregation ; Cell Adhesion Molecules/metabolism
    Chemical Substances Ligands ; Receptors, Cell Surface ; PEAR1 protein, human ; SVEP1 protein, human ; Cell Adhesion Molecules
    Language English
    Publishing date 2023-02-15
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-36486-0
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  5. Article ; Online: Inference of population mutation rate and detection of segregating sites from next-generation sequence data.

    Kang, Chul Joo / Marjoram, Paul

    Genetics

    2011  Volume 189, Issue 2, Page(s) 595–605

    Abstract: We live in an age in which our ability to collect large amounts of genome-wide genetic variation data offers the promise of providing the key to the understanding and treatment of genetic diseases. Over the next few years this effort will be spearheaded ... ...

    Abstract We live in an age in which our ability to collect large amounts of genome-wide genetic variation data offers the promise of providing the key to the understanding and treatment of genetic diseases. Over the next few years this effort will be spearheaded by so-called next-generation sequencing technologies, which provide vast amounts of short-read sequence data at relatively low cost. This technology is often used to detect unknown variation in regions that have been linked with a given disease or phenotype. However, error rates are significant, leading to some nontrivial issues when it comes to interpreting the data. In this article, we present a method with which to address questions of widespread interest: calling variants and estimating the population mutation rate. We show performance of the method using simulation studies before applying our approach to an analysis of data from the 1000 Genomes project.
    MeSH term(s) Algorithms ; Bayes Theorem ; Genetic Predisposition to Disease/genetics ; Genetic Variation ; Genetics, Population ; Genome, Human/genetics ; Genome-Wide Association Study/methods ; Genotype ; Humans ; Mutation Rate ; Phenotype ; Polymorphism, Single Nucleotide ; Sequence Analysis, DNA/methods
    Language English
    Publishing date 2011-08-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2167-2
    ISSN 1943-2631 ; 0016-6731
    ISSN (online) 1943-2631
    ISSN 0016-6731
    DOI 10.1534/genetics.111.130898
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: ANGPTL3 Deficiency and Risk of Hepatic Steatosis.

    D'Erasmo, Laura / Di Martino, Michele / Neufeld, Thomas / Fraum, Tyler J / Kang, Chul Joo / Burks, Kendall H / Di Costanzo, Alessia / Minicocci, Ilenia / Bini, Simone / Maranghi, Marianna / Pigna, Giovanni / Labbadia, Giancarlo / Zheng, Jie / Fierro, Davide / Montali, Anna / Ceci, Fabrizio / Catalano, Carlo / Davidson, Nicholas O / Lucisano, Giuseppe /
    Nicolucci, Antonio / Arca, Marcello / Stitziel, Nathan O

    Circulation

    2023  Volume 148, Issue 19, Page(s) 1479–1489

    Abstract: Background: ANGPTL3 (angiopoietin-like 3) is a therapeutic target for reducing plasma levels of triglycerides and low-density lipoprotein cholesterol. A recent trial with vupanorsen, an antisense oligonucleotide targeting hepatic production of ANGPTL3, ... ...

    Abstract Background: ANGPTL3 (angiopoietin-like 3) is a therapeutic target for reducing plasma levels of triglycerides and low-density lipoprotein cholesterol. A recent trial with vupanorsen, an antisense oligonucleotide targeting hepatic production of ANGPTL3, reported a dose-dependent increase in hepatic fat. It is unclear whether this adverse effect is due to an on-target effect of inhibiting hepatic ANGPTL3.
    Methods: We recruited participants with ANGPTL3 deficiency related to
    Results: We recruited participants with complete (n=6) or partial (n=32) ANGPTL3 deficiency related to
    Conclusions: ANGPTL3 deficiency related to LoF mutations in
    MeSH term(s) Humans ; Angiopoietin-like Proteins/genetics ; Angiopoietin-Like Protein 3 ; Triglycerides ; Cholesterol, LDL
    Chemical Substances Angiopoietin-like Proteins ; Angiopoietin-Like Protein 3 ; vupanorsen ; Triglycerides ; Cholesterol, LDL ; ANGPTL3 protein, human
    Language English
    Publishing date 2023-09-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.123.065866
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  7. Article ; Online: SVEP1 is a human coronary artery disease locus that promotes atherosclerosis.

    Jung, In-Hyuk / Elenbaas, Jared S / Alisio, Arturo / Santana, Katherine / Young, Erica P / Kang, Chul Joo / Kachroo, Puja / Lavine, Kory J / Razani, Babak / Mecham, Robert P / Stitziel, Nathan O

    Science translational medicine

    2021  Volume 13, Issue 586

    Abstract: A low-frequency variant of sushi, von Willebrand factor type A, EGF, and pentraxin domain-containing protein 1 (SVEP1), an extracellular matrix protein, is associated with risk of coronary disease in humans independent of plasma lipids. Despite a robust ... ...

    Abstract A low-frequency variant of sushi, von Willebrand factor type A, EGF, and pentraxin domain-containing protein 1 (SVEP1), an extracellular matrix protein, is associated with risk of coronary disease in humans independent of plasma lipids. Despite a robust statistical association, if and how SVEP1 might contribute to atherosclerosis remained unclear. Here, using Mendelian randomization and complementary mouse models, we provide evidence that SVEP1 promotes atherosclerosis in humans and mice and is expressed by vascular smooth muscle cells (VSMCs) within the atherosclerotic plaque. VSMCs also interact with SVEP1, causing proliferation and dysregulation of key differentiation pathways, including integrin and Notch signaling. Fibroblast growth factor receptor transcription increases in VSMCs interacting with SVEP1 and is further increased by the coronary disease-associated
    MeSH term(s) Animals ; Atherosclerosis/genetics ; Cell Adhesion Molecules/genetics ; Cell Proliferation ; Cells, Cultured ; Coronary Artery Disease/genetics ; Humans ; Mice ; Mice, Inbred C57BL ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle ; Plaque, Atherosclerotic/genetics
    Chemical Substances Cell Adhesion Molecules ; SVEP1 protein, human
    Language English
    Publishing date 2021-03-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.abe0357
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  8. Article ; Online: Methods for detecting associations between phenotype and aggregations of rare variants.

    Yang, Fan / Kang, Chul Joo / Marjoram, Paul

    BMC proceedings

    2011  Volume 5 Suppl 9, Page(s) S51

    Abstract: Although genome-wide association studies have uncovered variants associated with more than 150 traits, the percentage of phenotypic variation explained by these associations remains small. This has led to the search for the dark matter that explains this ...

    Abstract Although genome-wide association studies have uncovered variants associated with more than 150 traits, the percentage of phenotypic variation explained by these associations remains small. This has led to the search for the dark matter that explains this missing genetic component of heritability. One potential explanation for dark matter is rare variants, and several statistics have been devised to detect associations resulting from aggregations of rare variants in relatively short regions of interest, such as candidate genes. In this paper we investigate the feasibility of extending this approach in an agnostic way, in which we consider all variants within a much broader region of interest, such as an entire chromosome or even the entire exome. Our method searches for subsets of variant sites using either Markov chain Monte Carlo or genetic algorithms. The analysis was performed with knowledge of the Genetic Analysis Workshop 17 answers.
    Language English
    Publishing date 2011-11-29
    Publishing country England
    Document type Journal Article
    ZDB-ID 2411867-9
    ISSN 1753-6561 ; 1753-6561
    ISSN (online) 1753-6561
    ISSN 1753-6561
    DOI 10.1186/1753-6561-5-S9-S51
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  9. Article ; Online: Mitochondrial genome copy number measured by DNA sequencing in human blood is strongly associated with metabolic traits via cell-type composition differences.

    Ganel, Liron / Chen, Lei / Christ, Ryan / Vangipurapu, Jagadish / Young, Erica / Das, Indraniel / Kanchi, Krishna / Larson, David / Regier, Allison / Abel, Haley / Kang, Chul Joo / Scott, Alexandra / Havulinna, Aki / Chiang, Charleston W K / Service, Susan / Freimer, Nelson / Palotie, Aarno / Ripatti, Samuli / Kuusisto, Johanna /
    Boehnke, Michael / Laakso, Markku / Locke, Adam / Stitziel, Nathan O / Hall, Ira M

    Human genomics

    2021  Volume 15, Issue 1, Page(s) 34

    Abstract: Background: Mitochondrial genome copy number (MT-CN) varies among humans and across tissues and is highly heritable, but its causes and consequences are not well understood. When measured by bulk DNA sequencing in blood, MT-CN may reflect a combination ... ...

    Abstract Background: Mitochondrial genome copy number (MT-CN) varies among humans and across tissues and is highly heritable, but its causes and consequences are not well understood. When measured by bulk DNA sequencing in blood, MT-CN may reflect a combination of the number of mitochondria per cell and cell-type composition. Here, we studied MT-CN variation in blood-derived DNA from 19184 Finnish individuals using a combination of genome (N = 4163) and exome sequencing (N = 19034) data as well as imputed genotypes (N = 17718).
    Results: We identified two loci significantly associated with MT-CN variation: a common variant at the MYB-HBS1L locus (P = 1.6 × 10
    Conclusion: These results suggest that measurements of MT-CN in blood-derived DNA partially reflect differences in cell-type composition and that these differences are causally linked to insulin and related traits.
    MeSH term(s) Adult ; Aged ; Apoptosis Regulatory Proteins/genetics ; Cell Lineage/genetics ; DNA Copy Number Variations/genetics ; DNA, Mitochondrial/blood ; DNA, Mitochondrial/genetics ; Female ; GTP-Binding Proteins/genetics ; Genetic Predisposition to Disease ; Genome, Mitochondrial/genetics ; Genome-Wide Association Study ; Humans ; Male ; Membrane Proteins/genetics ; Mendelian Randomization Analysis ; Middle Aged ; Phenotype ; Polymorphism, Single Nucleotide/genetics ; Proto-Oncogene Proteins c-myb/genetics ; Sequence Analysis, DNA ; Exome Sequencing
    Chemical Substances Apoptosis Regulatory Proteins ; DNA, Mitochondrial ; MYB protein, human ; Membrane Proteins ; Proto-Oncogene Proteins c-myb ; TMBIM1 protein, human ; GTP-Binding Proteins (EC 3.6.1.-) ; HBS1L protein, human (EC 3.6.1.-)
    Language English
    Publishing date 2021-06-07
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2147618-4
    ISSN 1479-7364 ; 1479-7364
    ISSN (online) 1479-7364
    ISSN 1479-7364
    DOI 10.1186/s40246-021-00335-2
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  10. Article ; Online: Association of structural variation with cardiometabolic traits in Finns.

    Chen, Lei / Abel, Haley J / Das, Indraniel / Larson, David E / Ganel, Liron / Kanchi, Krishna L / Regier, Allison A / Young, Erica P / Kang, Chul Joo / Scott, Alexandra J / Chiang, Colby / Wang, Xinxin / Lu, Shuangjia / Christ, Ryan / Service, Susan K / Chiang, Charleston W K / Havulinna, Aki S / Kuusisto, Johanna / Boehnke, Michael /
    Laakso, Markku / Palotie, Aarno / Ripatti, Samuli / Freimer, Nelson B / Locke, Adam E / Stitziel, Nathan O / Hall, Ira M

    American journal of human genetics

    2021  Volume 108, Issue 4, Page(s) 583–596

    Abstract: The contribution of genome structural variation (SV) to quantitative traits associated with cardiometabolic diseases remains largely unknown. Here, we present the results of a study examining genetic association between SVs and cardiometabolic traits in ... ...

    Abstract The contribution of genome structural variation (SV) to quantitative traits associated with cardiometabolic diseases remains largely unknown. Here, we present the results of a study examining genetic association between SVs and cardiometabolic traits in the Finnish population. We used sensitive methods to identify and genotype 129,166 high-confidence SVs from deep whole-genome sequencing (WGS) data of 4,848 individuals. We tested the 64,572 common and low-frequency SVs for association with 116 quantitative traits and tested candidate associations using exome sequencing and array genotype data from an additional 15,205 individuals. We discovered 31 genome-wide significant associations at 15 loci, including 2 loci at which SVs have strong phenotypic effects: (1) a deletion of the ALB promoter that is greatly enriched in the Finnish population and causes decreased serum albumin level in carriers (p = 1.47 × 10
    MeSH term(s) Alleles ; Cardiovascular Diseases/genetics ; Cholesterol/blood ; DNA Copy Number Variations/genetics ; Female ; Finland ; Genome, Human/genetics ; Genomic Structural Variation/genetics ; Genotype ; High-Throughput Nucleotide Sequencing ; Humans ; Male ; Mitochondrial Proteins/genetics ; Promoter Regions, Genetic/genetics ; Pyruvate Dehydrogenase (Lipoamide)-Phosphatase/genetics ; Pyruvic Acid/metabolism ; Serum Albumin, Human/genetics
    Chemical Substances ALB protein, human ; Mitochondrial Proteins ; PDPR protein, human ; Pyruvic Acid (8558G7RUTR) ; Cholesterol (97C5T2UQ7J) ; Pyruvate Dehydrogenase (Lipoamide)-Phosphatase (EC 3.1.3.43) ; Serum Albumin, Human (ZIF514RVZR)
    Language English
    Publishing date 2021-04-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 219384-x
    ISSN 1537-6605 ; 0002-9297
    ISSN (online) 1537-6605
    ISSN 0002-9297
    DOI 10.1016/j.ajhg.2021.03.008
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