Biological knowledge-driven analysis of epistasis in human GWAS with application to lipid traits.

[1]  Andrew G. Clark,et al.  Gene-Based Testing of Interactions in Association Studies of Quantitative Traits , 2013, PLoS genetics.

[2]  Steve Horvath,et al.  Adipose Co-expression networks across Finns and Mexicans identify novel triglyceride-associated genes , 2012, BMC Medical Genomics.

[3]  Tom R. Gaunt,et al.  Large-scale gene-centric meta-analysis across 32 studies identifies multiple lipid loci. , 2012, American journal of human genetics.

[4]  J. Belmont,et al.  Interaction between SNPs in the RXRA and near ANGPTL3 gene region inhibits apoB reduction after statin-fenofibric acid therapy in individuals with mixed dyslipidemia[S] , 2012, Journal of Lipid Research.

[5]  M. Perlman,et al.  Multivariate Detection of Gene‐Gene Interactions , 2012, Genetic epidemiology.

[6]  Yuehua Cui,et al.  Gene-centric gene–gene interaction: A model-based kernel machine method , 2012, 1209.6502.

[7]  Taesung Park,et al.  A novel method to identify high order gene-gene interactions in genome-wide association studies: Gene-based MDR , 2012, BMC Bioinformatics.

[8]  Christophe G. Lambert,et al.  Learning from our GWAS mistakes: from experimental design to scientific method , 2012, Biostatistics.

[9]  E. Lander,et al.  The mystery of missing heritability: Genetic interactions create phantom heritability , 2012, Proceedings of the National Academy of Sciences.

[10]  Haiyuan Yu,et al.  HINT: High-quality protein interactomes and their applications in understanding human disease , 2012, BMC Systems Biology.

[11]  M. Fornage,et al.  Genetic Loci Associated with Plasma Phospholipid n-3 Fatty Acids: A Meta-Analysis of Genome-Wide Association Studies from the CHARGE Consortium , 2011, PLoS genetics.

[12]  Emmanouil Collab.  A map of human genome variation from population-scale sequencing , 2011, Nature.

[13]  Wei Zheng,et al.  dmGWAS: dense module searching for genome-wide association studies in protein-protein interaction networks , 2011, Bioinform..

[14]  Jing He,et al.  Gene-based interaction analysis by incorporating external linkage disequilibrium information , 2010, European Journal of Human Genetics.

[15]  Yan V. Sun,et al.  Identification of epistatic effects using a protein-protein interaction database. , 2010, Human molecular genetics.

[16]  Sharon R Grossman,et al.  Integrating common and rare genetic variation in diverse human populations , 2010, Nature.

[17]  Momiao Xiong,et al.  A Novel Statistic for Genome-Wide Interaction Analysis , 2010, PLoS genetics.

[18]  Tanya M. Teslovich,et al.  Biological, Clinical, and Population Relevance of 95 Loci for Blood Lipids , 2010, Nature.

[19]  Jason H. Moore,et al.  Missing heritability and strategies for finding the underlying causes of complex disease , 2010, Nature Reviews Genetics.

[20]  Marcus W Feldman,et al.  On the Classification of Epistatic Interactions , 2010, Genetics.

[21]  Luigi Ferrucci,et al.  Genome-wide association analysis of total cholesterol and high-density lipoprotein cholesterol levels using the Framingham Heart Study data , 2010, BMC Medical Genetics.

[22]  Judy H. Cho,et al.  Finding the missing heritability of complex diseases , 2009, Nature.

[23]  Scott M. Williams,et al.  Epistasis and its implications for personal genetics. , 2009, American journal of human genetics.

[24]  F. Collins,et al.  Potential etiologic and functional implications of genome-wide association loci for human diseases and traits , 2009, Proceedings of the National Academy of Sciences.

[25]  H. Cordell.  Detecting gene–gene interactions that underlie human diseases , 2009, Nature Reviews Genetics.

[26]  P. Donnelly,et al.  A Flexible and Accurate Genotype Imputation Method for the Next Generation of Genome-Wide Association Studies , 2009, PLoS genetics.

[27]  K. Frazer,et al.  Human genetic variation and its contribution to complex traits , 2009, Nature Reviews Genetics.

[28]  Lincoln Stein,et al.  Reactome knowledgebase of human biological pathways and processes , 2008, Nucleic Acids Res..

[29]  Christian Gieger,et al.  Loci influencing lipid levels and coronary heart disease risk in 16 European population cohorts , 2009, Nature Genetics.

[30]  B. Maher.  Personal genomes: The case of the missing heritability , 2008, Nature.

[31]  M. Daly,et al.  Common SNPs in HMGCR in Micronesians and Whites Associated With LDL-Cholesterol Levels Affect Alternative Splicing of Exon13 , 2008, Arteriosclerosis, thrombosis, and vascular biology.

[32]  Li Ma,et al.  Parallel and serial computing tools for testing single-locus and epistatic SNP effects of quantitative traits in genome-wide association studies , 2008, BMC Bioinformatics.

[33]  Daniel Dvorkin,et al.  Genome-wide analysis of single-locus and epistasis single-nucleotide polymorphism effects on anti-cyclic citrullinated peptide as a measure of rheumatoid arthritis , 2007, BMC proceedings.

[34]  K. Sirotkin,et al.  The NCBI dbGaP database of genotypes and phenotypes , 2007, Nature Genetics.

[35]  Manuel A. R. Ferreira,et al.  PLINK: a tool set for whole-genome association and population-based linkage analyses. , 2007, American journal of human genetics.

[36]  D. Reich,et al.  Principal components analysis corrects for stratification in genome-wide association studies , 2006, Nature Genetics.

[37]  P. Donnelly,et al.  Genome-wide strategies for detecting multiple loci that influence complex diseases , 2005, Nature Genetics.

[38]  M. Purugganan,et al.  Epistatic interaction between Arabidopsis FRI and FLC flowering time genes generates a latitudinal cline in a life history trait. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[39]  Chris S. Haley,et al.  Epistasis: too often neglected in complex trait studies? , 2004, Nature Reviews Genetics.

[40]  S. Kerje,et al.  A global search reveals epistatic interaction between QTL for early growth in the chicken. , 2003, Genome research.

[41]  R. Kronmal,et al.  Multi-Ethnic Study of Atherosclerosis: objectives and design. , 2002, American journal of epidemiology.

[42]  H. Cordell.  Epistasis: what it means, what it doesn't mean, and statistical methods to detect it in humans. , 2002, Human molecular genetics.

[43]  Tom H. Pringle,et al.  The human genome browser at UCSC. , 2002, Genome research.

[44]  G A Churchill,et al.  Genome-wide epistatic interaction analysis reveals complex genetic determinants of circadian behavior in mice. , 2001, Genome research.

[45]  J. Cheverud,et al.  Epistasis and its contribution to genetic variance components. , 1995, Genetics.

[46]  A. Folsom,et al.  The Atherosclerosis Risk in Communities (ARIC) Study: design and objectives. The ARIC investigators. , 1989, American journal of epidemiology.

[47]  W. W. Doane,et al.  INTERACTIONS BETWEEN THE AMYLASE AND ADIPOSE CHROMOSOMAL REGIONS OF DROSOPHILA MELANOGASTER , 1984, Evolution; international journal of organic evolution.

[48]  C. Cockerham,et al.  An Extension of the Concept of Partitioning Hereditary Variance for Analysis of Covariances among Relatives When Epistasis Is Present. , 1954, Genetics.

[49]  T. Dawber,et al.  Epidemiological approaches to heart disease: the Framingham Study. , 1951, American journal of public health and the nation's health.

[50]  Genomewide association study of 14 , 000 cases of seven common diseases and 3 , 000 shared controls Supplementary Information , 2022 .