An Expanded View of Complex Traits: From Polygenic to Omnigenic
暂无分享,去创建一个
[1] Gerome Breen,et al. Psychiatric Genomics: An Update and an Agenda , 2017, bioRxiv.
[2] Stephen Burgess,et al. Consequences of natural perturbations in the human plasma proteome , 2017, bioRxiv.
[3] Wei Cheng,et al. Contribution of copy number variants to schizophrenia from a genome-wide study of 41,321 subjects , 2016, Nature Genetics.
[4] Abhijeet R. Sonawane,et al. Understanding Tissue-Specific Gene Regulation , 2017, bioRxiv.
[5] Nikolaos A Patsopoulos,et al. Limited statistical evidence for shared genetic effects of eQTLs and autoimmune disease-associated loci in three major immune cell types , 2017, Nature Genetics.
[6] M. Rienstra,et al. Letter to editor: Reply on question of Marques JR et al. regarding the paper entitled: "The LifeLines cohort study: Prevalence and treatment of cardiovascular disease and risk factors". , 2019, International journal of cardiology.
[7] Kaur Alasoo,et al. Genetic effects on chromatin accessibility foreshadow gene expression changes in macrophage immune response , 2017, bioRxiv.
[8] Marcelo P. Segura-Lepe,et al. Rare and low-frequency coding variants alter human adult height , 2016, Nature.
[9] Jakob Grove,et al. Polygenic transmission disequilibrium confirms that common and rare variation act additively to create risk for autism spectrum disorders , 2016, Nature Genetics.
[10] Len A. Pennacchio,et al. Enhancer Variants Synergistically Drive Dysfunction of a Gene Regulatory Network In Hirschsprung Disease , 2016, Cell.
[11] Eleazar Eskin,et al. Distant regulatory effects of genetic variation in multiple human tissues , 2016, bioRxiv.
[12] B. Pasaniuc,et al. Contrasting the genetic architecture of 30 complex traits from summary association data , 2016, bioRxiv.
[13] P. Visscher,et al. A plethora of pleiotropy across complex traits , 2016, Nature Genetics.
[14] Steven P. Gygi,et al. Defining the consequences of genetic variation on a proteome-wide scale , 2016, Nature.
[15] A. Chakravarti,et al. Revealing rate‐limiting steps in complex disease biology: The crucial importance of studying rare, extreme‐phenotype families , 2016, BioEssays : news and reviews in molecular, cellular and developmental biology.
[16] Joseph K. Pickrell,et al. Detection and interpretation of shared genetic influences on 42 human traits , 2015, Nature Genetics.
[17] Kyle J. Gaulton,et al. Detection of human adaptation during the past 2000 years , 2016, Science.
[18] David A. Knowles,et al. RNA splicing is a primary link between genetic variation and disease , 2016, Science.
[19] C. Spencer,et al. A contribution of novel CNVs to schizophrenia from a genome-wide study of 41,321 subjects: CNV Analysis Group and the Schizophrenia Working Group of the Psychiatric Genomics Consortium , 2016, bioRxiv.
[20] N. Barton,et al. The infinitesimal model , 2016, bioRxiv.
[21] Matthew Stephens,et al. False discovery rates: a new deal , 2016, bioRxiv.
[22] Giulio Genovese,et al. Schizophrenia risk from complex variation of complement component 4 , 2016, Nature.
[23] Yakir A Reshef,et al. Partitioning heritability by functional annotation using genome-wide association summary statistics , 2015, Nature Genetics.
[24] Manolis Kellis,et al. FTO Obesity Variant Circuitry and Adipocyte Browning in Humans. , 2015, The New England journal of medicine.
[25] G. Kempermann. Faculty Opinions recommendation of Human genomics. The Genotype-Tissue Expression (GTEx) pilot analysis: multitissue gene regulation in humans. , 2015 .
[26] Jun S. Liu,et al. The Genotype-Tissue Expression (GTEx) pilot analysis: Multitissue gene regulation in humans , 2015, Science.
[27] Kali T. Witherspoon,et al. Excess of rare, inherited truncating mutations in autism , 2015, Nature Genetics.
[28] M. Daly,et al. An Atlas of Genetic Correlations across Human Diseases and Traits , 2015, Nature Genetics.
[29] N. Wray,et al. Contrasting genetic architectures of schizophrenia and other complex diseases using fast variance components analysis , 2015, Nature Genetics.
[30] Ross M. Fraser,et al. Genetic studies of body mass index yield new insights for obesity biology , 2015, Nature.
[31] Alexis Battle,et al. Impact of regulatory variation from RNA to protein , 2015, Science.
[32] Michael Q. Zhang,et al. Integrative analysis of 111 reference human epigenomes , 2015, Nature.
[33] M. Daly,et al. Genetic and Epigenetic Fine-Mapping of Causal Autoimmune Disease Variants , 2014, Nature.
[34] M. Daly,et al. LD Score regression distinguishes confounding from polygenicity in genome-wide association studies , 2014, Nature Genetics.
[35] Benjamin M. Neale,et al. Genetic Consortium for Anorexia Nervosa of the Wellcome Trust Case Control Consortium , 2015 .
[36] Christopher S. Poultney,et al. Synaptic, transcriptional, and chromatin genes disrupted in autism , 2014, Nature.
[37] Ross M. Fraser,et al. Defining the role of common variation in the genomic and biological architecture of adult human height , 2014, Nature Genetics.
[38] C. Spencer,et al. Biological Insights From 108 Schizophrenia-Associated Genetic Loci , 2014, Nature.
[39] G. Davey Smith,et al. Mendelian randomization: genetic anchors for causal inference in epidemiological studies , 2014, Human molecular genetics.
[40] N. Cox,et al. Obesity-associated variants within FTO form long-range functional connections with IRX3 , 2014, Nature.
[41] Eric S. Lander,et al. A polygenic burden of rare disruptive mutations in schizophrenia , 2014, Nature.
[42] E. Banks,et al. De novo mutations in schizophrenia implicate synaptic networks , 2014, Nature.
[43] Peggy Hall,et al. The NHGRI GWAS Catalog, a curated resource of SNP-trait associations , 2013, Nucleic Acids Res..
[44] Joseph K. Pickrell. Joint analysis of functional genomic data and genome-wide association studies of 18 human traits , 2013, bioRxiv.
[45] J. Pritchard,et al. The deleterious mutation load is insensitive to recent population history , 2013, Nature Genetics.
[46] Sharon R Grossman,et al. Detecting natural selection in genomic data. , 2013, Annual review of genetics.
[47] M. Peters,et al. Systematic identification of trans eQTLs as putative drivers of known disease associations , 2013, Nature Genetics.
[48] L. Furlong. Human diseases through the lens of network biology. , 2013, Trends in genetics : TIG.
[49] Greg Gibson,et al. Blood-Informative Transcripts Define Nine Common Axes of Peripheral Blood Gene Expression , 2013, PLoS genetics.
[50] Buhm Han,et al. Chromatin marks identify critical cell types for fine mapping complex trait variants , 2012 .
[51] David C. Wilson,et al. Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease , 2012, Nature.
[52] Shane J. Neph,et al. Systematic Localization of Common Disease-Associated Variation in Regulatory DNA , 2012, Science.
[53] A. Butte,et al. Leveraging models of cell regulation and GWAS data in integrative network-based association studies , 2012, Nature Genetics.
[54] Cameron D. Palmer,et al. Evidence of widespread selection on standing variation in Europe at height-associated SNPs , 2012, Nature Genetics.
[55] Kasper Lage,et al. Pervasive Sharing of Genetic Effects in Autoimmune Disease , 2011, PLoS genetics.
[56] G. Wagner,et al. The pleiotropic structure of the genotype–phenotype map: the evolvability of complex organisms , 2011, Nature Reviews Genetics.
[57] Alkes L. Price,et al. Single-Tissue and Cross-Tissue Heritability of Gene Expression Via Identity-by-Descent in Related or Unrelated Individuals , 2011, PLoS genetics.
[58] M. Daly,et al. Integrating Autoimmune Risk Loci with Gene-Expression Data Identifies Specific Pathogenic Immune Cell Subsets. , 2011, American journal of human genetics.
[59] E. Davidson. Emerging properties of animal gene regulatory networks , 2010, Nature.
[60] P. Visscher,et al. Common SNPs explain a large proportion of heritability for human height , 2011 .
[61] Joseph K. Pickrell,et al. The Genetics of Human Adaptation: Hard Sweeps, Soft Sweeps, and Polygenic Adaptation , 2010, Current Biology.
[62] D. Goldstein. Common genetic variation and human traits. , 2009, The New England journal of medicine.
[63] B. Walsh,et al. Abundant Genetic Variation + Strong Selection = Multivariate Genetic Constraints: A Geometric View of Adaptation , 2009 .
[64] Judy H. Cho,et al. Finding the missing heritability of complex diseases , 2009, Nature.
[65] P. Visscher,et al. Common polygenic variation contributes to risk of schizophrenia and bipolar disorder , 2009, Nature.
[66] Manuel A. R. Ferreira,et al. Assumption-Free Estimation of Heritability from Genome-Wide Identity-by-Descent Sharing between Full Siblings , 2006, PLoS genetics.
[67] M. Olivier. A haplotype map of the human genome. , 2003, Nature.
[68] M. Olivier. A haplotype map of the human genome , 2003, Nature.
[69] D. Botstein,et al. Discovering genotypes underlying human phenotypes: past successes for mendelian disease, future approaches for complex disease , 2003, Nature Genetics.
[70] S. Strogatz. Exploring complex networks , 2001, Nature.
[71] Courtney A. Harper,et al. A genomic screen of autism: evidence for a multilocus etiology. , 1999, American journal of human genetics.
[72] Duncan J. Watts,et al. Collective dynamics of ‘small-world’ networks , 1998, Nature.
[73] R. Suzman,et al. An Overview of the Health and Retirement Study , 1995 .
[74] N. Barton,et al. Pleiotropic models of quantitative variation. , 1990, Genetics.
[75] R. Fisher. XV.—The Correlation between Relatives on the Supposition of Mendelian Inheritance. , 1919, Transactions of the Royal Society of Edinburgh.
[76] L. Penrose,et al. THE CORRELATION BETWEEN RELATIVES ON THE SUPPOSITION OF MENDELIAN INHERITANCE , 2022 .