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CPAG: software for leveraging pleiotropy in GWAS to reveal similarity between human traits links plasma fatty acids and intestinal inflammation.

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Date
2015-09-15
Authors
Wang, L
Oehlers, SH
Espenschied, ST
Rawls, JF
Tobin, DM
Ko, DC
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Abstract
Meta-analyses of genome-wide association studies (GWAS) have demonstrated that the same genetic variants can be associated with multiple diseases and other complex traits. We present software called CPAG (Cross-Phenotype Analysis of GWAS) to look for similarities between 700 traits, build trees with informative clusters, and highlight underlying pathways. Clusters are consistent with pre-defined groups and literature-based validation but also reveal novel connections. We report similarity between plasma palmitoleic acid and Crohn's disease and find that specific fatty acids exacerbate enterocolitis in zebrafish. CPAG will become increasingly powerful as more genetic variants are uncovered, leading to a deeper understanding of complex traits. CPAG is freely available at www.sourceforge.net/projects/CPAG/.
Type
Journal article
Subject
Animals
Cluster Analysis
Crohn Disease
Enterocolitis
Fatty Acids, Monounsaturated
Genetic Pleiotropy
Genome-Wide Association Study
Humans
Phenotype
Polymorphism, Single Nucleotide
Software
Zebrafish
Permalink
https://hdl.handle.net/10161/10609
Published Version (Please cite this version)
10.1186/s13059-015-0722-1
Publication Info
Wang, L; Oehlers, SH; Espenschied, ST; Rawls, JF; Tobin, DM; & Ko, DC (2015). CPAG: software for leveraging pleiotropy in GWAS to reveal similarity between human traits links plasma fatty acids and intestinal inflammation. Genome Biol, 16. pp. 190. 10.1186/s13059-015-0722-1. Retrieved from https://hdl.handle.net/10161/10609.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
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Scholars@Duke

Ted Espenschied

Research Scholar
Ko

Dennis Ko

Associate Professor in Molecular Genetics and Microbiology
Using Pathogens to Decipher Genetic Variation Connecting Cell Biology and Disease SusceptibilityDespite improvements in public health, advancements in vaccines, and the development of many classes of antibiotics, infectious disease is still responsible for over a quarter of all deaths worldwide. However, even for the most devastating of pandemics, individuals demonstrate a large variability in the severity of infection. The long-term goal of the lab is to understand the ge
Rawls

John Franklin Rawls

Professor of Molecular Genetics and Microbiology
We seek to understand how the intestinal microbiome contributes to vertebrate physiology and disease. To that end, we leverage complementary zebrafish and mouse models to study the integrative physiology of host-microbiome interactions. This work has identified novel and conserved mechanisms by which intestinal bacteria regulate dietary fat metabolism and systemic innate immunity. We also apply genomic approaches in these animal models to understand the transcriptional regulatory pathways utiliz
Tobin

David M. Tobin

Associate Professor of Molecular Genetics and Microbiology
Tuberculosis: Mycobacterial Pathogenesis and Host Susceptibility Tuberculosis kills 1.5 million people annually. Our laboratory aims to understand the intricate interplay between mycobacteria and their hosts using a combination of model organism genetics, human genetics, pharmacology and high-resolution microscopy. By identifying key pathways utilized by the infecting bacteria and the host innate immune system, we hope to discover new therapeutic targets and interventi

Liuyang Wang

Assistant Research Professor of Molecular Genetics and Microbiology
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