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CPAG: software for leveraging pleiotropy in GWAS to reveal similarity between human traits links plasma fatty acids and intestinal inflammation.
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 articleSubject
AnimalsCluster Analysis
Crohn Disease
Enterocolitis
Fatty Acids, Monounsaturated
Genetic Pleiotropy
Genome-Wide Association Study
Humans
Phenotype
Polymorphism, Single Nucleotide
Software
Zebrafish
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https://hdl.handle.net/10161/10609Published Version (Please cite this version)
10.1186/s13059-015-0722-1Publication Info
(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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Show full item recordScholars@Duke
Ted Espenschied
Research Scholar
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
John Franklin Rawls
James B. Duke Distinguished Professor
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
David M. Tobin
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
Leveraging bioinformatics and big data to understand the intricacies of human diseases.
My overall research goals are centered on unraveling the molecular mechanism underpinning
human disease susceptibility and harnessing these findings to innovative diagnostic
and therapeutic strategies. I have adopted a multidisciplinary approach that integrates
genomics, transcriptomics, and computational biology. Leveraging high-throughput cellular
screening and genome-wide associ
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