The Comparative Toxicogenomics Database: update 2019

被引:705
作者
Davis, Allan Peter [1 ]
Grondin, Cynthia J. [1 ]
Johnson, Robin J. [1 ]
Sciaky, Daniela [1 ]
McMorran, Roy [2 ]
Wiegers, Jolene [1 ]
Wiegers, Thomas C. [1 ]
Mattingly, Carolyn J. [1 ,3 ]
机构
[1] North Carolina State Univ, Dept Biol Sci, Raleigh, NC 27695 USA
[2] Mt Desert Isl Biol Lab, Dept Bioinformat, Salsbury Cove, ME 04672 USA
[3] North Carolina State Univ, Ctr Human Hlth & Environm, Raleigh, NC 27695 USA
关键词
ONTOLOGY; DISEASES; RESOURCE; EXPOSURE; GENES; TOOL; CTD;
D O I
10.1093/nar/gky868
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The Comparative Toxicogenomics Database (CTD; http://ctdbase.org/) is a premier public resource for literature-based, manually curated associations between chemicals, gene products, phenotypes, diseases, and environmental exposures. In this biennial update, we present our new chemical-phenotype module that codes chemical-induced effects on phenotypes, curated using controlled vocabularies for chemicals, phenotypes, taxa, and anatomical descriptors; this module provides unique opportunities to explore cellular and system-level phenotypes of the pre-disease state and allows users to construct predictive adverse outcome pathways (linking chemical-gene molecular initiating events with phenotypic key events, diseases, and population-level health outcomes). We also report a 46% increase in CTD manually curated content, which when integrated with other datasets yields more than 38 million toxicogenomic relationships. We describe new querying and display features for our enhanced chemical-exposure science module, providing greater scope of content and utility. As well, we discuss an updated MEDIC disease vocabulary with over 1700 new terms and accession identifiers. To accommodate these increases in data content and functionality, CTD has upgraded its computational infrastructure. These updates continue to improve CTD and help inform new testable hypotheses about the etiology and mechanisms underlying environmentally influenced diseases.
引用
收藏
页码:D948 / D954
页数:7
相关论文
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