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dc.contributor.authorProkopec, Stephenie D.
dc.contributor.authorHoulahan, Kathleen E.
dc.contributor.authorSun, Ren X.
dc.contributor.authorWatson, John D.
dc.contributor.authorYao, Cindy Q.
dc.contributor.authorLee, Jamie
dc.contributor.authorP’ng, Christine
dc.contributor.authorPang, Renee
dc.contributor.authorWu, Alexander H.
dc.contributor.authorChong, Lauren C.
dc.contributor.authorSmith, Ashley B.
dc.contributor.authorHarding, Nicholas J.
dc.contributor.authorMoffat, Ivy D.
dc.contributor.authorLindén, Jere
dc.contributor.authorLensu, Sanna
dc.contributor.authorOkey, Allan B.
dc.contributor.authorPohjanvirta, Raimo
dc.contributor.authorBoutros, Paul C.
dc.identifier.citationProkopec, S. D., Houlahan, K. E., Sun, R. X., Watson, J. D., Yao, C. Q., Lee, J., . . . Boutros, P. C. (2017). Compendium of TCDD-mediated transcriptomic response datasets in mammalian model systems. <em>BMC Genomics</em>, 18, 78. <a href="">doi:10.1186/s12864-016-3446-z</a>
dc.description.abstractBackground 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is the most potent congener of the dioxin class of environmental contaminants. Exposure to TCDD causes a wide range of toxic outcomes, ranging from chloracne to acute lethality. The severity of toxicity is highly dependent on the aryl hydrocarbon receptor (AHR). Binding of TCDD to the AHR leads to changes in transcription of numerous genes. Studies evaluating the transcriptional changes brought on by TCDD may provide valuable insight into the role of the AHR in human health and disease. We therefore compiled a collection of transcriptomic datasets that can be used to aid the scientific community in better understanding the transcriptional effects of ligand-activated AHR. Results Specifically, we have created a datasets package – TCDD.Transcriptomics – for the R statistical environment, consisting of 63 unique experiments comprising 377 samples, including various combinations of 3 species (human derived cell lines, mouse and rat), 4 tissue types (liver, kidney, white adipose tissue and hypothalamus) and a wide range of TCDD exposure times and doses. These datasets have been fully standardized using consistent preprocessing and annotation packages (available as of September 14, 2015). To demonstrate the utility of this R package, a subset of “AHR-core” genes were evaluated across the included datasets. Ahrr, Nqo1 and members of the Cyp family were significantly induced following exposure to TCDD across the studies as expected while Aldh3a1 was induced specifically in rat liver. Inmt was altered only in liver tissue and primarily by rat-AHR. Conclusions Analysis of the “AHR-core” genes demonstrates a continued need for studies surrounding the impact of AHR-activity on the transcriptome; genes believed to be consistently regulated by ligand-activated AHR show surprisingly little overlap across species and tissues. Until now, a comprehensive assessment of the transcriptome across these studies was challenging due to differences in array platforms, processing methods and annotation versions. We believe that this package, which is freely available for download ( will prove to be a highly beneficial resource to the scientific community evaluating the effects of TCDD exposure as well as the variety of functions of the AHR.
dc.publisherBioMed Central
dc.relation.ispartofseriesBMC Genomics
dc.subject.othermicroarray datasets
dc.titleCompendium of TCDD-mediated transcriptomic response datasets in mammalian model systems
dc.contributor.laitosLiikuntabiologian laitosfi
dc.contributor.laitosDepartment of Biology of Physical Activityen
dc.type.coarjournal article
dc.rights.copyright© The Author(s). 2017 This article is distributed under the terms of the Creative Commons Attribution 4.0 International License.

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This article is distributed under the terms of the Creative Commons Attribution 4.0
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Except where otherwise noted, this item's license is described as © The Author(s). 2017 This article is distributed under the terms of the Creative Commons Attribution 4.0 International License.