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Lyle D. Burgoon

Researcher at Engineer Research and Development Center

Publications -  98
Citations -  3635

Lyle D. Burgoon is an academic researcher from Engineer Research and Development Center. The author has contributed to research in topics: Gene expression & Gene. The author has an hindex of 34, co-authored 94 publications receiving 3223 citations. Previous affiliations of Lyle D. Burgoon include Oak Ridge Institute for Science and Education & United States Environmental Protection Agency.

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The minimum information required for reporting a molecular interaction experiment (MIMIx)

TL;DR: MIMIx, the minimum information required for reporting a molecular interaction experiment, is proposed, which will support the rapid, systematic capture of molecular interaction data in public databases, thereby improving access to valuable interaction data.
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Comparative analysis of dioxin response elements in human, mouse and rat genomic sequences

TL;DR: The results suggest that AhR-mediated gene expression may not be well conserved across species, which could have significant implications in human risk assessment.
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Comparative toxicogenomic analysis of the hepatotoxic effects of TCDD in Sprague Dawley rats and C57BL/6 mice.

TL;DR: Understanding of TCDD-mediated gene expression responses is expanded and indicates that species-specific toxicity may be mediated by differences in gene expression which may help explain the wide range of species sensitivities and will have important implications in risk assessment strategies.
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Temporal and Dose-Dependent Hepatic Gene Expression Patterns in Mice Provide New Insights into TCDD-Mediated Hepatotoxicity

TL;DR: The data support a proposed mechanism for TCDD-mediated hepatotoxicity, including fatty liver, which involves mobilization of peripheral fat and inappropriate increases in hepatic uptake of fatty acids.
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Hypoxia-inducible factor-1α regulates the expression of genes in hypoxic hepatic stellate cells important for collagen deposition and angiogenesis.

TL;DR: The hypothesis was tested that HIF‐1α is activated in HSCs and regulates the expression of genes important for HSC activation and liver fibrosis.