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Filtering by: Academic Affiliation Environmental and Molecular Toxicology Date 2016 Non-Academic Affiliation Oregon State University. Undergraduate Research, Scholarship, and the Arts (URSA) Rights Statement In Copyright

1. LncRNA regulation in mouse lung tumor from dibenzo[def,p]chrysene induced carcinogenesis in a transplacental Nrf2 knockout mouse model

Creator:: Patel, Karan, You, Hyekyoung, Siddens, Lisbeth, and Williams, David
Abstract:: Dibenzo[def,p]chrysene (DBC) is a highly potent, but less prevalent, environmental carcinogen belonging to a class of compounds known as Polycyclic Aromatic Hydrocarbons (PAHs). They are highly ubiquitous and arise as a byproduct of natural and anthropogenic combustion processes. Previous studies have documented carcinogenic effects upon in utero exposure of PAHs....
Resource Type:: Poster

2. Alternative Exon 3 Inclusion in the Vitamin D Receptor (VDR) Modulates Transcriptional Activity for Target Genes in a Ligand-Independent Manner

Creator:: Cameron, Alex N., Annalora, Andrew, and Marcus, Craig
Abstract:: Xenobiotic exposures may induce alternative splicing in the pre-mRNA of nuclear hormone receptor (NHR) genes, yielding unpredictable patterns of gene expression that may promote adverse drug events and promote environmental disease. Informed by observations in the androgen receptor (AR; class I NHR), whereby alternatively-spliced AR transcripts induce ligand-independent hormone signaling...
Resource Type:: Poster

ScholarsArchive@OSU

1. LncRNA regulation in mouse lung tumor from dibenzo[def,p]chrysene induced carcinogenesis in a transplacental Nrf2 knockout mouse model

2. Alternative Exon 3 Inclusion in the Vitamin D Receptor (VDR) Modulates Transcriptional Activity for Target Genes in a Ligand-Independent Manner

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1. LncRNA regulation in mouse lung tumor from dibenzo[def,p]chrysene induced carcinogenesis in a transplacental Nrf2 knockout mouse model

2. Alternative Exon 3 Inclusion in the Vitamin D Receptor (VDR) Modulates Transcriptional Activity for Target Genes in a Ligand-Independent Manner

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