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Titanium Dioxide Nanoparticles Induce DNA Damage and Genetic Instability In vivo in Mice

Cancer research (Chicago, Ill.), 2009-11, Vol.69 (22), p.8784-8789

2009

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Determination of Antibiotic Hypersensitivity among 4,000 Single-Gene-Knockout Mutants of Escherichia coli

Journal of Bacteriology, 2008-09, Vol.190 (17), p.5981-5988

2008

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Treatment of mice with 2,3,7,8-Tetrachlorodibenzo-p-dioxin markedly increases the levels of a number of cytochrome P450 metabolites of omega-3 polyunsaturated fatty acids in the liver and lung

The Journal of Toxicological Sciences, 2013/12/01, Vol.38(6), pp.833-836

2013

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2,3,7,8-Tetrachlorodibenzo-p-dioxin treatment alters eicosanoid levels in several organs of the mouse in an aryl hydrocarbon receptor-dependent fashion

Toxicology and applied pharmacology, 2012-03, Vol.259 (2), p.143-151

2012

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SIN3A, Generally Regarded as a Transcriptional Repressor, Is Required for Induction of Gene Transcription by the Aryl Hydrocarbon Receptor

The Journal of biological chemistry, 2014-11, Vol.289 (48), p.33655-33662

2014

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Exposure to ambient ultrafine particulate matter alters the expression of genes in primary human neurons

Neurotoxicology (Park Forest South), 2017-01, Vol.58, p.50-57

2017

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Genome-wide RNAi high-throughput screen identifies proteins necessary for the AHR-dependent induction of CYP1A1 by 2,3,7,8-tetrachlorodibenzo-p-dioxin

Toxicological sciences, 2013-11, Vol.136 (1), p.107-119

2013

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Human brain derived cells respond in a type-specific manner after exposure to urban particulate matter (PM)

Toxicology in vitro, 2014-10, Vol.28 (7), p.1290-1295

2014

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CYP2S1 is negatively regulated by corticosteroids in human cell lines

Toxicology letters, 2012-02, Vol.209 (1), p.30-34

2012

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2,3,7,8- Te trachlorodibenzo-p-dioxin treatment alters eicosanoid levels in several organs of the mouse in an aryl hydrocarbon receptor-dependent fashion

Toxicology and applied pharmacology, 2011-12, Vol.259 (2), p.143-151

2011

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RNAi High Throughput Screenings Facilitate the Identification of Proteins Necessary for TCDD-induced CYP1A1 Enzymatic Activity and Aid in the Discovery of a Novel Role for Sin3A in AHR-Mediated Gene Expression

Solaimani, Parrisa Sherry

2012

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Oxidative and Inflammatory Pathways in Age-Related Chronic Disease Processes

Inflammation, Aging, and Oxidative Stress, 2016, p.95-106

2016

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Mice, Inbred C57bl
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Polychlorinated Dibenzodioxins - Toxicity
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Ahr
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Aryl Hydrocarbon Receptor
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Brain - Cytology
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Cell Line, Tumor
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Cells, Cultured
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Cytochrome P-450 Cyp1a1 - Biosynthesis
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Cytochrome P-450 Cyp1a1 - Genetics
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Eicosanoids
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Titanium Dioxide Nanoparticles Induce DNA Damage and Genetic Instability In vivo in Mice

Determination of Antibiotic Hypersensitivity among 4,000 Single-Gene-Knockout Mutants of Escherichia coli

Treatment of mice with 2,3,7,8-Tetrachlorodibenzo-p-dioxin markedly increases the levels of a number of cytochrome P450 metabolites of omega-3 polyunsaturated fatty acids in the liver and lung

2,3,7,8-Tetrachlorodibenzo-p-dioxin treatment alters eicosanoid levels in several organs of the mouse in an aryl hydrocarbon receptor-dependent fashion

SIN3A, Generally Regarded as a Transcriptional Repressor, Is Required for Induction of Gene Transcription by the Aryl Hydrocarbon Receptor

Exposure to ambient ultrafine particulate matter alters the expression of genes in primary human neurons

Genome-wide RNAi high-throughput screen identifies proteins necessary for the AHR-dependent induction of CYP1A1 by 2,3,7,8-tetrachlorodibenzo-p-dioxin

Human brain derived cells respond in a type-specific manner after exposure to urban particulate matter (PM)

CYP2S1 is negatively regulated by corticosteroids in human cell lines

2,3,7,8- Te trachlorodibenzo-p-dioxin treatment alters eicosanoid levels in several organs of the mouse in an aryl hydrocarbon receptor-dependent fashion

RNAi High Throughput Screenings Facilitate the Identification of Proteins Necessary for TCDD-induced CYP1A1 Enzymatic Activity and Aid in the Discovery of a Novel Role for Sin3A in AHR-Mediated Gene Expression

Oxidative and Inflammatory Pathways in Age-Related Chronic Disease Processes

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