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GSE109508
Homo sapiens
90 Downloadable Samples
Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)
Description
A673 cells were exposed in triplicate to three agrichemicals for 24hrs at 8 concentrations and a DMSO vehicle control (0.001, 0.003, 0.01, 0.03, 0.1, 0.3, 1, 3, and 10 M plus DMSO vehicle controls). While a common set of DMSO controls was used, these CEL files were RMA normalized independently with each of the chemical treated groups. Gene expression was measured on an Affymetrix GeneTitan system. The compounds used were fenbuconazole (a.k.a FENB, CAS # 114369-43-6) a triazole fungicide, imazalil (a.k.a. IMAZ, CAS # 35554-44-0), an azole pesticide, and 2,4-dichlorophenoxyacetic acid (a.k.a. 2,4-D or 2-4-D in file names, CAS # 94-75-7), a chlorophenoxy herbicide.
Publication Title
A Qualitative Modeling Approach for Whole Genome Prediction Using High-Throughput Toxicogenomics Data and Pathway-Based Validation.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 90 Downloadable Samples
- Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)
Description
MCF7 cells were exposed in triplicate to three agrichemicals for 24hrs at 8 concentrations and a DMSO vehicle control (0.001, 0.003, 0.01, 0.03, 0.1, 0.3, 1, 3, and 10 M plus DMSO vehicle controls). While a common set of DMSO controls was used, these CEL files were RMA normalized independently with each of the chemical treated groups. Gene expression was measured on an Affymetrix GeneTitan system. The compounds used were fenbuconazole (a.k.a FENB, CAS # 114369-43-6) a triazole fungicide, imazalil (a.k.a. IMAZ, CAS # 35554-44-0), an azole pesticide, and 2,4-dichlorophenoxyacetic acid (a.k.a. 2,4-D or 2-4-D in file names, CAS # 94-75-7), a chlorophenoxy herbicide.
Publication Title
A Qualitative Modeling Approach for Whole Genome Prediction Using High-Throughput Toxicogenomics Data and Pathway-Based Validation.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 90 Downloadable Samples
- Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)
Description
HepaRG cells were exposed in triplicate to three agrichemicals for 24hrs at 8 concentrations and a DMSO vehicle control (0.001, 0.003, 0.01, 0.03, 0.1, 0.3, 1, 3, and 10 M plus DMSO vehicle controls). While a common set of DMSO controls was used, these CEL files were RMA normalized independently with each of the chemical treated groups. Gene expression was measured on an Affymetrix GeneTitan system. The compounds used were fenbuconazole (a.k.a FENB, CAS # 114369-43-6) a triazole fungicide, imazalil (a.k.a. IMAZ, CAS # 35554-44-0), an azole pesticide, and 2,4-dichlorophenoxyacetic acid (a.k.a. 2,4-D or 2-4-D in file names, CAS # 94-75-7), a chlorophenoxy herbicide.
Publication Title
A Qualitative Modeling Approach for Whole Genome Prediction Using High-Throughput Toxicogenomics Data and Pathway-Based Validation.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 90 Downloadable Samples
- Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)
Description
HpeG2 cells were exposed in triplicate to three agrichemicals for 24hrs at 8 concentrations and a DMSO vehicle control (0.001, 0.003, 0.01, 0.03, 0.1, 0.3, 1, 3, and 10 M plus DMSO vehicle controls). While a common set of DMSO controls was used, these CEL files were RMA normalized independently with each of the chemical treated groups. Gene expression was measured on an Affymetrix GeneTitan system. The compounds used were fenbuconazole (a.k.a FENB, CAS # 114369-43-6) a triazole fungicide, imazalil (a.k.a. IMAZ, CAS # 35554-44-0), an azole pesticide, and 2,4-dichlorophenoxyacetic acid (a.k.a. 2,4-D or 2-4-D in file names, CAS # 94-75-7), a chlorophenoxy herbicide.
Publication Title
A Qualitative Modeling Approach for Whole Genome Prediction Using High-Throughput Toxicogenomics Data and Pathway-Based Validation.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Rattus norvegicus
- 81 Downloadable Samples
- Affymetrix Rat Gene 2.0 ST Array (ragene20st)
Description
Exposure to common environmental chemicals, including those found in personal care products has been linked to mammary cancer at high doses in animal models. Their effects at low doses at levels comparable to human exposure, especially during critical windows of development remain poorly understood. Using a Sprague-Dawley rat model, we investigated the effects of of three environmental chemicals diethyl phthalate (DEP), methyl paraben (MPB) and triclosan (TCS) on the transcriptome of normal developing mammary glands at low doses mimicking human exposure. Rats were exposed during three windows of early development perinatal (gestation day (GD) 1 - 20 or postnatal day (PND) 1 - 20), prepubertal (PND 21 - 41) and pubertal (PND 42 - 62), as well as chronic exposure from birth to end of lactation (PND 1 - 146). Mammary gland whole-transcriptomes were profiled by Affymetrix rat gene 2.0 st arrays.
Publication Title
Changes in mammary histology and transcriptome profiles by low-dose exposure to environmental phenols at critical windows of development.
Sample Metadata Fields
Sex, Specimen part
View Samples- Rattus norvegicus
- 31 Downloadable Samples
- Affymetrix Rat Gene 2.0 ST Array (ragene20st)
Description
There is a lack of systematic investigations of large-scale transcriptome patterns associated with normal breast development. Herein, we profiled whole-transcriptome (by microarrays) of normal mammary glands in female Sprague-Dawley rats, an animal model widely used in breast cancer research, across six distinctive developmental stages pre-pubertal, peri-pubertal, pubertal, lactation, and adult parous and age-matched nulliparous.
Publication Title
Histology and Transcriptome Profiles of the Mammary Gland across Critical Windows of Development in Sprague Dawley Rats.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 56 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The dendritic cell (DC) is a master regulator of immune responses. Pathogenic viruses subvert normal immune function in DCs through the expression of immune antagonists. Understanding how these antagonists interact with the host immune system requires knowledge of the underlying genetic regulatory network that operates during an uninhibited antiviral response. In order to isolate and identify this network, we studied DCs infected with Newcastle Disease Virus (NDV), which is able to stimulate innate immunity and DC maturation through activation of RIG-I signaling, but lacks the ability to evade the human interferon response. To analyze this experimental model, we developed a new approach integrating genome-wide expression kinetics and time-dependent promoter analysis. We found that the genetic program underlying the antiviral cell state transition during the first 18-hours post-infection could be explained by a single regulatory network. Gene expression changes were driven by a step-wise multi-factor cascading control mechanism, where the specific transcription factors controlling expression changed over time. Within this network, most individual genes are regulated by multiple factors, indicating robustness against virus-encoded immune evasion genes. In addition to effectively recapitulating current biological knowledge, we predicted, and validated experimentally, antiviral roles for several novel transcription factors. More generally, our results show how a genetic program can be temporally controlled through a single regulatory network to achieve the large-scale genetic reprogramming characteristic of cell state transitions.
Publication Title
Antiviral response dictated by choreographed cascade of transcription factors.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 31 Downloadable Samples
Illumina HiSeq 2500
Description
C5aR1, a receptor for the complement activation proinflammatory fragment, C5a, is primarily expressed on cells of the myeloid lineage, and to a lesser extent on endothelial cells and neurons in brain. Previous work demonstrated C5aR1 antagonist, PMX205, decreased amyloid pathology and suppressed cognitive deficits in Alzheimer Disease (AD) mouse models. In the Arctic AD mouse model, genetic deletion of C5aR1 prevented behavior deficits at 10 months. However, the molecular mechanisms of this protection has not been definitively demonstrated. To understand the role of microglial C5aR1 in the Arctic AD mouse model, we have taken advantage of the CX3CR1GFP and CCR2RFP reporter mice to distinguish microglia as GFP-positive and infiltrating monocytes as GFP and RFP positive, for subsequent transcriptome analysis on specifically sorted myeloid populations from wild type and AD mouse models. Immunohistochemical analysis of mice aged to 2, 5, 7 and 10 months showed no change in amyloid beta (Ab) deposition in the Arctic C5aR1 knockout (KO) mice relative to that seen in the Arctic mice. Of importance, no CCR2+ monocytes/macrophages were found near the plaques in the Arctic brain with or without C5aR1. RNA-seq analysis on microglia from these mice identified inflammation related genes as differentially expressed, with increased expression in the Arctic mice relative to wildtype and decreased expression in the Arctic/C5aR1KO relative to Arctic. In addition, phagosomal-lysosomal proteins and protein degradation pathways that were increased in the Arctic mice were further increased in the Arctic/C5aR1KO mice. These data are consistent with a microglial polarization state with restricted induction of inflammatory genes and enhancement of clearance pathways. Overall design: Microglia mRNA profiles of wildtype (WT), C5aR1 knockout (C5aR1KO), Arctic (ARC) and Arctic C5aR1 knockout (ARCKO) mice at 2, 5, 7 and 10-11 month. Duplicates were sequenced for each genotype on Illumina HiSeq 2500 platform.
Publication Title
Prevention of C5aR1 signaling delays microglial inflammatory polarization, favors clearance pathways and suppresses cognitive loss.
Sample Metadata Fields
Age, Specimen part, Subject
View Samples- Homo sapiens
- 150 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Human Dendritic Cell Response Signatures Distinguish 1918, Pandemic, and Seasonal H1N1 Influenza Viruses.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 30 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
An 8 hours timecourse was performed with human DCs infected either with A/California/7/2009 and A/Brevig Mission/1/1918 (pandemic) or A/New Caledonia/20/99 and A/Texas/36/91 seosonal.
Publication Title
Human Dendritic Cell Response Signatures Distinguish 1918, Pandemic, and Seasonal H1N1 Influenza Viruses.
Sample Metadata Fields
Specimen part, Treatment
View Samples