DrugMatrix is a comprehensive rat toxicogenomics database and analysis tool developed to facilitate the integration of toxicogenomics into hazard assessment. Using the whole genome and a diverse set of compounds allows a comprehensive view of most pharmacological and toxicological questions and is applicable to other situations such as disease and development.
Genomic models of short-term exposure accurately predict long-term chemical carcinogenicity and identify putative mechanisms of action.
Sex, Specimen part, Compound, Time
View SamplesDrugMatrix is a comprehensive rat toxicogenomics database and analysis tool developed to facilitate the integration of toxicogenomics into hazard assessment. Using the whole genome and a diverse set of compounds allows a comprehensive view of most pharmacological and toxicological questions and is applicable to other situations such as disease and development.
Genomic models of short-term exposure accurately predict long-term chemical carcinogenicity and identify putative mechanisms of action.
Specimen part, Compound, Time
View SamplesDrugMatrix is a comprehensive rat toxicogenomics database and analysis tool developed to facilitate the integration of toxicogenomics into hazard assessment. Using the whole genome and a diverse set of compounds allows a comprehensive view of most pharmacological and toxicological questions and is applicable to other situations such as disease and development.
Genomic models of short-term exposure accurately predict long-term chemical carcinogenicity and identify putative mechanisms of action.
Sex, Specimen part, Compound, Time
View SamplesDrugMatrix is a comprehensive rat toxicogenomics database and analysis tool developed to facilitate the integration of toxicogenomics into hazard assessment. Using the whole genome and a diverse set of compounds allows a comprehensive view of most pharmacological and toxicological questions and is applicable to other situations such as disease and development.
Genomic models of short-term exposure accurately predict long-term chemical carcinogenicity and identify putative mechanisms of action.
Sex, Specimen part, Compound, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genomic models of short-term exposure accurately predict long-term chemical carcinogenicity and identify putative mechanisms of action.
Sex, Specimen part, Compound, Time
View SamplesDrugMatrix is a comprehensive rat toxicogenomics database and analysis tool developed to facilitate the integration of toxicogenomics into hazard assessment. Using the whole genome and a diverse set of compounds allows a comprehensive view of most pharmacological and toxicological questions and is applicable to other situations such as disease and development.
Genomic models of short-term exposure accurately predict long-term chemical carcinogenicity and identify putative mechanisms of action.
Sex, Specimen part, Compound, Time
View SamplesEGFR and MEK pathways were activated alone or in combination in human mammary epithelial cells. We profiled the pathway gene expression signatures using RNA-Seq. Overall design: mRNA was extracted from human mammary epithelial cells overexpressing EGFR gene, MEK gene, or EGFR and MEK genes in combination (or GFP control) for RNA-Seq analysis. Experiment was performed in six replicates per condition.
ASSIGN: context-specific genomic profiling of multiple heterogeneous biological pathways.
No sample metadata fields
View SamplesWe obtained gene expression data and HD-SNP6.0 copy number data from PTL, PCNSL and PMLBCL samples and performed an integrative analysis on them. RNA was whole genome amplified using Nugen.
Targetable genetic features of primary testicular and primary central nervous system lymphomas.
Disease, Disease stage
View SamplesAffymetrix MG430 2.0 expression levels of wild-type (STHdhQ7/Q7), 3NP-treated wild-type (STHdhQ7/Q7+3-NP), and mutant (STHdhQ111/Q111) striatal cells
Unbiased gene expression analysis implicates the huntingtin polyglutamine tract in extra-mitochondrial energy metabolism.
No sample metadata fields
View SamplesHuntingtons disease (HD) involves marked early neurodegeneration in the striatum whereas the cerebellum is relatively spared despite the ubiquitous expression of full-length mutant huntingtin, implying that inherent tissue-specific differences determine susceptibility to the HD CAG mutation. To understand this tissue specificity, we compared early mutant huntingtin-induced gene expression changes in striatum to those in cerebellum in young Hdh CAG knock-in mice, prior to onset of evident pathological alterations. Endogenous levels of full-length mutant huntingtin caused qualitatively similar, but quantitatively different gene expression changes in the two brain regions. Importantly, the quantitatively different responses in striatum and cerebellum in mutant mice were well accounted for by the intrinsic molecular differences in gene expression between striatum and cerebellum in wild-type animals. Tissue-specific gene expression changes in response to the HD mutation, therefore, appear to reflect the different inherent capacities of these tissues to buffer qualitatively similar effects of mutant huntingtin. These findings highlight a role for intrinsic quantitative tissue differences in contributing to HD pathogenesis, and likely to other neurodegenerative disorders exhibiting tissue-specificity, thereby guiding the search for effective therapeutic interventions.
Differential effects of the Huntington's disease CAG mutation in striatum and cerebellum are quantitative not qualitative.
Specimen part
View Samples