Wild-type and the acs2Ts1 mutant yeasts were shifted from 25deg to 37deg. After 60 minutes, Yeasts were harvested and divided into 2 x 2 cell samples. Total RNAs were purified from 4 populations.
Nucleocytosolic acetyl-coenzyme a synthetase is required for histone acetylation and global transcription.
No sample metadata fields
View SamplesRat mammary glands were obtained from individual rats in RXR treated (a) and control (b) conditions (12 rats in each condition). The 24 samples were hybridized individually. Also, in each condition, samples were combined into different pools of 2, pools of 3, pools of 12. Technical replicates were also run.
On the utility of pooling biological samples in microarray experiments.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The Gene Expression Barcode: leveraging public data repositories to begin cataloging the human and murine transcriptomes.
Treatment
View SamplesWe used yeast RNA to estimate background binding for each probe on the human U133 plus 2.0 array.
The Gene Expression Barcode: leveraging public data repositories to begin cataloging the human and murine transcriptomes.
Treatment
View SamplesWe hybridized yeast RNA to the mouse 430 2.0 array to estimate the background binding for each probe.
The Gene Expression Barcode: leveraging public data repositories to begin cataloging the human and murine transcriptomes.
Treatment
View SamplesDespite investment in toxicogenomics, nonclinical safety studies are still used to predict clinical liabilities for new drug candidates. Network-based approaches for genomic analysis help overcome challenges with whole-genome transcriptional profiling using limited numbers of treatments for phenotypes of interest. Herein, we apply co-expression network analysis to safety assessment using rat liver gene expression data to define 415 modules, exhibiting unique transcriptional control, organized in a visual representation of the transcriptome (the TXG-MAP). Accounting for the overall transcriptional activity resulting from treatment, we explain mechanisms of toxicity and predict distinct toxicity phenotypes using module associations. We demonstrate that early network responses compliment traditional histology-based assessment in predicting outcomes for longer studies and identify a novel mechanism of hepatotoxicity involving endoplasmic reticulum stress and Nrf2 activation. Module-based molecular subtypes of cholestatic injury derived using rat translate to human. Moreover, compared to gene-level analysis alone, combining module and gene-level analysis performed in sequence identifies significantly more phenotype-gene associations, including established and novel biomarkers of liver injury.
Toxicogenomic module associations with pathogenesis: a network-based approach to understanding drug toxicity.
Sex, Specimen part
View SamplesBoth cellular senescence and organismic aging are known to be dynamic processes that start early in life and progress constantly during the whole life of the individual. In this work, with the objective of identifying signatures of age-related progressive change at the transcriptomic level, we have performed a whole-genome gene expression analysis of peripheral blood leukocytes in a group of healthy individuals with ages ranging from 14 to 93 years. A set of genes with progressively changing gene expression (either increase or decrease with age) has been identified and contextualized in a coexpression network. A modularity analysis has been performed on this network and biological-term and pathway enrichment analyses have been used for biological interpretation of each module. In summary, the results of the present work reveal the existence of a transcriptomic component that shows progressive expression changes associated to age in peripheral blood leukocytes, highlighting both the dynamic nature of the process and the need to complement young vs. elder studies with longitudinal studies that includes middle aged individuals. From the transcriptional point of view, immunosenescence seems to be occurring from a relatively early age, at least from the late 20s/early 30s, and the 49 56 y/o age-range appears to be critical. In general, the genes that, according to our results, show progressive expression changes with aging are involved in pathogenic/cellular processes that have classically been linked to aging in humans: cancer, immune processes and cellular growth vs. maintenance.
Age gene expression and coexpression progressive signatures in peripheral blood leukocytes.
Age, Specimen part
View SamplesPre-LVAD and explanted ischemic and nonischemic cardiomyopathy and nonfailing hearts all normalized with RMA
Gene expression analysis of ischemic and nonischemic cardiomyopathy: shared and distinct genes in the development of heart failure.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Age and sun exposure-related widespread genomic blocks of hypomethylation in nonmalignant skin.
Sex, Age, Specimen part
View SamplesGene expression profiling of epidermal samples obtained from sun-exposed and sun-protected body sites from younger (<35 years old) and older (>60 years old) individuals. The Affymetrix U133A plus 2.0 array was used to obtain gene expression data. Samples included 4 younger sun exposed epidermal samples, 4 older sun exposed epidermal samples, 3 younger sun protected epidermal samples, 5 older sun protected epidermal samples.
Age and sun exposure-related widespread genomic blocks of hypomethylation in nonmalignant skin.
Sex, Age, Specimen part
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