mRNA-sequencing from ribosomal RNA-depleted cardiac total RNA was performed 9 weeks after injection of rAAV6-PLCb1a, rAAV6-PLCb1b or rAAV6-blank viri into the tail vein of C57BL/6 male mice (7-8 weeks of age at time of injection). Overall design: 6 biological replicates each of rAAV6-PLCb1a, rAAV6-PLCb1b or rAAV6-blank-treated mice.
Chronic Contractile Dysfunction without Hypertrophy Does Not Provoke a Compensatory Transcriptional Response in Mouse Hearts.
Sex, Age, Specimen part, Cell line, Subject
View SamplesThis dataset is a time series (1 hour [h], 4 hours, 24 hours, 48 hours, 1 week [w], and 8 weeks) intended to compare normal functioning left ventricles [lv + lv2] with infarcted [ilv] and non-infarcted left ventricles [nilv]. Ilv samples are taken from the region between the LAD artery and the apex on a mouse with myocardial infarction. Lv2 samples are from the same region in a sham operated mouse. Nilv samples are taken from the region above the infartion and the left ventricle [lv] samples mimic that region in a sham mouse. The lv and lv2 samples can be compared as both are from normal functioning hearts. For more information visit http://cardiogenomics.med.harvard.edu/groups/proj1/pages/mi_home.html
Mouse cardiac surgery: comprehensive techniques for the generation of mouse models of human diseases and their application for genomic studies.
No sample metadata fields
View SamplesMYC is induced early in human adipose stem cells in response to a standard MDIR adipogenic cocktail. The objective of this experiment was to identify key gene networks impacted by MYC loss-of-function in a mixed donor pool of human derived adipose stem cells.
MYC is an early response regulator of human adipogenesis in adipose stem cells.
Sex, Race
View SamplesA673 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.
A Qualitative Modeling Approach for Whole Genome Prediction Using High-Throughput Toxicogenomics Data and Pathway-Based Validation.
Specimen part, Cell line
View SamplesMCF7 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.
A Qualitative Modeling Approach for Whole Genome Prediction Using High-Throughput Toxicogenomics Data and Pathway-Based Validation.
Specimen part, Cell line
View SamplesHepaRG 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.
A Qualitative Modeling Approach for Whole Genome Prediction Using High-Throughput Toxicogenomics Data and Pathway-Based Validation.
Specimen part, Cell line
View SamplesHpeG2 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.
A Qualitative Modeling Approach for Whole Genome Prediction Using High-Throughput Toxicogenomics Data and Pathway-Based Validation.
Specimen part, Cell line
View SamplesGene expression in larval, early third instar eye-antenna discs was assessed to reveal an ATF4 contribution to target gene induction following COX7a knockdown. As hypothesised, these COX7a-RNAi induced target genes require the transcription factor ATF4 for induction, irrespective of concomitant Notch pathway activation through Delta over-expression.
ATF4-Induced Warburg Metabolism Drives Over-Proliferation in Drosophila.
No sample metadata fields
View SamplesGene expression in larval, early third instar eye-antenna discs was assesed in genotypes with Notch Gain-of-Function (UAS-Delta or UAS-Notch[intra2]) over-expression or mitochondrial COX7a Loss-of-function (UAS-COX7a-RNAi) or a combination of both (UAS-Delta, UAS-COX7a-RNAi). The analysis revealed that, despite a strong genetic interaction between Notch pathway activation and knockdown of COX7a, no transcriptional cooperation or synergy was detectable in early L3 eye-antenna discs. Rather, COX7a knockdown induced a unique transcriptional signature, which further experiments revealed to be mediated by the transcription factor ATF4.
ATF4-Induced Warburg Metabolism Drives Over-Proliferation in Drosophila.
No sample metadata fields
View SamplesAs part of a larger effort to provide proof-of-concept in vitro only risk assessments, we have developed a suite of high throughput assays for key readouts in the p53 DNA damage response toxicity pathway: DSB DNA damage (p-H2AX), permanent chromosomal damage (micronuclei; MN), p53 activation, p53 transcriptional activity, and cell fate (cell cycle arrest, apoptosis,MN). Dose-response studies were performed with these protein and cell fate assays, together with whole genome transcriptomics, for three prototype chemicals: etoposide (ETP), quercetin (QUE) and methyl methanesulfonate (MMS). Data were collected in a human cell line expressing wild-type p53 (HT1080) and results were confirmed in a second p53 competent cell line (HCT 116). At chemical concentrations causing similar increases in p53 protein expression, p53-mediated protein expression and cellular processes showed substantial chemical-specific differences. These chemical-specific differences in the p53 transcriptional response appear to be determined by augmentation of the p53 response by co-regulators. More importantly, dose-response data for each of the chemicals indicates that the p53 transcriptional response does not prevent MN induction at low concentrations. In fact, the no observed effect levels (NOELs) and benchmark doses (BMDs) for MN induction were less than or equal to those for p53-mediated gene transcription regardless of the test chemical, indicating that p53s post-translational responses may be more important than transcriptional activation in the response to low dose DNA damage. This effort demonstrates the process of defining key assays required for a pathway-based, in vitro-only risk assessment, using the p53-mediated DNA damage response pathway as a prototype.
Profiling dose-dependent activation of p53-mediated signaling pathways by chemicals with distinct mechanisms of DNA damage.
Specimen part, Cell line
View Samples