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Links from GEO DataSets

Items: 9

1.

Shifted Metabolic Bias in Livers of Mice Lacking Hepatocytic Thioredoxin Reductase-1 Protects Against Acetaminophen Toxicity

(Submitter supplied) Genetic disruption of thioredoxin reductase 1 protects against acetaminophen (APAP) toxicity. To determine the role of the thioredoxin system on xenobiotic metabolism we challeneged wildtype and txnrd1liver-null mice with acetaminophen.
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS4928
Platform:
GPL8321
12 Samples
Download data: CEL
Series
Accession:
GSE37874
ID:
200037874
2.
Full record GDS4928

Acetaminophen effect on thioredoxin reductase 1-null liver

Analysis of liver from hepatocyte-specific, thioredoxin reductase 1 (TrxR1)-null mutants treated with the pro-toxin acetaminophen. The Trx system impacts bioenergetics and drug metabolism. Results provide insight into the role of the Trx system in detoxifying certain xenobiotic challenges.
Organism:
Mus musculus
Type:
Expression profiling by array, transformed count, 2 genotype/variation, 2 protocol sets
Platform:
GPL8321
Series:
GSE37874
12 Samples
Download data: CEL
3.

Mouse Gsr-null and TrxR1/Gsr-null liver transcriptomes

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL8321
19 Samples
Download data: CEL
Series
Accession:
GSE124446
ID:
200124446
4.

Elevated Nrf2 response in TrxR1/Gsr-null livers

(Submitter supplied) Liver-specific depletion of both of the cytosolic NADPH-dependent disulfide reductases, TrxR1 and Gsr, was shown to result in increased activation of Nrf2 as compared to elimination of either of these enzymes alone. Activation of transcription factor Nrf2 and its downstream cytoprotective target genes by oxidative and electrophilic insults can protect cells from potentially carcinogenic damage. However, many cancers have an activated Nrf2 response, which can protect cancer cells from oxidative stress radiation. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL8321
8 Samples
Download data: CEL
Series
Accession:
GSE124445
ID:
200124445
5.

Mouse Gsr-null liver transcriptome

(Submitter supplied) Genetic disruption of Gsr in mouse elicits only subtle changes in the liver transcriptome. Transcriptome analysis of Gsr-null livers was performed to further our understanding of pathways that may compensate for loss of Gsr, one of the two NADPH-dependent cytosolic disulfide reductases.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL8321
11 Samples
Download data: CEL
Series
Accession:
GSE124444
ID:
200124444
6.

Single cell RNA sequencing on the early hepatic transcriptomic landscape

(Submitter supplied) Single cell RNA sequencing, spatial reconstruction of the liver lobule after acetaminophen (300 mg/kg)
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
6 Samples
Download data: H5
Series
Accession:
GSE200771
ID:
200200771
7.

Transcriptional profile of Mouse liver after MitoCDNB application

(Submitter supplied) To assess the effect of MitoCDNB on transcriptional profile of mouse liver tissue we injected mice with either vehicle (0.1 % ethanol) or 5 mg/kg of MitoCDNB. Liver was taken from both vehicle or MitoCDNB injected mice after 1 or 4 hours and the transcriptome assessed using Illumina RNASeq.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21273
24 Samples
Download data: CSV
Series
Accession:
GSE117425
ID:
200117425
8.

High-throughput sequencing reveals induction of drug metabolism in various cholestatic livers

(Submitter supplied) Cholestasis is a multifactorial disorder that compromises liver function. We wanted to examine Phase I and II drug metabolism in cholestatic livers. We performed high-throughput sequencing on livers from Fxr-/- Shp-/- double knockout mice, which mimic juvenile cholestasis. Next, we used comparative transcriptomic approach to test if the induction in drug metabolism is also seen in models of liver injury, including steatosis, regeneration and bile acid-stressed livers. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
26 Samples
Download data: CSV
Series
Accession:
GSE116627
ID:
200116627
9.

Deletion of thioredoxin reductase disrupts redox homeostasis and impairs β-cell function

(Submitter supplied) Reactive oxygen species (ROS) have been implicated as mediators of pancreatic β-cell damage. While β-cells are thought to be vulnerable to oxidative damage, we have shown, using inhibitors and acute depletions, that thioredoxin reductase, thioredoxin, and peroxiredoxins are the primary mediators of antioxidant defense in β-cells. However, the role of this antioxidant cycle in maintaining redox homeostasis and β-cell survival in vivo remains unclear. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
13 Samples
Download data: XLSX
Series
Accession:
GSE200965
ID:
200200965
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