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Mus musculus
72 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Genetic predisposition and environmental components contribute to an individuals non-alcoholic fatty liver disease (NAFLD) susceptibility. Therefore, we compared phenotypic variations of mouse strains extensively used in biomedical research during induction of high-fat diet (HFD)-mediated NAFLD and assessed transcriptional alterations in livers. In a time-resolved fashion we determined a wide spectrum of physiological parameters in C3HeB/FeJ (C3H), C57BL/6NTac, C57BL/6J, and 129P2/OlaHsd (129) males during a 7, 14, or 21 days HFD challenge and performed gene transcription analyses in steatotic livers.
Publication Title
Phenotypic comparison of common mouse strains developing high-fat diet-induced hepatosteatosis.
Sample Metadata Fields
Sex, Age, Treatment
View Samples- Mus musculus
- 32 Downloadable Samples
- Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
BACKGROUND. Dietary intake of saturated fat is a likely contributor to nonalcoholic fatty liver disease (NAFLD) and insulin resistance, but the mechanisms that initiate these abnormalities in humans remain unclear. We examined the effects of a single oral saturated fat load on insulin sensitivity, hepatic glucose metabolism, and lipid metabolism in humans. Similarly, initiating mechanisms were examined after an equivalent challenge in mice.
Publication Title
Acute dietary fat intake initiates alterations in energy metabolism and insulin resistance.
Sample Metadata Fields
Sex, Age, Specimen part, Treatment
View Samples- Mus musculus
- 42 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
In this survey we effectively combined transcriptomics, proteomics and targeted-metabolomics to analyse the temporal relationship of alterations in liver preceding and accompanying the development of HFD-mediated hepatic insulin resistance. To assess HFD-mediated alterations in physiological parameters, insulin sensitivity, and molecular adaptations in liver male C3HeB/FeJ mice treated with a high-fat diet (HFD) for 7, 14, or 21 days and compared to age- matched controls fed low-fat diet (LFD).
Publication Title
High fat diet-induced modifications in membrane lipid and mitochondrial-membrane protein signatures precede the development of hepatic insulin resistance in mice.
Sample Metadata Fields
Sex, Age, Treatment, Time
View Samples- Mus musculus
- 13 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Objective: To study if diabetic and insulin-resistant states lead to mitochondrial dysfunction in the liver, or alternatively, if there is adaption of mitochondrial function to these states in the long-term range.
Publication Title
Liver adapts mitochondrial function to insulin resistant and diabetic states in mice.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples- Mus musculus
- 11 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
White adipose tissue is primary involved in the response to insulin after feeding, while brain is not directly sensitive to insulin levels.
Publication Title
eIF6 coordinates insulin sensitivity and lipid metabolism by coupling translation to transcription.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Liver is primary involved in the response to insulin after feeding. Hepatocytes activates a tightly controlled genetic programme where specific sets of genes are modulates in response to insulin, for activation of the anabolic pathways.
Publication Title
eIF6 coordinates insulin sensitivity and lipid metabolism by coupling translation to transcription.
Sample Metadata Fields
Specimen part
View Samples
GSE2815- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
The transcriptional activities of c-Myb and its oncogenic variant v-Myb were compared by expressing them in human MCF7 cells using recombinant adenovirus vectors. A hybrid construct, 3Mutc, which is a variant of c-Myb harboring three v-Myb-derived DNA binding domain mutations was also analyzed. All the samples were compared to cells infected with a control adenovirus. The results showed that v-Myb, which differs from c-Myb only by N- and C-terminal deletions and eleven amino acid substitutions, has a qualitatively different transcriptional activity.
Publication Title
Oncogenic mutations cause dramatic, qualitative changes in the transcriptional activity of c-Myb.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 5 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The transcriptional activities of c-Myb and its oncogenic variant v-Myb were compared by expressing them in primary human monocytes using recombinant adenovirus vectors. All the samples were compared to cells infected with a control adenovirus expressing only GFP. The results showed that v-Myb, which differs from c-Myb only by N- and C-terminal deletions and eleven amino acid substitutions, has a qualitatively different transcriptional activity.
Publication Title
Oncogenic mutations cause dramatic, qualitative changes in the transcriptional activity of c-Myb.
Sample Metadata Fields
No sample metadata fields
View Samples GSE1318- Homo sapiens
- 25 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Recombinant adenovirus vectors were used to express wild type or domain swap mutants of A-Myb and c-Myb transcription factors in MCF-7 cells or pimary lung epithelial cells or fibroblasts. The results show that Myb proteins have extreme context specificity and identify sub-domains responsible for the activation of specific sets of target genes.
Publication Title
Positive and negative determinants of target gene specificity in myb transcription factors.
Sample Metadata Fields
No sample metadata fields
View Samples- Rattus norvegicus
- 24 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
While prion infections have been extensively characterized in the laboratory mouse, little is known regarding the molecular responses to prions in other rodents. To explore these responses and make comparisons, we generated a prion disease in the laboratory rat by successive passage of mouse RML prions. Here we describe the accumulation of prions and associated pathology in the rat and describe the transcriptional impact throughout prion disease. Comparative transcriptional profiling between laboratory mice and rats suggests that similar molecular processes are unfolding in response to prion infection. At the level of individual transcripts, however, variability exists between mice and rats and many genes deregulated in mouse scrapie are not affected in rats. Notwithstanding these differences, many transcriptome responses are conserved between mice and rats infected with scrapie. Our findings highlight the usefulness of comparative approaches to understanding neurodegeneration and prion diseases in particular.
Publication Title
Transcriptomic responses to prion disease in rats.
Sample Metadata Fields
Specimen part, Disease
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