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GSE8316
Mus musculus, Homo sapiens, Rattus norvegicus
46 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302), Affymetrix Mouse Expression 430A Array (moe430a)
Description
PPARalpha is a ligand-activated transcription factor involved in the regulation of nutrient metabolism and inflammation. Although much is already known about the function of PPARalpha in hepatic lipid metabolism, many PPARalpha-dependent pathways and genes have yet to be discovered. In order to obtain an overview of PPARalpha-regulated genes relevant to lipid metabolism, and to probe for novel candidate PPARalpha target genes, livers from several animal studies in which PPARalpha was activated and/or disabled were analyzed by Affymetrix GeneChips. Numerous novel PPARalpha-regulated genes relevant to lipid metabolism were identified. Out of this set of genes, eight genes were singled out for study of PPARalpha-dependent regulation in mouse liver and in mouse, rat, and human primary hepatocytes, including thioredoxin interacting protein (Txnip), electron-transferring-flavoprotein beta polypeptide (Etfb), electron-transferring-flavoprotein dehydrogenase (Etfdh), phosphatidylcholine transfer protein (Pctp), endothelial lipase (EL, Lipg), adipose triglyceride lipase (Pnpla2), hormone-sensitive lipase (HSL, Lipe), and monoglyceride lipase (Mgll). Using an in silico screening approach, one or more PPAR response elements (PPREs) were identified in each of these genes. Regulation of Pnpla2, Lipe, and Mgll, which are involved in triglyceride hydrolysis, was studied under conditions of elevated hepatic lipids. In wild-type mice fed a high fat diet, the decrease in hepatic lipids following treatment with the PPARalpha agonist Wy14643 was paralleled by significant up-regulation of Pnpla2, Lipe, and Mgll, suggesting that induction of triglyceride hydrolysis may contribute to the anti-steatotic role of PPARalpha. Our study illustrates the power of transcriptional profiling to uncover novel PPARalpha-regulated genes and pathways in liver.
Publication Title
Comprehensive analysis of PPARalpha-dependent regulation of hepatic lipid metabolism by expression profiling.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 16 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302), Affymetrix Mouse Expression 430A Array (moe430a)
Description
PPAR is a ligand-activated transcription factor involved in the regulation of nutrient metabolism and inflammation. Although much is already known about the function of PPAR in hepatic lipid metabolism, many PPAR-dependent pathways and genes have yet to be discovered. In order to obtain an overview of PPAR-regulated genes relevant to lipid metabolism, and to probe for novel candidate PPAR target genes, livers from several animal studies in which PPAR was activated and/or disabled were analyzed by Affymetrix GeneChips. Numerous novel PPAR-regulated genes relevant to lipid metabolism were identified. Out of this set of genes, eight genes were singled out for study of PPAR-dependent regulation in mouse liver and in mouse, rat, and human primary hepatocytes, including thioredoxin interacting protein (Txnip), electron-transferring-flavoprotein polypeptide (Etfb), electron-transferring-flavoprotein dehydrogenase (Etfdh), phosphatidylcholine transfer protein (Pctp), endothelial lipase (EL, Lipg), adipose triglyceride lipase (Pnpla2), hormone-sensitive lipase (Lipe), and monoglyceride lipase (Mgll). Using an in silico screening approach, one or more PPAR response elements (PPREs) were identified in each of these genes. Since Pnpla2, Lipe, and Mgll contribute to hepatic triglyceride hydrolysis, gene regulation was studied under conditions of elevated hepatic lipids. In wild-type mice fed a high fat diet, the decrease in hepatic lipids following treatment with the PPAR agonist Wy14643 was paralleled by significant up-regulation of Pnpla2, Lipe, and Mgll, suggesting that induction of triglyceride hydrolysis may contribute to the anti-steatotic role of PPAR. Our study illustrates the power of transcriptional profiling to uncover novel PPAR-regulated genes and pathways in liver.
Publication Title
Comprehensive analysis of PPARalpha-dependent regulation of hepatic lipid metabolism by expression profiling.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 16 Downloadable Samples
- Affymetrix Mouse Expression 430A Array (moe430a)
Description
PPAR is a ligand-activated transcription factor involved in the regulation of nutrient metabolism and inflammation. Although much is already known about the function of PPAR in hepatic lipid metabolism, many PPAR-dependent pathways and genes have yet to be discovered. In order to obtain an overview of PPAR-regulated genes relevant to lipid metabolism, and to probe for novel candidate PPAR target genes, livers from several animal studies in which PPAR was activated and/or disabled were analyzed by Affymetrix GeneChips. Numerous novel PPAR-regulated genes relevant to lipid metabolism were identified. Out of this set of genes, eight genes were singled out for study of PPAR-dependent regulation in mouse liver and in mouse, rat, and human primary hepatocytes, including thioredoxin interacting protein (Txnip), electron-transferring-flavoprotein polypeptide (Etfb), electron-transferring-flavoprotein dehydrogenase (Etfdh), phosphatidylcholine transfer protein (Pctp), endothelial lipase (EL, Lipg), adipose triglyceride lipase (Pnpla2), hormone-sensitive lipase (Lipe), and monoglyceride lipase (Mgll). Using an in silico screening approach, one or more PPAR response elements (PPREs) were identified in each of these genes. Since Pnpla2, Lipe, and Mgll contribute to hepatic triglyceride hydrolysis, gene regulation was studied under conditions of elevated hepatic lipids. In wild-type mice fed a high fat diet, the decrease in hepatic lipids following treatment with the PPAR agonist Wy14643 was paralleled by significant up-regulation of Pnpla2, Lipe, and Mgll, suggesting that induction of triglyceride hydrolysis may contribute to the anti-steatotic role of PPAR. Our study illustrates the power of transcriptional profiling to uncover novel PPAR-regulated genes and pathways in liver.
Publication Title
Comprehensive analysis of PPARalpha-dependent regulation of hepatic lipid metabolism by expression profiling.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus, Homo sapiens, Rattus norvegicus
- 6 Downloadable Samples
- Affymetrix Mouse Expression 430A Array (moe430a)
Description
PPAR is a ligand-activated transcription factor involved in the regulation of nutrient metabolism and inflammation. Although much is already known about the function of PPAR in hepatic lipid metabolism, many PPAR-dependent pathways and genes have yet to be discovered. In order to obtain an overview of PPAR-regulated genes relevant to lipid metabolism, and to probe for novel candidate PPAR target genes, livers from several animal studies in which PPAR was activated and/or disabled were analyzed by Affymetrix GeneChips. Numerous novel PPAR-regulated genes relevant to lipid metabolism were identified. Out of this set of genes, eight genes were singled out for study of PPAR-dependent regulation in mouse liver and in mouse, rat, and human primary hepatocytes, including thioredoxin interacting protein (Txnip), electron-transferring-flavoprotein polypeptide (Etfb), electron-transferring-flavoprotein dehydrogenase (Etfdh), phosphatidylcholine transfer protein (Pctp), endothelial lipase (EL, Lipg), adipose triglyceride lipase (Pnpla2), hormone-sensitive lipase (Lipe), and monoglyceride lipase (Mgll). Using an in silico screening approach, one or more PPAR response elements (PPREs) were identified in each of these genes. Since Pnpla2, Lipe, and Mgll contribute to hepatic triglyceride hydrolysis, gene regulation was studied under conditions of elevated hepatic lipids. In wild-type mice fed a high fat diet, the decrease in hepatic lipids following treatment with the PPAR agonist Wy14643 was paralleled by significant up-regulation of Pnpla2, Lipe, and Mgll, suggesting that induction of triglyceride hydrolysis may contribute to the anti-steatotic role of PPAR. Our study illustrates the power of transcriptional profiling to uncover novel PPAR-regulated genes and pathways in liver.
Publication Title
Comprehensive analysis of PPARalpha-dependent regulation of hepatic lipid metabolism by expression profiling.
Sample Metadata Fields
Sex
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Expression 430A Array (moe430a)
Description
PPAR is a ligand-activated transcription factor involved in the regulation of nutrient metabolism and inflammation. Although much is already known about the function of PPAR in hepatic lipid metabolism, many PPAR-dependent pathways and genes have yet to be discovered. In order to obtain an overview of PPAR-regulated genes relevant to lipid metabolism, and to probe for novel candidate PPAR target genes, livers from several animal studies in which PPAR was activated and/or disabled were analyzed by Affymetrix GeneChips. Numerous novel PPAR-regulated genes relevant to lipid metabolism were identified. Out of this set of genes, eight genes were singled out for study of PPAR-dependent regulation in mouse liver and in mouse, rat, and human primary hepatocytes, including thioredoxin interacting protein (Txnip), electron-transferring-flavoprotein polypeptide (Etfb), electron-transferring-flavoprotein dehydrogenase (Etfdh), phosphatidylcholine transfer protein (Pctp), endothelial lipase (EL, Lipg), adipose triglyceride lipase (Pnpla2), hormone-sensitive lipase (Lipe), and monoglyceride lipase (Mgll). Using an in silico screening approach, one or more PPAR response elements (PPREs) were identified in each of these genes. Since Pnpla2, Lipe, and Mgll contribute to hepatic triglyceride hydrolysis, gene regulation was studied under conditions of elevated hepatic lipids. In wild-type mice fed a high fat diet, the decrease in hepatic lipids following treatment with the PPAR agonist Wy14643 was paralleled by significant up-regulation of Pnpla2, Lipe, and Mgll, suggesting that induction of triglyceride hydrolysis may contribute to the anti-steatotic role of PPAR. Our study illustrates the power of transcriptional profiling to uncover novel PPAR-regulated genes and pathways in liver.
Publication Title
Comprehensive analysis of PPARalpha-dependent regulation of hepatic lipid metabolism by expression profiling.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Expression 430A Array (moe430a)
Description
PPAR is a ligand-activated transcription factor involved in the regulation of nutrient metabolism and inflammation. Although much is already known about the function of PPAR in hepatic lipid metabolism, many PPAR-dependent pathways and genes have yet to be discovered. In order to obtain an overview of PPAR-regulated genes relevant to lipid metabolism, and to probe for novel candidate PPAR target genes, livers from several animal studies in which PPAR was activated and/or disabled were analyzed by Affymetrix GeneChips. Numerous novel PPAR-regulated genes relevant to lipid metabolism were identified. Out of this set of genes, eight genes were singled out for study of PPAR-dependent regulation in mouse liver and in mouse, rat, and human primary hepatocytes, including thioredoxin interacting protein (Txnip), electron-transferring-flavoprotein polypeptide (Etfb), electron-transferring-flavoprotein dehydrogenase (Etfdh), phosphatidylcholine transfer protein (Pctp), endothelial lipase (EL, Lipg), adipose triglyceride lipase (Pnpla2), hormone-sensitive lipase (Lipe), and monoglyceride lipase (Mgll). Using an in silico screening approach, one or more PPAR response elements (PPREs) were identified in each of these genes. Since Pnpla2, Lipe, and Mgll contribute to hepatic triglyceride hydrolysis, gene regulation was studied under conditions of elevated hepatic lipids. In wild-type mice fed a high fat diet, the decrease in hepatic lipids following treatment with the PPAR agonist Wy14643 was paralleled by significant up-regulation of Pnpla2, Lipe, and Mgll, suggesting that induction of triglyceride hydrolysis may contribute to the anti-steatotic role of PPAR. Our study illustrates the power of transcriptional profiling to uncover novel PPAR-regulated genes and pathways in liver.
Publication Title
Comprehensive analysis of PPARalpha-dependent regulation of hepatic lipid metabolism by expression profiling.
Sample Metadata Fields
Sex, Specimen part
View Samples- Caenorhabditis elegans
- 10 Downloadable Samples
Affymetrix C. elegans Genome Array (celegans)
Description
Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented.
Publication Title
Active transcriptomic and proteomic reprogramming in the C. elegans nucleotide excision repair mutant xpa-1.
Sample Metadata Fields
No sample metadata fields
View Samples- Rattus norvegicus
- 9 Downloadable Samples
- Affymetrix Rat Expression 230A Array (rae230a)
Description
FK1706 potentiated nerve growth factor-induced neurite outgrowth, putatively mediated via FKBP-52 and the Ras/Raf/MAPK signaling pathway. It also improved mechanical allodynia accompanied by the recovery of intraepidermal nerve fiber density in a painful diabetic neuropathy in rats.
Publication Title
FK1706, a novel non-immunosuppressive immunophilin ligand, modifies gene expression in the dorsal root ganglia during painful diabetic neuropathy.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 14 Downloadable Samples
- Affymetrix Mouse Clariom S Array (clariomsmouse)
Description
Scope: As a result of population ageing, the number of Alzheimer’s disease (AD) patients has rapidly increased. There are many hypothesises on the pathogenesis of AD, but its detailed molecular mechanism is still unknown, and so no effective preventive or therapeutic measures have been established. Some reports showed a decrease in levels of norepinephrine (NE) has been suspected to be involved in the decline of cognitive function in AD patients and NE concentrations were decreased in postmortem AD patient brains. Tyr-Trp was identified as being the most effective dipeptide in enhancing norepinephrine (NE) synthesis and metabolism. And Tyr-Trp treatment ameliorated the short-term memory dysfunction in AD model mice caused by amyloid beta (Aβ) 25-35. So, the purpose of this study was to investigate the preventive or/and protective effects of Tyr-Trp administration in AD model mice.
Publication Title
Tyr-Trp administration facilitates brain norepinephrine metabolism and ameliorates a short-term memory deficit in a mouse model of Alzheimer's disease.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 10 Downloadable Samples
- Affymetrix Mouse Expression 430A Array (moe430a)
Description
Ataxin 1 (Atxn1) is a protein of unknown function associated with cerebellar neurodegeneration in spinocerebellar ataxia type 1 (SCA1). SCA1 is caused by an expanded polyglutamine within Atxn1 by gain-of-function mechanisms. Lack of Atxn1 in mice triggers motor deficits in the absence of neurodegeneration or apparent neuropathological abnormalities.We extracted RNA from cerebellum of 5 Atxn1-null mice and 5 WT. Cerebellar gene expression profiles at 15 weeks of age were generated usSCA1 ing Affymetrix MOE430A arrays. Identifying the molecular pathways regulated by Atxn1 can provide insights into the early molecular mechanisms underlying neuronal dysfunction.
Publication Title
Down-regulation of the dopamine receptor D2 in mice lacking ataxin 1.
Sample Metadata Fields
Age, Specimen part
View Samples