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accession-icon GSE31217
A zebrafish transgenic model of Ewing's Sarcoma reveals conserved mediators of EWS-FLI1 tumorigenesis
  • organism-icon Danio rerio
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A zebrafish transgenic model of Ewing's sarcoma reveals conserved mediators of EWS-FLI1 tumorigenesis.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE31186
The human Ewing's Sarcoma oncoprotein EWS-FLI1 causes Ewing's-type tumors in zebrafish
  • organism-icon Danio rerio
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

The fusion oncoprotein EWS-FLI1 arises from a t(11;22)(q24;q12) chromosomal translocation and causes Ewing's Sarcoma, a malignant bone tumor. The mechanism whereby EWS-FLI1 transforms cells is unknown. Somatic, mosaic expression of human EWS-FLI1 in zebrafish from the heat shock promoter [Tg(HSP:EWS-FLI1)] caused small round blue cell tumors (SRBCTs) similar to human Ewing's sarcoma.

Publication Title

A zebrafish transgenic model of Ewing's sarcoma reveals conserved mediators of EWS-FLI1 tumorigenesis.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE31185
The human Ewing's Sarcoma oncoprotein EWS-FLI1 causes developmental defects in zebrafish embryos
  • organism-icon Danio rerio
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

The fusion oncoprotein EWS-FLI1 arises from a t(11;22)(q24;q12) chromosomal translocation and causes Ewing's Sarcoma, a malignant bone tumor. The mechanism whereby EWS-FLI1 transforms cells is unknown. We made germline transgenic zebrafish expressing human EWS-FLI1 under the control of the heat shock promoter. Induction of EWS-FLI1 expression causes multiple defects in embryonic development.

Publication Title

A zebrafish transgenic model of Ewing's sarcoma reveals conserved mediators of EWS-FLI1 tumorigenesis.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE114621
Exon level expression analysis from rhabdomyosarcoma patient tumors.
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Rhabdomyosarcoma is a childhood tumor with features of aberrant muscle differentiation. We studied samples from 101 rhabdomyosarcoma patients to determine core gene expression signatures relevant in the disease.

Publication Title

Integrative Bayesian Analysis Identifies Rhabdomyosarcoma Disease Genes.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE17254
Comparative analysis of gene regulation by the transcription factor PPAR between mouse and human
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 46 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Studies in mice have shown that PPAR is an important regulator of hepatic lipid metabolism and the acute phase response. However, little information is available on the role of PPAR in human liver. Here we set out to compare the function of PPAR in mouse and human hepatocytes via analysis of target gene regulation. Primary hepatocytes from 6 human and 6 mouse donors were treated with PPAR agonist Wy14643 and gene expression profiling was performed using Affymetrix GeneChips followed by a systems biology analysis. Baseline PPAR expression was similar in human and mouse hepatocytes. Depending on species and time of exposure, Wy14643 significantly induced the expression of 362-672 genes. Surprisingly minor overlap was observed between the Wy14643-regulated genes from mouse and human, although more substantial overlap was observed at the pathway level. Xenobiotics metabolism and apolipoprotein synthesis were specifically regulated by PPAR in human hepatocytes, whereas glycolysis-gluconeogenesis was regulated specifically in mouse hepatocytes. Most of the genes commonly regulated in mouse and human were involved in lipid metabolism and many represented known PPAR targets, including CPT1A, HMGCS2, FABP, ACSL, and ADFP. Several genes were identified that were specifically induced by PPAR in human (MBL2, ALAS1, CYP1A1, TSKU) or mouse (Fbp2, lgals4, Cd36, Ucp2, Pxmp4). Furthermore, several putative novel PPAR targets were identified that were commonly regulated in both species, including CREB3L3, KLF10, KLF11 and MAP3K8. Our results suggest that PPAR activation has a major impact on gene regulation in human hepatocytes. Importantly, the role of PPAR as master regulator of hepatic lipid metabolism is generally well-conserved between mouse and human. Overall, however, PPAR regulates a mostly divergent set of genes in mouse and human hepatocytes.

Publication Title

Comparative analysis of gene regulation by the transcription factor PPARalpha between mouse and human.

Sample Metadata Fields

Sex, Age, Specimen part, Subject, Time

View Samples
accession-icon GSE17251
Comparative analysis of gene regulation by the transcription factor PPAR_human
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Studies in mice have shown that PPAR is an important regulator of hepatic lipid metabolism and the acute phase response. However, little information is available on the role of PPAR in human liver. Here we set out to compare the function of PPAR in mouse and human hepatocytes via analysis of target gene regulation. Primary hepatocytes from 6 human and 6 mouse donors were treated with PPAR agonist Wy14643 and gene expression profiling was performed using Affymetrix GeneChips followed by a systems biology analysis. Baseline PPAR expression was similar in human and mouse hepatocytes. Depending on species and time of exposure, Wy14643 significantly induced the expression of 362-672 genes. Surprisingly minor overlap was observed between the Wy14643-regulated genes from mouse and human, although more substantial overlap was observed at the pathway level. Xenobiotics metabolism and apolipoprotein synthesis were specifically regulated by PPAR in human hepatocytes, whereas glycolysis-gluconeogenesis was regulated specifically in mouse hepatocytes. Most of the genes commonly regulated in mouse and human were involved in lipid metabolism and many represented known PPAR targets, including CPT1A, HMGCS2, FABP, ACSL, and ADFP. Several genes were identified that were specifically induced by PPAR in human (MBL2, ALAS1, CYP1A1, TSKU) or mouse (Fbp2, lgals4, Cd36, Ucp2, Pxmp4). Furthermore, several putative novel PPAR targets were identified that were commonly regulated in both species, including CREB3L3, KLF10, KLF11 and MAP3K8. Our results suggest that PPAR activation has a major impact on gene regulation in human hepatocytes. Importantly, the role of PPAR as master regulator of hepatic lipid metabolism is generally well-conserved between mouse and human. Overall, however, PPAR regulates a mostly divergent set of genes in mouse and human hepatocytes.

Publication Title

Comparative analysis of gene regulation by the transcription factor PPARalpha between mouse and human.

Sample Metadata Fields

Sex, Age, Specimen part, Subject, Time

View Samples
accession-icon GSE17250
Comparative analysis of gene regulation by the transcription factor PPAR_mouse
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Studies in mice have shown that PPAR is an important regulator of hepatic lipid metabolism and the acute phase response. However, little information is available on the role of PPAR in human liver. Here we set out to compare the function of PPAR in mouse and human hepatocytes via analysis of target gene regulation. Primary hepatocytes from 6 human and 6 mouse donors were treated with PPAR agonist Wy14643 and gene expression profiling was performed using Affymetrix GeneChips followed by a systems biology analysis. Baseline PPAR expression was similar in human and mouse hepatocytes. Depending on species and time of exposure, Wy14643 significantly induced the expression of 362-672 genes. Surprisingly minor overlap was observed between the Wy14643-regulated genes from mouse and human, although more substantial overlap was observed at the pathway level. Xenobiotics metabolism and apolipoprotein synthesis were specifically regulated by PPAR in human hepatocytes, whereas glycolysis-gluconeogenesis was regulated specifically in mouse hepatocytes. Most of the genes commonly regulated in mouse and human were involved in lipid metabolism and many represented known PPAR targets, including CPT1A, HMGCS2, FABP, ACSL, and ADFP. Several genes were identified that were specifically induced by PPAR in human (MBL2, ALAS1, CYP1A1, TSKU) or mouse (Fbp2, lgals4, Cd36, Ucp2, Pxmp4). Furthermore, several putative novel PPAR targets were identified that were commonly regulated in both species, including CREB3L3, KLF10, KLF11 and MAP3K8. Our results suggest that PPAR activation has a major impact on gene regulation in human hepatocytes. Importantly, the role of PPAR as master regulator of hepatic lipid metabolism is generally well-conserved between mouse and human. Overall, however, PPAR regulates a mostly divergent set of genes in mouse and human hepatocytes.

Publication Title

Comparative analysis of gene regulation by the transcription factor PPARalpha between mouse and human.

Sample Metadata Fields

Sex, Age, Specimen part, Time

View Samples
accession-icon GSE8316
Comprehensive analysis of PPARa-dependent regulation of hepatic lipid metabolism by expression profiling
  • organism-icon Mus musculus, Homo sapiens, Rattus norvegicus
  • sample-icon 46 Downloadable Samples
  • Technology Badge Icon 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
accession-icon GSE8292
Comprehensive analysis of PPAR-dependent regulation of hepatic lipid metabolism by expression profiling - 3
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon 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
accession-icon GSE8295
Comprehensive analysis of PPAR-dependent regulation of hepatic lipid metabolism by expression profiling - 4
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon 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
...

refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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