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accession-icon GSE10280
MF1 outbred stock liver gene expression data
  • organism-icon Mus musculus
  • sample-icon 110 Downloadable Samples
  • Technology Badge IconSentrix MouseRef-8 Expression BeadChip

Description

Linkage analysis of complex traits in mice is a powerful tool to find loci affecting the phenotype but it has a poor resolution making it difficult to identify the underlying genes. We show here, using whole genome association analysis of gene expression traits in an outbred mouse population, the MF1 stock, that mapping resolution is greatly increased as compared to linkage. The fact that eQTLs discovered in other crosses were replicated and successfully mapped with high resolution in this population provides a strong proof of concept. In addition, we show that this population is a useful resource to resolve the eQTL hotspots detected in other studies. Finally, we highlight the importance of correcting for population structure in whole genome association studies in the outbred stock.

Publication Title

High-resolution mapping of gene expression using association in an outbred mouse stock.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE38705
Macrophage samples from the HMDP
  • organism-icon Mus musculus
  • sample-icon 510 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Mouse Genome 430A Array (htmg430a)

Description

Identify genes involved in regulation of inflammatory responses and gene-environemnt interactions, in macrophages from a set of mouse inbred strains termed the HMDP. The HMDP is a genetically diverse mapping panel comprised of classical inbred and recombinant inbred wild type mice. The RMA values of genes were used for genome wide association as described in Bennett et al Genome Research 2010.

Publication Title

Unraveling inflammatory responses using systems genetics and gene-environment interactions in macrophages.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE16780
Hybrid Mouse diversity Panel Liver Expression Profile
  • organism-icon Mus musculus
  • sample-icon 288 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Mouse Genome 430A Array (htmg430a)

Description

Novel, systems-based approach to mouse genetics.

Publication Title

A high-resolution association mapping panel for the dissection of complex traits in mice.

Sample Metadata Fields

Specimen part

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accession-icon GSE65111
Genome-wide prediction and analysis of yeast RNase III-dependent snoRNA processing signals
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome S98 Array (ygs98)

Description

In Saccharomyces cerevisiae, the maturation of both pre-rRNA and pre-small nucleolar RNAs (pre-snoRNAs) involves common factors, thereby providing a potential mechanism for the coregulation of snoRNA and rRNA synthesis. In this study, we examined the global impact of the double-stranded-RNA-specific RNase Rnt1p, which is required for pre-rRNA processing, on the maturation of all known snoRNAs. In silico searches for Rnt1p cleavage signals, and genome-wide analysis of the Rnt1p-dependent expression profile, identified seven new Rnt1p substrates. Interestingly, two of the newly identified Rnt1p-dependent snoRNAs, snR39 and snR59, are located in the introns of the ribosomal protein genes RPL7A and RPL7B. In vitro and in vivo experiments indicated that snR39 is normally processed from the lariat of RPL7A, suggesting that the expressions of RPL7A and snR39 are linked. In contrast, snR59 is produced by a direct cleavage of the RPL7B pre-mRNA, indicating that a single pre-mRNA transcript cannot be spliced to produce a mature RPL7B mRNA and processed by Rnt1p to produce a mature snR59 simultaneously. The results presented here reveal a new role of yeast RNase III in the processing of intron-encoded snoRNAs that permits independent regulation of the host mRNA and its associated snoRNA.

Publication Title

Genome-wide prediction and analysis of yeast RNase III-dependent snoRNA processing signals.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE51075
Transcriptional responses of murine macrophages to the adenylate cyclase toxin of Bordetella pertussis
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Three different recombinant forms of CyaA were used to investigate transcriptional responses of murine bone marrow-derived macrophages (BMDMs) using Affymetrix Mouse Genome Genechips. These forms were enzymically active, invasive CyaA, nonenzymically active, invasive CyaA (CyaA*) and non-enzymically active, non-invasive CyaA (proCyaA*). BMMs, treated with 20 ng/ml of CyaA for 24 h, showed over 1000 significant changes in gene transcription compared with control cells. CyaA caused an increase in transcription of many inflammatory genes and genes associated with various signalling cascades such as those involved in cyclic AMP-dependent protein kinase A signalling. Most strikingly, CyaA caused down-regulation of numerous genes involved in cell proliferation. CyaA* at 20 ng/ml significantly up-regulated the transcription of only twelve genes after 24 h whereas proCyaA* at this concentration significantly increased the transcription of only two genes.

Publication Title

Transcriptional responses of murine macrophages to the adenylate cyclase toxin of Bordetella pertussis.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

View Samples
accession-icon GSE12000
Obesity study in transgenic and knockout animals
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge IconSentrix MouseRef-8 Expression BeadChip (Target ID), Rosetta/Merck Mouse TOE 75k Array 1 microarray

Description

A major task in dissecting the genetics of complex traits is to identify causal genes for disease phenotypes. We previously developed a method to infer causal relationships among genes through the integration of DNA variation, gene transcription, and phenotypic information. Here we validated our method through the characterization of transgenic and knockout mouse models of candidate genes that were predicted to be causal for abdominal obesity. Perturbation of eight out of the nine genes, with Gas7, Me1 and Gpx3 being novel, resulted in significant changes in obesity related traits. Liver expression signatures revealed alterations in common metabolic pathways and networks contributing to abdominal obesity and overlapped with a macrophage-enriched metabolic network module that is highly associated with metabolic traits in mice and humans. Integration of gene expression in the design and analysis of traditional F2 intercross studies allows high confidence prediction of causal genes, and identification of involved pathways and networks.

Publication Title

Validation of candidate causal genes for obesity that affect shared metabolic pathways and networks.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE11999
Lactb male transgenic liver expression vs FVB male wildtype control
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconSentrix MouseRef-8 Expression BeadChip (Target ID)

Description

A major task in dissecting the genetics of complex traits is to identify causal genes for disease phenotypes. We previously developed a method to infer causal relationships among genes through the integration of DNA variation, gene transcription, and phenotypic information. Here we validated our method through the characterization of transgenic and knockout mouse models of candidate genes that were predicted to be causal for abdominal obesity. Perturbation of eight out of the nine genes, with Gas7, Me1 and Gpx3 being novel, resulted in significant changes in obesity related traits. Liver expression signatures revealed alterations in common metabolic pathways and networks contributing to abdominal obesity and overlapped with a macrophage-enriched metabolic network module that is highly associated with metabolic traits in mice and humans. Integration of gene expression in the design and analysis of traditional F2 intercross studies allows high confidence prediction of causal genes, and identification of involved pathways and networks.

Publication Title

Validation of candidate causal genes for obesity that affect shared metabolic pathways and networks.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE11996
Gas7 male transgenic liver expression vs FVB male wildtype control
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconSentrix MouseRef-8 Expression BeadChip (Target ID)

Description

A major task in dissecting the genetics of complex traits is to identify causal genes for disease phenotypes. We previously developed a method to infer causal relationships among genes through the integration of DNA variation, gene transcription, and phenotypic information. Here we validated our method through the characterization of transgenic and knockout mouse models of candidate genes that were predicted to be causal for abdominal obesity. Perturbation of eight out of the nine genes, with Gas7, Me1 and Gpx3 being novel, resulted in significant changes in obesity related traits. Liver expression signatures revealed alterations in common metabolic pathways and networks contributing to abdominal obesity and overlapped with a macrophage-enriched metabolic network module that is highly associated with metabolic traits in mice and humans. Integration of gene expression in the design and analysis of traditional F2 intercross studies allows high confidence prediction of causal genes, and identification of involved pathways and networks.

Publication Title

Validation of candidate causal genes for obesity that affect shared metabolic pathways and networks.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE11998
Gyk female heterozygous liver expression vs C57Bl/6J female wildtype control
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconSentrix MouseRef-8 Expression BeadChip (Target ID)

Description

A major task in dissecting the genetics of complex traits is to identify causal genes for disease phenotypes. We previously developed a method to infer causal relationships among genes through the integration of DNA variation, gene transcription, and phenotypic information. Here we validated our method through the characterization of transgenic and knockout mouse models of candidate genes that were predicted to be causal for abdominal obesity. Perturbation of eight out of the nine genes, with Gas7, Me1 and Gpx3 being novel, resulted in significant changes in obesity related traits. Liver expression signatures revealed alterations in common metabolic pathways and networks contributing to abdominal obesity and overlapped with a macrophage-enriched metabolic network module that is highly associated with metabolic traits in mice and humans. Integration of gene expression in the design and analysis of traditional F2 intercross studies allows high confidence prediction of causal genes, and identification of involved pathways and networks.

Publication Title

Validation of candidate causal genes for obesity that affect shared metabolic pathways and networks.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE11997
Gpx3 male transgenic liver expression vs B6/DBA male wildtype control
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconSentrix MouseRef-8 Expression BeadChip (Target ID)

Description

A major task in dissecting the genetics of complex traits is to identify causal genes for disease phenotypes. We previously developed a method to infer causal relationships among genes through the integration of DNA variation, gene transcription, and phenotypic information. Here we validated our method through the characterization of transgenic and knockout mouse models of candidate genes that were predicted to be causal for abdominal obesity. Perturbation of eight out of the nine genes, with Gas7, Me1 and Gpx3 being novel, resulted in significant changes in obesity related traits. Liver expression signatures revealed alterations in common metabolic pathways and networks contributing to abdominal obesity and overlapped with a macrophage-enriched metabolic network module that is highly associated with metabolic traits in mice and humans. Integration of gene expression in the design and analysis of traditional F2 intercross studies allows high confidence prediction of causal genes, and identification of involved pathways and networks.

Publication Title

Validation of candidate causal genes for obesity that affect shared metabolic pathways and networks.

Sample Metadata Fields

No sample metadata fields

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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Developed by the Childhood Cancer Data Lab

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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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