Open Access Research article

Analysis of the heat shock response in mouse liver reveals transcriptional dependence on the nuclear receptor peroxisome proliferator-activated receptor α (PPARα)

Beena Vallanat1, Steven P Anderson2, Holly M Brown-Borg3, Hongzu Ren1, Sander Kersten4, Sudhakar Jonnalagadda5, Rajagopalan Srinivasan56 and J Christopher Corton1*

Author Affiliations

1 NHEERL Toxicogenomics Core, US EPA, Research Triangle Park, NC 27711, USA

2 Safety Assessment, Merial, Ltd., Duluth, GA 30096, USA

3 Department of Pharmacology, Physiology and Therapeutics, University of North Dakota, School of Medicine, 501 N. Columbia Road, Grand Forks, ND 58203-2817, USA

4 Nutrition, Metabolism and Genomics Group, Wageningen University and Nutrigenomics Consortium, TI Food and Nutrition, Wageningen, the Netherlands

5 Institute of Chemical and Engineering Sciences, A*STAR (Agency for Science, Technology and Research), 1 Pesek Road, Jurong Island, Singapore

6 Department of Chemical and Biomolecular Engineering, National University of Singapore, 10 Kent Ridge Crescent, Singapore

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BMC Genomics 2010, 11:16  doi:10.1186/1471-2164-11-16

Published: 7 January 2010

Additional files

Additional file 1:

Sequences of primers. Sequences of primers used in TaqMan studies.

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Additional file 2:

Gene expression changes after WY, heat shock or heat shock+WY in wild-type and PPARα-null mouse livers. Table represents the gene annotations and fold changes for gene expression changes after WY, heat shock or heat shock+WY in wild-type and PPARα-null mouse livers.

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Additional file 3:

Table of genesets significantly up-regulated by heat shock in wild-type mice. Table describes GSEA genesets significantly up-regulated by heat shock in wild-type mice.

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Additional file 4:

Table of genesets significantly up-regulated by heat shock in PPARα-null mice. Table describes GSEA genesets significantly up-regulated by heat shock in PPARα-null mice.

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Additional file 5:

Table of genesets significantly down-regulated by heat shock in PPARα-null mice. Table describes GSEA genesets significantly down-regulated by heat shock in PPARα-null mice.

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Additional file 6:

Table of transcription factor genesets significantly up-regulated by heat shock in wild-type mice. Table describes the GSEA transcription factor genesets significantly up-regulated by heat shock in wild-type mice.

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Additional file 7:

Table of transcription factor genesets significantly up-regulated by heat shock in PPARα-null mice. Table describes the GSEA transcription factor genesets significantly up-regulated by heat shock in PPARα-null mice.

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Additional file 8:

Analysis of interactions between WY and HS in wild-type mice. Interactions between WY and HS in wild-type mice using Ingenuity Pathway Analysis Tool.

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Additional file 9:

Canonical pathways analysis using Ingenuity. Canonical pathways in an Ingenuity comparison between genes only regulated by WY or only by WY+HS in wild-type mice.

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Additional file 10:

Excel spreadsheet of genes regulated by heat shock or by strain differences between wild-type and HSF1-null mice. Genes were originally from the Trinklein et al. (2004) study. Excel spreadsheet of genes regulated by heat shock or by strain differences between wild-type and HSF1-null mice.

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Additional file 11:

Figures of expression of heat shock genes in wild-type and HSF1-null mouse embryonic fibroblasts. Mouse embryonic fibroblasts were given a HS and cells were harvested at the indicated times as described (Trinklein et al., 2004). Genes which exhibited significant changes after HS or that exhibited significant differences between wild-type and HSF1-null strains were identified as described in the Methods. A. HSF1-dependent HS genes. B. HSF1-independent HS genes. C. Genes which exhibited differences in expression between control wild-type and control HSF1-null strains.

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