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Raw gene Expression data is sourced from GEO, and the appropriate db package for mapping probes to gene symbols was sourced from the Bioconductor AnnotationData packages.
You can read more about microarray data here.
Select conditions below to toggle them from the plot:
| GROUP | CONDITION | SAMPLES |
|---|---|---|
| Male mice: 129P2/OlaHsd |
GSM1056631 GSM1056632 GSM1056633 GSM1056634 GSM1056635 GSM1056636 GSM1056637
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GSM1056623 GSM1056624 GSM1056625 GSM1056626 GSM1056627 GSM1056628 GSM1056629 GSM1056630
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| Male mice: C3HeB/FeJ |
GSM1056687 GSM1056688 GSM1056689 GSM1056690 GSM1056691 GSM1056692 GSM1056693 GSM1056694
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GSM1056669 GSM1056670 GSM1056671 GSM1056672 GSM1056673 GSM1056674 GSM1056675 GSM1056676 GSM1056677 GSM1056678 GSM1056679 GSM1056680 GSM1056681 GSM1056682 GSM1056683 GSM1056684 GSM1056685 GSM1056686
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| Male mice: C57BL/6J |
GSM1056646 GSM1056647 GSM1056648 GSM1056649 GSM1056650 GSM1056651 GSM1056652
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GSM1056638 GSM1056639 GSM1056640 GSM1056641 GSM1056642 GSM1056643 GSM1056644 GSM1056645
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| Male mice: C57BL/6NTac |
GSM1056661 GSM1056662 GSM1056663 GSM1056664 GSM1056665 GSM1056666 GSM1056667 GSM1056668
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GSM1056653 GSM1056654 GSM1056655 GSM1056656 GSM1056657 GSM1056658 GSM1056659 GSM1056660
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Submission Date: Dec 21, 2012
Summary: 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.
HFD exposure for 21 days progressively increased liver triacylglycerol concentrations (TAG) in 129. Strain-specific liver transcription profiles in this model suggest a transition from benign fatty liver to inflammation-associated NAFLD. No comparable changes were observed in C3H males where after an initial increase, hepatic TAG declined. In all genetic backgrounds hepatosteatosis was paralleled by a concerted repression of genes potentially increasing the liver's vulnerability to oxidative stress damage thereby contributing to the progression of benign hepatosteatosis to NASH later on. The products of further identified strain-independent gene candidates might represent putative molecular links between the pathogenesis of NAFLD and cancer, insulin resistance, type 2 diabetes, and neurodegenerative disorders. Phenotypic characteristics and strain-dependent and -independent transcriptional changes in liver in different murine genetic backgrounds in this work can be exploited in the search for molecular mechanisms implicated in the development of HFD-mediated NAFLD, the investigation of potential therapeutic targets and in selecting a suitable murine genetic background for studies and mouse mutant engineering.
GEO Accession ID: GSE43106
PMID: 24327959
Submission Date: Dec 21, 2012
Summary: 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.
HFD exposure for 21 days progressively increased liver triacylglycerol concentrations (TAG) in 129. Strain-specific liver transcription profiles in this model suggest a transition from benign fatty liver to inflammation-associated NAFLD. No comparable changes were observed in C3H males where after an initial increase, hepatic TAG declined. In all genetic backgrounds hepatosteatosis was paralleled by a concerted repression of genes potentially increasing the liver's vulnerability to oxidative stress damage thereby contributing to the progression of benign hepatosteatosis to NASH later on. The products of further identified strain-independent gene candidates might represent putative molecular links between the pathogenesis of NAFLD and cancer, insulin resistance, type 2 diabetes, and neurodegenerative disorders. Phenotypic characteristics and strain-dependent and -independent transcriptional changes in liver in different murine genetic backgrounds in this work can be exploited in the search for molecular mechanisms implicated in the development of HFD-mediated NAFLD, the investigation of potential therapeutic targets and in selecting a suitable murine genetic background for studies and mouse mutant engineering.
GEO Accession ID: GSE43106
PMID: 24327959
Visualize Samples
Visualizations are precomputed using the Python package scanpy on the top 5000 most variable genes.
Precomputed Differential Gene Expression
Differential expression signatures are automatically computed using the limma R package.
More options for differential expression are available to compute below.
Signatures:
Select conditions:
Control Condition
Perturbation Condition
Only conditions with at least 1 replicate are available to select
Differential expression signatures can be computed using DESeq2 or characteristic direction.