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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 |
|---|---|---|
| Liver |
GSM1238920 GSM1238921 GSM1238922
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GSM1238917 GSM1238918 GSM1238919
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Submission Date: Sep 23, 2013
Summary: The hypothalamus has recently emerged as a key regulator of metabolism and aging in mammals. We have examined the impact of targeted disruption of hypothalamic hypophysiotropic peptide: Growth Hormone-releasing Hormone (GHRH) in mice on longevity, and the putative mechanisms of delayed aging. GHRH knockout (KO) mice are remarkably long-lived and in comparison to genetically normal (wild type) animals exhibiting major shifts in the expression of genes related to xenobiotic detoxification, stress resistance, and insulin signaling. These mutant mice also have increased adiponectin levels and alterations in glucose homeostasis consistent with the removal of the counter-insulin effects of GH. While these effects overlap with those of caloric restriction (CR), we show that effects of CR and the GHRH mutation are additive, with lifespan of GHRH-KO mutants further increased by CR. We conclude that GHRH-KO mice feature perturbations in a network of signaling pathways related to stress resistance, metabolic control and inflammation, and therefore provide a new model that can be used to explore links between GHRH repression, downregulation of the somatotropic axis, and extended longevity.
GEO Accession ID: GSE51108
PMID: 24175087
Submission Date: Sep 23, 2013
Summary: The hypothalamus has recently emerged as a key regulator of metabolism and aging in mammals. We have examined the impact of targeted disruption of hypothalamic hypophysiotropic peptide: Growth Hormone-releasing Hormone (GHRH) in mice on longevity, and the putative mechanisms of delayed aging. GHRH knockout (KO) mice are remarkably long-lived and in comparison to genetically normal (wild type) animals exhibiting major shifts in the expression of genes related to xenobiotic detoxification, stress resistance, and insulin signaling. These mutant mice also have increased adiponectin levels and alterations in glucose homeostasis consistent with the removal of the counter-insulin effects of GH. While these effects overlap with those of caloric restriction (CR), we show that effects of CR and the GHRH mutation are additive, with lifespan of GHRH-KO mutants further increased by CR. We conclude that GHRH-KO mice feature perturbations in a network of signaling pathways related to stress resistance, metabolic control and inflammation, and therefore provide a new model that can be used to explore links between GHRH repression, downregulation of the somatotropic axis, and extended longevity.
GEO Accession ID: GSE51108
PMID: 24175087
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.