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Updated: Apr 6, 2026
A Chemical Screening Procedure for Glucocorticoid Signaling with a Zebrafish Larva Luciferase Reporter System
Published on: September 10, 2013
Animal Models of Altered Glucocorticoid Signaling
1Division of Endocrinology, Metabolism and Lipid Research, Department of Internal Medicine, Washington University School of Medicine, 660 S Euclid Avenue, Campus Box 8127, St. Louis, MO, 63110, USA, caharris@dom.wustl.edu.
Abstract:
In this chapter we will review genetically engineered mice with alterations in glucocorticoid signaling. Most of the mice involve direct alterations to the glucocorticoid receptor locus, but we will touch briefly on other relevant models including 11-β-HSD transgenics which alter tissue levels of ligand as well as mice with glucocorticoid excess. Of course, the number of mice with mutations in genes such as GR targets and transcriptional coregulators is beyond the scope of this chapter.
Insights
This chapter reviews genetically engineered mice models. These models investigate glucocorticoid receptor (GR) signaling pathways and their effects on cellular processes.
Area of Science:
- Endocrinology and Molecular Biology
- Genetics and Genomics
Background:
- Glucocorticoid signaling is crucial for numerous physiological processes.
- Genetically engineered mouse models are vital tools for studying complex signaling pathways.
- Understanding glucocorticoid receptor (GR) function requires sophisticated genetic models.
Purpose of the Study:
- To provide a comprehensive review of genetically engineered mice used to study glucocorticoid signaling.
- To highlight models with direct alterations to the glucocorticoid receptor locus.
- To briefly discuss related models, including those affecting ligand levels or involving glucocorticoid excess.
Main Methods:
- Review of existing literature on genetically engineered mouse models.
- Focus on mice with modifications to the glucocorticoid receptor (GR) locus.
- Inclusion of models such as 11-β-HSD transgenics and those with glucocorticoid excess.
Main Results:
- Detailed examination of mice with direct GR locus alterations.
- Discussion of how altered ligand availability (e.g., via 11-β-HSD transgenics) impacts signaling.
- Consideration of models exhibiting glucocorticoid excess.
Conclusions:
- Genetically engineered mice provide powerful insights into glucocorticoid signaling.
- Direct GR modifications and altered ligand availability are key areas of study.
- Further research into GR targets and coregulators in mouse models is warranted but beyond this chapter's scope.
