Glucocorticoid receptor function in hepatocytes is essential to promote postnatal body growth
Copyright policy )Glucocorticoid receptor function in hepatocytes is essential to promote postnatal body growth
Mice carrying a hepatocyte-specific inactivation of the glucorticoid receptor (GR) gene show a dramatic reduction in body size. Growth hormone signaling mediated by the Stat5 transcription factors is impaired. We show that Stat5 proteins physically interact with GR and GR is present in vivo on Stat5-dependent IGF-I and ALS regulatory regions. Interestingly, mice with a DNA-binding-deficient GR but an unaltered ability to interact with STAT5 (GRdim/dim) have a normal body size and normal levels of Stat5-dependent mRNAs. These findings strongly support the model in which GR acts as a coactivator for Stat5-dependent transcription upon GH stimulation and reveal an essential role of hepatic GR in the control of body growth.
- Collège de France France
- Institut Pasteur France
- German Cancer Research Center Germany
- Research Institute of Molecular Pathology Austria
Male, Transcription, Genetic, Growth, Milk Proteins, Mice, Mutant Strains, DNA-Binding Proteins, Mice, Receptors, Glucocorticoid, Organ Specificity, Growth Hormone, Hepatocytes, STAT5 Transcription Factor, Trans-Activators, Animals, Body Constitution, Female, RNA, Messenger, Protein Binding, Signal Transduction
Male, Transcription, Genetic, Growth, Milk Proteins, Mice, Mutant Strains, DNA-Binding Proteins, Mice, Receptors, Glucocorticoid, Organ Specificity, Growth Hormone, Hepatocytes, STAT5 Transcription Factor, Trans-Activators, Animals, Body Constitution, Female, RNA, Messenger, Protein Binding, Signal Transduction
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