The Synergistic Effect of Dexamethasone and All-trans-retinoic Acid on Hepatic Phosphoenolpyruvate Carboxykinase Gene Expression Involves the Coactivator p300

Wang, Xiaohui L.; Herzog, Birger; Waltner-Law, Mary; Hall, Robert K.; Shiota, Masakazu; Granner, Daryl K.

doi:10.1074/jbc.m403455200

Cited by 37 publications

(21 citation statements)

References 35 publications

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“…Furthermore, combined treatment of hepatocytes with GCs and retinoic acid promotes the recruitment of additional transcriptional co-factors apart from SRC-1, including the acetyltransferases p300/CREB binding protein (CBP) and p300/CBP/cointegrator-associated protein (p/CIP). Ablation of p300 expression in isolated hepatocytes strongly diminishes PEPCK activity, supporting the critical role of histone-modifying co-factors for hormone-inducible PEPCK gene expression [86].…”

Section: Molecular Control Of Gluconeogenic Enzyme Expressionmentioning

confidence: 70%

Glucocorticoids, metabolism and metabolic diseases

Vegiopoulos

Herzig

2007

Molecular and Cellular Endocrinology

440

370

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Since the discovery of the beneficial effects of adrenocortical extracts for treating adrenal insufficiency more than 80 years ago, glucocorticoids (GC) and their cognate, intracellular receptor, the glucocorticoid receptor (GR) have been characterized as critical components of the delicate hormonal control system that determines energy homeostasis in mammals.Whereas physiological levels of GCs are required for proper metabolic control, excessive GC action has been tied to a variety of pandemic metabolic diseases, such as type II diabetes and obesity. Highlighted by its importance for human health, the investigation of molecular mechanisms of GC/GR action has become a major focus in biomedical research. In particular, the understanding of tissue-specific functions of the GC-GR pathway has been proven to be of substantial value for the identification of novel therapeutic options in the treatment of severe metabolic disorders. Therefore, this review focuses on the role of the GC-GR axis for metabolic homeostasis and dysregulation, emphasizing tissue-specific functions of GCs in the control of energy metabolism.

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Section: Molecular Control Of Gluconeogenic Enzyme Expressionmentioning

confidence: 70%

Glucocorticoids, metabolism and metabolic diseases

Vegiopoulos

Herzig

2007

Molecular and Cellular Endocrinology

440

370

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“…html) was conducted by using a kit from Upstate Biotechnology (Lake Placid, NY, USA). The immunoprecipitated DNAs were used as the template for PCR that was performed by using specific primers for the promoter region of the PCK1 17) or G6PC genes (Table 1) with an Applied Biosystems 7300 sequence detection system. The relative amounts of DNA of the PCK1 or G6PC genes were normalized by the amount of EEF1A1 gene DNA.…”

Section: Methodsmentioning

confidence: 99%

Effect of Biotin Treatment on Hepatic Gene Expression in Streptozotocin-Induced Diabetic Rats

Sugita

Shirakawa

Sugimoto

et al. 2008

Bioscience, Biotechnology, and Biochemistry

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“…1A). Because of the extremely low transfection efficiency of H4IIE cells (data not shown) (17,18) and the observed qualitatively identical impact of CARM1 on gluconeogenic gene transcription in H4IIE and HepG2 cells (Fig. 1), human HepG2 cells were used for all subsequent promoter studies.…”

Section: Carm1 Controls Gluconeogenic Gene Expression-to Test Whethermentioning

confidence: 99%

Signal-dependent Control of Gluconeogenic Key Enzyme Genes through Coactivator-associated Arginine Methyltransferase 1

Krones-Herzig

Mesaros

Metzger

et al. 2006

Journal of Biological Chemistry

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Together with impaired glucose uptake in skeletal muscle, elevated hepatic gluconeogenesis is largely responsible for the hyperglycemic phenotype in type II diabetic patients. Intracellular glucocorticoid and cyclic adenosine monophosphate (cAMP)/protein kinase A-dependent signaling pathways contribute to aberrant hepatic glucose production through the induction of gluconeogenic enzyme gene expression. Here we show that the coactivator-associated arginine methyltransferase 1 (CARM1) is required for cAMP-mediated activation of ratelimiting gluconeogenic phosphoenolpyruvate carboxykinase (PEPCK; EC 4.1.1.32) and glucose-6-phosphatase genes. Mutational analysis showed that CARM1 mediates its effect via the cAMP-responsive element within the PEPCK promoter, which is identified here as a CARM1 target in vivo. In hepatocytes, endogenous CARM1 physically interacts with cAMP-responsive element binding factor CREB and is recruited to the PEPCK and glucose-6-phosphatase promoters in a cAMP-dependent manner associated with increased promoter methylation. CARM1 might, therefore, represent a critical component of cAMP-dependent glucose metabolism in the liver.

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The Synergistic Effect of Dexamethasone and All-trans-retinoic Acid on Hepatic Phosphoenolpyruvate Carboxykinase Gene Expression Involves the Coactivator p300

Cited by 37 publications

References 35 publications

Glucocorticoids, metabolism and metabolic diseases

Glucocorticoids, metabolism and metabolic diseases

Effect of Biotin Treatment on Hepatic Gene Expression in Streptozotocin-Induced Diabetic Rats

Signal-dependent Control of Gluconeogenic Key Enzyme Genes through Coactivator-associated Arginine Methyltransferase 1

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