Roles of 14-3-3 beta and gamma in regulation of the glucocorticoid receptor transcriptional activation and hepatic gluconeogenesis
- Authors
- Hwang, Yunhee; An, Hyoung-Tae; Kang, Minsoo; Ko, Jesang
- Issue Date
- 27-6월-2018
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- 14-3-3; Glucocorticoid receptor; Phosphoenolpyruvate carboxykinase; Glucose-6-phosphatase; Gluconeogenesis
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.501, no.3, pp.800 - 806
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 501
- Number
- 3
- Start Page
- 800
- End Page
- 806
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/74890
- DOI
- 10.1016/j.bbrc.2018.05.077
- ISSN
- 0006-291X
- Abstract
- The glucocorticoid receptor (GR) is a ligand-dependent transcription factor that mediates the effects of glucocorticoids, and plays a crucial role in cell growth, development, inflammation, and gluconeogenesis. The 14-3-3 proteins bind to target proteins via phosphorylation, and influence many cellular events by altering their subcellular localization or by acting as chaperones. However, the mechanisms by which 14-3-3 proteins regulate GR transactivation and their involvement in gluconeogenesis remain uncharacterized. We found that 14-3-3 beta and gamma increased GR transcriptional activity and the promoter activities of phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase in the presence of glucocorticoids. Inhibition of the endogenous 14-3-3 beta and gamma decreased dexamethasone- and cAMP-stimulated PEPCK expression. Further, both 14-3-3 beta and gamma increased glucose production in response to glucocorticoids. Our findings suggest that 14-3-3 beta and gamma function as positive regulators of GR transactivation and glucocorticoid-mediated hepatic gluconeogenesis. (C) 2018 Elsevier Inc. All rights reserved.
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