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A new function of glucocorticoid receptor: regulation of mRNA stability
A new function of glucocorticoid receptor: regulation of mRNA stability
BMB Reports. 2015. Jul, 48(7): 367-368
Copyright © 2015, Korean Society for Biochemistry and Molecular Biology
This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
  • Received : July 02, 2015
  • Published : July 31, 2015
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About the Authors
Ok Hyun Park
Eunjin Do
Yoon Ki Kim
yk-kim@korea.ac.kr

Abstract
It has long been thought that glucocorticoid receptor (GR) functions as a DNA-binding transcription factor in response to its ligand (a glucocorticoid) and thus regulates various cellular and physiological processes. It is also known that GR can bind not only to DNA but also to mRNA; this observation points to the possible role of GR in mRNA metabolism. Recent data revealed a molecular mechanism by which binding of GR to target mRNA elicits rapid mRNA degradation. GR binds to specific RNA sequences regardless of the presence of a ligand. In the presence of a ligand, however, the mRNA-associated GR can recruit PNRC2 and UPF1, both of which are specific factors involved in nonsense-mediated mRNA decay (NMD). PNRC2 then recruits the decapping complex, consequently promoting mRNA degradation. This mode of mRNA decay is termed “GR-mediated mRNA decay” (GMD). Further research demonstrated that GMD plays a critical role in chemotaxis of immune cells by targeting CCL2 mRNA. All these observations provide molecular insights into a previously unappreciated function of GR in posttranscriptional regulation of gene expression. [BMB Reports 2015; 48(7): 367-368]
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Acknowledgements
This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIP) (2012R1A2A1A01002469 and 2014R1A2A1A11050412), and by a Korea University Grant (K1505301). O.H.P was in part supported by the Global PhD Fellowship Program through the National Research Foundation funded by the Korean Government.
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