The role of calpains in ligand-induced degradation of the glucocorticoid receptor
- Authors
- Kim, Yoon Suk; Kim, Jeonghan; Kim, Yoonseo; Lee, Young Han; Kim, Jae-Hong; Lee, Seung-Jae; Shin, Soon Young; Ko, Jesang
- Issue Date
- 19-9월-2008
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- glucocorticoid receptor; calpain; dexamethasone
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.374, no.2, pp.373 - 377
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 374
- Number
- 2
- Start Page
- 373
- End Page
- 377
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/122701
- DOI
- 10.1016/j.bbrc.2008.07.040
- ISSN
- 0006-291X
- Abstract
- The glucocorticoid receptor (GR) is a ligand-activated transcription factor that mediates the effects of glucocorticoids in diverse cellular processes, including homeostasis, stress response, and inflammation. Glucocorticoids induce clown-regulation of GR at both the mRNA and Protein levels, Causing reduced hormone responsiveness in response to long-term treatment with glucocorticoid. However, the mechanism involved in this process is still obscure. In this study, we examined whether calpain, a calcium-activated cysteine protease, is involved in ligand-stimulated degradation of GR. In COS-7 cells expressing the human GR, treatment with a calpain inhibitor abolished glucocorticoid-induced clown-regulation of GR in a dose dependent manner. The protein level of endogenous GR was also elevated by inhibition of the calpain activity in HeLa cells treated with glucocorticoid. Furthermore, glucocorticoid-induced transcriptional activation of GR was enhanced in cells treated with a calpain inhibitor. These results indicate that calpain is involved in ligand-dependent degradation of GR, thus causing reduced hormone responsiveness. (C) 2008 Elsevier Inc. All rights reserved.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - College of Life Sciences and Biotechnology > Division of Life Sciences > 1. Journal Articles
- Graduate School > Department of Life Sciences > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.