Glucose regulates the function of glucocorticoid receptor via O-GlcNAc modification.

2014 Fiscal Year Final Research Report

• Project/Area Number: 24591357
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Endocrinology
• Research Institution: The University of Tokushima (2013-2014); Gunma University (2012)
• Principal Investigator: SAWATSUBASHI Shun 徳島大学, 藤井節郎記念医科学センター, 特任講師 (70535103)
• Co-Investigator(Renkei-kenkyūsha): KITAGAWA Hirochika 群馬大学, 生体調節研究所, 教授 (20345234) ; SATO Takashi 群馬大学, 生体調節研究所, 准教授 (70344934)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: グルココルチコイド / 翻訳後修飾 / O-GlcNAc / 核内受容体

Outline of Final Research Achievements

Glucocorticoids are widely used as anti-inflammatory drugs, the molecular mechanisms involved in this anti-inflammatory effect and associated with serious side effects remain unknown. In this study, we performed the proteomic analysis of post-translational modification on glucocorticoid receptor (GR) and identified a novel O-linked beta-N-acetylglucosamine (O-GlcNAc) modified sites. Moreover, this O-GlcNAcylation was regulated under conditions of glucose concentration in culture medium and detected in nucleus of mouse liver and cerebrum. Based on these results, we propose that this O-GlcNAcylation regulates the tissue-specific transcriptional activity of GR.

Free Research Field

分子生物学