Functional analysis of glucocorticoid induced transcript 1(GLCCI1)

• Project/Area Number: 21591398
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Pediatrics
• Research Institution: Kyorin University
• Principal Investigator: YAN Kunimasa 杏林大学, 医学部, 教授 (70255389)
• Co-Investigator(Kenkyū-buntansha): AKIMOTO Yoshihiro 杏林大学, 医学部, 准教授 (60184115) ; ISHIGAKI Yasuhito 金沢医科大学, 医学部, 講師 (20232275)
• Project Period (FY): 2009 – 2011
• Project Status: Completed (Fiscal Year 2011)
• Budget Amount: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000); Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000); Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000); Fiscal Year 2009: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
• Keywords: 糖質ステロイド / Ｔ細胞 / アポトーシス / Glcci1 / Dlc8 / PAK1 / T細胞 / 胸腺 / 細胞内骨格 / ステロイド / 精巣 / 糸球体 / ネフローゼ

Research Abstract

The aim of the present study was to identify the protein function of GLCCI1, a novel gene induced by synthetic glucocorticoid. We found that GLCCI was a tubulin-associated phosphoprotein migrated at ～70 kDa that was induced via glucocorticoid-glucocorticoid receptor complex. We also found that both PAK1 anddynein-light chain 8 were the ligand proteins of GLCCI1, and that GLCCI1 interfered the PAK1 kinase activity against LC8 biogenesis, which led to T cell apoptosis. Our data suggested that the functional implication of GLCCI1 in PAK1-LC8 interaction might be a novel downstream cascade resembling synthetic glucocorticoid action as an immunosuppressant.