Expression and behavior of related proteins to exocytosis in salivary acinar cells

2014 Fiscal Year Final Research Report

• Project/Area Number: 24592820
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Functional basic dentistry
• Research Institution: THE NIPPON DENTAL UNIVERSITY COLLEGE AT NIIGATA (2014); The Nippon Dental University (2012-2013)
• Principal Investigator: IMAI Akane 日本歯科大学新潟短期大学, その他部局等, 教授 (60180080)
• Co-Investigator(Kenkyū-buntansha): NASHIDA Tomoko 日本歯科大学, 新潟生命歯学部, 准教授 (10133464) ; YOSHIE Sumio 日本歯科大学, 新潟生命歯学部, 教授 (30095278) ; TSUJIMURA Maiko 日本歯科大学, 新潟生命歯学部, 講師 (60535219)
• Co-Investigator(Renkei-kenkyūsha): FUKUDA Mitsunori 東北大学, 生命研究科, 教授 (50311361)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 耳下腺 / Rabタンパク質 / 開口分泌

Outline of Final Research Achievements

We study about small GTPase Rab27 and its effectors regulate isoproterenol (IPR)-stimulated amylase release from rat parotid acinar cells. We investigated the possible involvement of MADD/DENN/Rab3GEP in amylase release from rat parotid acinar cells. mRNA and protein of MADD was expressed in parotid acinar cells. MADD protein was also expressed in the cytosolic fraction of parotid acinar cells. Introduction of an antibody against the C-terminal 150 amino acids of MADD (anti-MADD-C antibody) into streptolysin O-permeabilized parotid acinar cells caused not only inhibition of IPR-induced amylase release but also reduction in the amount of GTP-Rab27. Our findings indicated that MADD functions as a GEF for Rab27 in parotid acinar cells and that its Rab27-GEF activity, that is GDP/GTP cycle, is required for IPR-induced amylase release.

Free Research Field

口腔生化学