Regulation of ectodomian shedding by ADAM17 and remnant signaling

2014 Fiscal Year Final Research Report

• Project/Area Number: 24390074
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: General medical chemistry
• Research Institution: Ehime University
• Principal Investigator: HIGASHIYAMA Shigeki 愛媛大学, プロテオサイエンスセンター, 教授 (60202272)
• Co-Investigator(Renkei-kenkyūsha): FUKUDA Shinji 愛媛大学, プロテオサイエンスセンター, 助教 (70398238) ; INOUE Hirofumi 愛媛大学, 大学院医学系研究科, 講師 (70321635) ; MATSUSHITA Natsuki 愛媛大学, 医学部附属病院, 研究員 (40271556) ; JHO Takashi 名古屋市立大学, 大学院医学系研究科, 教授 (30231369)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: ectodomian shedding / ADAM17 / proHB-EGF / proamphiregulin / proTNF-α / annexin / レムナントペプチドシグナル

Outline of Final Research Achievements

ADAM17, a transmembrane-type metalloprotease, sheds various transmembrane proteins on cell surface, which regulates cell signaling. Both type I transmembrane protein proHB-EGF and proAREG, and type II transmembrane protein proTNF-α are equally shed. However, ADAM17 binding proteins annexin reversibly affected on their ADAM17-induced shedding. We propose that the catalytic domain of ADAM17 can swing by binding different member of annexin and access to the different types of membrane proteins.

Free Research Field

生化学、分子細胞生物学、