Regulation of NF-kB signaling by post-translational modifications and its relation to disease onsets

2015 Fiscal Year Final Research Report

• Project Area: Regulation of signal transduction by post-translational modifications and its pathogenic dysregulation
• Project/Area Number: 22117002
• Research Category: Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
• Allocation Type: Single-year Grants
• Review Section: Biological Sciences
• Research Institution: The University of Tokyo
• Principal Investigator: Inoue Jun-ichiro 東京大学, 医科学研究所, 教授 (70176428)
• Co-Investigator(Kenkyū-buntansha): OYAMA Masaaki 東京大学, 医科学研究所, 准教授 (30422398)
• Co-Investigator(Renkei-kenkyūsha): GOHDA Jin 東京大学, 医科学研究所, 特任講師 (90361617) ; YAMAGUCHI Noritaka 千葉大学, 大学院薬学研究院, 助教 (80399469) ; TAGUCHI Yuu 東京大学, 医科学研究所, 助教 (20549472)
• Project Period (FY): 2010-04-01 – 2016-03-31
• Keywords: 翻訳後修飾 / シグナル伝達 / 疾患 / 数理モデル / 構造生物学 / ユビキチン

Outline of Final Research Achievements

1. p47 inhibits NF-kB activation by inducing degradation of NEMO in lysosome. 2. NF-kB activation by HTLV-1 Tax protein requires generation of K63-linked polyubiquitin chains. 3. NF-kB activation in non-cancer stem cells induces expression of JAG1, which in turn stimulates cancer stem cells to increase stem cell population. NF-kB activation also induces expression of TMOD1, which leads to induction of MMP13, a protease that degrades extracellular matrix. 4. RelB-Venus knock-in mice is a tool to analyze spatiotemporal regulation of RelB.

Free Research Field

分子生物学