• Search Research Projects
  • Search Researchers
  • How to Use
  1. Back to previous page

Investigation on inhibitory mechanism of soluble ST2 protein (secreted IL-33 receptor) against LPS signal

Research Project

Project/Area Number 26460376
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field General medical chemistry
Research InstitutionJichi Medical University

Principal Investigator

Yanagisawa Ken  自治医科大学, 医学部, 教授 (50182366)

Co-Investigator(Kenkyū-buntansha) 多胡 憲治  自治医科大学, 医学部, 講師 (20306111)
太田 聡  自治医科大学, 医学部, 講師 (40528428)
Project Period (FY) 2014-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
KeywordsST2 / LPS / シグナル伝達 / 細胞がん化 / LPS受容体 / 細胞形質転換 / 炎症反応 / TLR4 / MD2 / IL-33 / CD14
Outline of Final Research Achievements

We investigated the mechanism of inhibitory effect of soluble ST2 protein, which is the extracellular domain of IL-33 receptor (ST2L protein), against the LPS signal transduction. ST2 protein did not inhibit the binding of LPS with LPS receptor. Each component of LPS receptor complex, TLR 4, CD14 and MD2, did not show the binding with ST2 protein, and each combination of two components of above also failed to bind with ST2, which suggests higher structure of LPS receptor complex is required for the binding with ST2.
Furthermore, We found novel proteins such as IFITM3 which bind with ST2L protein, and IL-33 is indispensable for the cellular transformation by Ras independent of ST2 protein, and IL-33 promotes the translation of cyclin D.

Report

(4 results)
  • 2016 Annual Research Report   Final Research Report ( PDF )
  • 2015 Research-status Report
  • 2014 Research-status Report
  • Research Products

    (4 results)

All 2017 2016 2015

All Journal Article (2 results) (of which Int'l Joint Research: 2 results,  Peer Reviewed: 2 results,  Open Access: 1 results,  Acknowledgement Compliant: 2 results) Presentation (2 results)

  • [Journal Article] STAT3 and ERK pathways are involved in cell growth stimulation of the ST2/IL1RL1 promoter2017

    • Author(s)
      Tago K, Ohta S, Funakoshi-Tago M, Aoki-Ohmura C, Matsugi J, Tominaga SI, Yanagisawa K
    • Journal Title

      FEBS Open Bio

      Volume: 7(2) Issue: 2 Pages: 293-302

    • DOI

      10.1002/2211-5463.12192

    • Related Report
      2016 Annual Research Report
    • Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
  • [Journal Article] Intracellular NF-HEV/IL-33 harbors essential roles in Ras-induced cellular transformation by contributing to cyclin D1 protein synthesis.2016

    • Author(s)
      S. Ohta, K. Tago, M. Funakoshi-Tago, J. Matsugi, K. Yanagisawa
    • Journal Title

      Cellular Signalling

      Volume: 0 Issue: 8 Pages: 0-0

    • DOI

      10.1016/j.cellsig.2016.04.013

    • Related Report
      2015 Research-status Report
    • Peer Reviewed / Int'l Joint Research / Acknowledgement Compliant
  • [Presentation] 新規IL-33シグナル調節蛋白質IFITM3の同定2015

    • Author(s)
      多胡 憲治、多胡 めぐみ、太田 聡、松儀 実広、柳澤 健
    • Organizer
      第38回日本分子生物学会年会 第88回日本生化学会大会 合同大会
    • Place of Presentation
      神戸
    • Year and Date
      2015-12-03
    • Related Report
      2015 Research-status Report
  • [Presentation] IL-33前駆体は、がん化型Ras変異体が誘導する形質転換とサイクリンD1タンパク質合成に必須の役割を担う2015

    • Author(s)
      太田 聡、多胡 憲治、多胡 めぐみ、松儀 実広、柳澤 健
    • Organizer
      第38回日本分子生物学会年会 第88回日本生化学会大会 合同大会
    • Place of Presentation
      神戸
    • Year and Date
      2015-12-01
    • Related Report
      2015 Research-status Report

URL: 

Published: 2014-04-04   Modified: 2018-03-22  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi