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2015 Fiscal Year Final Research Report

NF-kB inhibitory molecule mediated TNF responsiveness of rheumatoid arthritis delivered fibroblast-like synoviocyte

Research Project

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Project/Area Number 25462390
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Orthopaedic surgery
Research InstitutionKawasaki Medical School

Principal Investigator

IGARASHI HIDEYA  川崎医科大学, 医学部, 准教授 (40291538)

Project Period (FY) 2013-04-01 – 2016-03-31
Keywords関節リウマチ / 滑膜線維芽細胞 / NF-kappaB / ABIN-3 / NEDD4L / ユビキチンリガーゼ / アポトーシス
Outline of Final Research Achievements

To elucidate the molecular mechanisms for the pro-inflammatory effect of ABIN-3, an inhibitor for NF-κB activation, we established the stable transfectant constitutively expressing ABIN-3 by enforced expression in fibroblast-like synoviocyte cell line MH7A derived from rheumatoid arthritis patient designated as A3G. A3G showed the phenotypic changes as spindle-like appearance, growth retardation, decreased expression of MMPs and ALDH1A1, and down-regulated activity of Erk and Akt. We identified E3 ubiquitin ligase NEDD4L as a binding partner of ABIN-3 by mass-spectrometry and enforced expression.

Free Research Field

免疫学

URL: 

Published: 2017-05-10  

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