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2016 Fiscal Year Final Research Report

A novel trafficking mechanism regulated by bisecting GlcNAc, an Alzheimer's disease accelerator

Research Project

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Project/Area Number 26670148
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field General medical chemistry
Research InstitutionInstitute of Physical and Chemical Research

Principal Investigator

Kizuka Yasuhiko  国立研究開発法人理化学研究所, 疾患糖鎖研究チーム, 研究員 (20564743)

Research Collaborator SATO Keiko  国立研究開発法人理化学研究所, 疾患糖鎖研究チーム, パートタイマー
KITAZUME Shinobu  国立研究開発法人理化学研究所, 疾患糖鎖研究チーム, 副チームリーダー (80301753)
TANIGUCHI Naoyuki  国立研究開発法人理化学研究所, システム糖鎖生物学研究グループ, グループディレクター (90002188)
NAKANO Miyako  広島大学, 先端物質科学研究科, 准教授 (40397724)
NAKAJIMA Kazuki  藤田保健衛生大学, 研究支援推進センター, 講師 (10442998)
Project Period (FY) 2014-04-01 – 2017-03-31
Keywords糖鎖 / アルツハイマー病 / BACE1 / バイセクト糖鎖 / GnT-III
Outline of Final Research Achievements

The aim of this study is to clarify the mechanisms of Alzheimer's disease (AD) development, focusing on a neural glycan bisecting GlcNAc.
We focused on AD-related protein BACE1 and identified its new interacting partner Clec4g. Furthermore, our data suggest that oxidative stress induced in AD brain upregulates the level of bisecting GlcNAc on BACE1, which could lead to AD development. These findings will be useful to better understand the mechanisms of AD development.

Free Research Field

糖鎖生物学、生化学、分子生物学

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Published: 2018-03-22  

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