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

2016 Fiscal Year Final Research Report

• Project/Area Number: 26670148
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: General medical chemistry
• Research Institution: Institute 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