Elucidation of mechanisms of disease pathogenesis caused by ubiquitin ligase deficiency.

2014 Fiscal Year Final Research Report

• Project/Area Number: 25860241
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Pathological medical chemistry
• Research Institution: Kyushu University
• Principal Investigator: KANAE Yumimoto 九州大学, 生体防御医学研究所, 研究員 (30596838)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: ユビキチンリガーゼ

Outline of Final Research Achievements

We aim to reveal the mechanisms of pathogenesis by elucidating the relationship between a ubiquitin ligase and its substrates. We previously developed a new approach, termed DiPIUS (differential proteomics-based identification of ubiquitylation substrates), to discover substrates of ubiquitin ligases. We revealed that Fbxw7 controls osteoblast and chondrocyte differentiation by targeting OASIS and BBF2H7, basic leucine zipper (bZIP) type transcription factors, for proteasome-mediated degradation. We also showed that DEAD-box RNA helicase DDX24 is a substrate for MDM2.
We also showed that Fbxw7 inhibits cancer metastasis in non-cell autonomous manner by targeting Notch for degradation.

Free Research Field

タンパク質分解