mTOR signaling mechanisms dependent on amino acid transporter

2014 Fiscal Year Final Research Report

• Project/Area Number: 25860189
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: General pharmacology
• Research Institution: Kyoto Prefectural University of Medicine (2014); Osaka University (2013)
• Principal Investigator: TADAGAKI KENJIRO 京都府立医科大学, 医学(系)研究科(研究院), 助教 (30416268)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 薬理学 / シグナル伝達 / アミノ酸トランスポーター

Outline of Final Research Achievements

We performed this study to elucidate the signaling mechanisms leading to mTOR via L-type amino acid transporter (LAT1) by means of comprehensive phosphoproteomics and LAT1 inhibitors, revealing the overview of cellular responses mediated by LAT1 and to examine the possibilities of LAT1 as a molecular marker for cancer therapy. We found that the leucine uptake by LAT1 not only controls the phosphorylated proteins related to the translation regulations but induces the protein phosphorylations responsible for various cellular responses such as transcription, cell cycle regulation and cell structures. Our results indicated that co-administration of known anti-cancer agents with LAT1 inhibitors may be useful for cancer therapy.

Free Research Field

薬理学