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2022 Fiscal Year Final Research Report

Study of turn over mechanisms of tight junction

Research Project

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Project/Area Number 21K15089
Research Category

Grant-in-Aid for Early-Career Scientists

Allocation TypeMulti-year Fund
Review Section Basic Section 44010:Cell biology-related
Research InstitutionKyushu University

Principal Investigator

Shigetomi Kenta  九州大学, 理学研究院, 助教 (90878240)

Project Period (FY) 2021-04-01 – 2023-03-31
Keywordstight junction / cholesterol / ZO / claudin
Outline of Final Research Achievements

It has been widely accepted that the formation of tight junctions (TJ) requires ZO proteins, a scaffold protein. However, I found that proteasome inhibitors can induce TJ formation even in cell loss of ZO proteins. This result indicated that factors other than ZO proteins exist in TJ formation. Further analysis revealed a mechanism of TJ formation in which ZO proteins accumulate cholesterol and claudin accumulates in the cholesterol-rich membrane regions.

Free Research Field

細胞生物学

Academic Significance and Societal Importance of the Research Achievements

タイトジャンクションの形成には、他の細胞接着構造での解析を基にした類推から、裏打ちタンパク質であるZOタンパク質とclaudinの結合が必須であると考えられてきた。しかし、本研究によって、ZOタンパク質との結合は必須ではなく、ZOタンパク質がコレステロールを集積させ、コレステロールに富んだ膜領域にclaudinが集積し、タイトジャンクションの形成に至るという、他の細胞接着構造とは異なる形成機構を有していることを明らかにした点は学術的に大きな意義があると考える。

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Published: 2024-01-30  

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