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2022 Fiscal Year Final Research Report

Regulatory mechanism of calcium signaling in endoplasmic reticulum by novel K+ pump

Research Project

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Project/Area Number 20K07258
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 48020:Physiology-related
Research InstitutionUniversity of Toyama

Principal Investigator

Fujii Takuto  富山大学, 学術研究部薬学・和漢系, 助教 (50567980)

Project Period (FY) 2020-04-01 – 2023-03-31
Keywords小胞体 / K+ポンプ / カルシウム / 小胞体ストレス
Outline of Final Research Achievements

In this study, we examined the physiological function of a membrane transport protein (ER-ATPase) expressed in the endoplasmic reticulum (ER). K+-transport activity in the ER was significantly increased in ER-ATPase-overexpressing cells. ER Ca2+ levels were significantly increased in the ER-ATPase knockdown cells. ER-ATPase knockdown significantly decreased cell proliferation, and the rescue of ER-ATPase expression significantly restored the decreased proliferation. The expression of GRP78, a marker of ER stress, was significantly increased in ER-ATPase-knockdown cells. These results suggest that ER-ATPase functions as an ER K+-pump and is important for ER Ca2+ dynamics.

Free Research Field

細胞生理学

Academic Significance and Societal Importance of the Research Achievements

本研究では、小胞体においてK+ポンプとして機能する膜輸送タンパク質ER-ATPase(仮称)を見出し、小胞体Ca2+動態における生理的役割を明らかにした。本成果は、「新規K+ポンプの関与する小胞体Ca2+シグナリング制御機構」という細胞恒常性維持機構の新規概念につながることが期待される。生命活動における小胞体Ca2+シグナリングの重要性から考えて、本研究の学術的意義および多くの研究分野への普遍的波及効果は高い。またER-ATPaseの機能低下が、様々な病態発症に関与する小胞体ストレスを引き起こすことから、今後の研究により新たな病態発症機構が解明されることが期待される。

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Published: 2024-01-30  

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