| Project Area | Protein community: organization and maintenance of protein functions |
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| Project/Area Number |
19058010
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | Nara Institute of Science and Technology |
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Principal Investigator |
KOHNO Kenji 奈良先端科学技術大学院大学, バイオサイエンス研究科, 教授 (50142005)
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| Co-Investigator(Kenkyū-buntansha) |
TSURU Akio 奈良先端科学技術大学院大学, バイオサイエンス研究科, 助教 (80273861)
TERADA Kazutoyo 熊本大学, 大学院・生命科学研究部, 准教授 (00253724)
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| Research Collaborator |
KIMATA Yukio 奈良先端科学技術大学院大学, バイオサイエンス研究科, 准教授 (60263448)
YANAGITANI Kota 奈良先端科学技術大学院大学, バイオサイエンス研究科, 特任助教 (70614775)
SAITO Michiko 奈良先端科学技術大学院大学, バイオサイエンス研究科, 助教 (40379558)
KADOKURA Hiroshi 奈良先端科学技術大学院大学, バイオサイエンス研究科, 博士研究員 (70224558)
YAMAMOTO Yohei 奈良先端科学技術大学院大学, バイオサイエンス研究科, 博士研究員
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| Project Period (FY) |
2007 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥140,500,000 (Direct Cost: ¥140,500,000)
Fiscal Year 2011: ¥28,100,000 (Direct Cost: ¥28,100,000)
Fiscal Year 2010: ¥28,100,000 (Direct Cost: ¥28,100,000)
Fiscal Year 2009: ¥28,100,000 (Direct Cost: ¥28,100,000)
Fiscal Year 2008: ¥28,100,000 (Direct Cost: ¥28,100,000)
Fiscal Year 2007: ¥28,100,000 (Direct Cost: ¥28,100,000)
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| Keywords | 小胞体ストレス / タンパク質品質管理 / シグナル伝達 / 転写翻訳調節 / Hsp40 / ストレス / 小胞体 / 構造異常蛋白質 / 糖尿病 / ノックアウトマウス / 蛋白質品質管理 / HSP40 |
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| Research Abstract |
Activation process of ER stress sensor IRE1, which is an evolutionary highly conserved protein, has been studied. When misfolded and unfolded proteins accumulated in the ER by some various stresses, IRE1 sensors formed clusters and directly interacted with unfolded protein, resulting in the full activation of IRE1. Activated IRE1 attenuated ER stress by the transcriptional induction of UPR target genes. This activation process has been evolutionarily conserved from yeasts to humans. Specific inactivation of IRE1α gene in murine islet β cells caused diabetes in mice, whose mechanism has been unknown. Finally we found novel molecular chaperons located in the ER membrane stimulated the degradation of misfolded membrane proteins to attenuate ER stress.
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