| Project/Area Number |
06404083
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cell biology
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| Research Institution | KYOTO UNIVERSITY (1995)
Okazaki National Research Institutes (1994) |
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Principal Investigator |
TSUKITA Shoichiro KYOTO UNIVERSITY,FACULTY OF MEDICINE PROFESSOR, 医学研究科, 教授 (50155347)
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| Co-Investigator(Kenkyū-buntansha) |
YONEMURA Shigenobu KYOTO UNIVERSITY,FACULTY OF MEDICINE LECUTURER, 医学研究科, 講師 (60192811)
ITOH Masahiko KYOUTO UNIVERSITY,FACULTY OF MEDICINE ASSISTANT, 医学研究科, 助手 (70270486)
永渕 昭良 岡崎国立共同研究機構, 生理学研究所, 助手 (80218023)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥26,100,000 (Direct Cost: ¥26,100,000)
Fiscal Year 1995: ¥6,000,000 (Direct Cost: ¥6,000,000)
Fiscal Year 1994: ¥20,100,000 (Direct Cost: ¥20,100,000)
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| Keywords | cadherin / radixin / ezrin / moesin / catenin / ZO-1 / occuldin / claudin / αカテニン / Z0-1 / ノックアウト / 相同組換え / ES細胞 / 上皮細胞 / ERM蛋白質 / βカテニン |
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| Research Abstract |
We knocked out two important genes, occludin and moesin. Here we summarized the results on moesin-null mice.
ERM (ezrin/radixin/moesin) proteins are general cross-linkers between plasmamembranes and actin filaments. Since their expression is regulated in a tissue specific manner, unique function has been supposed for each of ERM proteins. On the other hand, experiments at the cellular level has suggested the functional redundancy of ERM proteins. To assess the possible overlapping functions of ERM proteins invivo, the moesin gene located on X chromosome was disrupted by gene targeting in embryonic stem cells. Hemizygous male as well as homozygous female mice for the mutation were completely devoid of moesin but were normally developed and fertile, showing no obvious histological abnormalities in all the tissues examined. In tissues of the mutant mice, moesin completely disappeared without affecting the expression levels and subcellular distribution of ezrin and radixin. Also in platelets, fibroblasts, and mast cells isolated from moesin-deficient mice, targeted disruption of moesin gene did not affect their ERM-dependent functions, i.e.platelet aggregation, stress fiber/focal contact formation of fibroblasts, and microvillar formation of mast cells, without compensatory up-regulation of ezrin and radixin. These findings favor the notion that ERM proteins are functionally redundant at the cellular as well as the whole body levels.
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