Reconstitution of intercellular gap junction by Wnt proteins
| Project/Area Number |
14570659
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Osaka University |
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Principal Investigator |
TOYOFUKU Toshihiko Osaka University, Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (60322179)
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| Co-Investigator(Kenkyū-buntansha) |
中土 義章 大阪大学, 医学部附属病院, 医員(臨床研究)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2002: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Connexin43 / cardiac myocytes / N-cadherin / GATA-4 / semaphorin / connexin43 / beta-catenin / TCF |
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| Research Abstract |
The biological effects of gap and adhesion on cardiac morphogenesis have been investigated.
1. Effects of gap and adhesion molecules on the cell proliferation
Connexin43 and N-cadherin suppress the cell proliferation by induction of P21, cell cycle regulator, mediated G2/M arrest.
2. Effects of adhesion molecules on the cardiac morphogenesis
Genetically targeted N-cadherin induces the cardia bifida, the failure of single heart formation. The N-cadherin expression is regulated by GATA-4, cardiogenic factor, establishing the biological role of signaling pathway from GATA-54 to N-cadherin.
3. Identification of novel type of semaphorin to regulate cardiac morphogenesis
Semaphorin are originally identified as a. regulator for neural development. We identified new member of sernaphorin family which regulates cardiac morphogenesis.
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Report
(3 results)
Research Products
(9 results)
