Project/Area Number |
17081011
|
Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
|
Allocation Type | Single-year Grants |
Review Section |
Biological Sciences
|
Research Institution | Kyoto University |
Principal Investigator |
MORI Yasuo Kyoto University, 大学院・工学研究科, 教授 (80212265)
|
Co-Investigator(Kenkyū-buntansha) |
FUJIMOTO Toyoshi 名古屋大学, 大学院・医学系研究科, 教授 (50115929)
WAKAMORI Minoru 東北大学, 大学院・歯学研究科, 教授 (50222401)
HARA Yuji アイオワ大学, 医学部, ポスドク (60362456)
|
Project Period (FY) |
2005 – 2009
|
Project Status |
Completed (Fiscal Year 2009)
|
Budget Amount *help |
¥76,500,000 (Direct Cost: ¥76,500,000)
Fiscal Year 2009: ¥17,100,000 (Direct Cost: ¥17,100,000)
Fiscal Year 2008: ¥17,100,000 (Direct Cost: ¥17,100,000)
Fiscal Year 2007: ¥17,100,000 (Direct Cost: ¥17,100,000)
Fiscal Year 2006: ¥18,000,000 (Direct Cost: ¥18,000,000)
Fiscal Year 2005: ¥7,200,000 (Direct Cost: ¥7,200,000)
|
Keywords | Ca^<2+>チャネル / 分子複合体 / 膜分子集積 / シグナル伝達 / バイオセンサー / カルシウムチャネル |
Research Abstract |
Ca^<2+> as a second messenger controls a wide variety of biological responses and contributes to formation of tissues such as bones, thereby playing a central role in regulating "homeostasis" at whole body, tissue, and cell levels. In my research, I have focused on voltage-dependent Ca^<2+> channels (VDCCs) and transient receptor potential (TRP) channels to aim at understanding mechanisms, that underlie formation and assembly at the biomembrane of Ca^<2+> channel protein complexes (Ca^<2+> channelplexes), and their physiological significance. Firstly, I have unveiled several unique activation mechanisms, that regulate cellular signal transduction for TRP Ca^<2+>-permeable caion channels. Secondly, I have demonstrated that channel proteins act not only as Ca^<2+>-permeating apparatus but also as assembly centers for receptors, signal-regulating proteins, and scaffolding proteins. Thirdly, important roles of Ca^<2+> channel protein complexes via formation of feedback regulation pathways in signal transduction have been demonstrated. Finally, I have also shown physiological significance of Ca^<2+> channelplexes at tissue levels. TRPC3 channelplexes in B lymphocyte activation and P/Q type VDCCplexes in presynaptic vesicle fusion are examples of the outcome of this study. Thus, my study clarifies how individual Ca^<2+> channels play roles in unique cellular responses.
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