Research on the role of microtubule plus-end tracking proteins in the reorganization of microtubule array upon cell membrane disruption
Project/Area Number |
19570175
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Cell biology
|
Research Institution | St.Marianna University School of Medicine |
Principal Investigator |
TOGO Tatsuru St.Marianna University School of Medicine, 医学部, 講師 (40334247)
|
Project Period (FY) |
2007 – 2009
|
Project Status |
Completed (Fiscal Year 2009)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2008: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2007: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
Keywords | 膜修復 / 微小管 / プラス端集積因子 / adenomatous polyposis coli / EB1 / カルシウム / GSK-3β / チロシンキナーゼ / 微小管プラス端集積因子 / CaMキナーゼ |
Research Abstract |
Microtubule (MT) plus end tracking proteins (+TIPs) are involved in the regulation of MT dynamics. It was reported previously that an increase in intracellular Ca^<2+> concentration ([Ca^<2+>]_i) induced by cell membrane disruption stimulates rearrangement of MTs, suggesting that some +TIPs are regulated by Ca^<2+>.In the present study. the behaviors of +TIPs following an increase in [Ca^<2+>]_i was observed. Disruption of plasma membrane and increase in [Ca^<2+>]_i stimulates redistribution of denomatous polyposis coli (APC) AND EB1. Present study also indicated that Ca^<2+> stimulates redistribution of APC throuht a tyrosine kinase- and GSK-3β-dependent pathway.
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Report
(4 results)
Research Products
(7 results)