| Project/Area Number |
10044261
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Nagoya University |
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Principal Investigator |
HAMAGUCHI Michiaki Nagoya University, School of Medicine, Professor, 医学部, 教授 (90135351)
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| Co-Investigator(Kenkyū-buntansha) |
MATSDA Satoru School of Medicine, Assistant Professor, 医学部, 講師 (50242110)
HANAFUSA Hidesaburo Osaka Bio Inst., Director, 所長
MAYER Bruce ハーバード大学, 医学部, 講師
PELLMAN Davi ハーバード大学, 医学部, 講師
DUTTA Anyndi ハーバード大学, 医学部, 講師
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,900,000)
Fiscal Year 1999: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1998: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | cell growth / cell cycle / tyrosine kinase / growth regulator / cell adhesion / 増殖抑制因子 |
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| Research Abstract |
The aim of this study is to clarify signaling pathway for the regulation of cell cycle that depends on protein-protein interactions regulated by SH2-phosphotyrosine binding or SH3-proline bindings, under the international collaborative study. Advance of recent study revealed that cell growth cycle is regulated by a variety of intracellular signaling pathway that activated by tyrosine phosphorylation of cellular proteins. Up to date, two types of signaling pathway, positive and negative ones, that regulate cell growth were identified.
In this study we mainly focused on a transmembrane glycoprotein, SHPS-1. SHPS-1 appears to have a function as a docking protein that reclutes the tyrosine phosphatase, SHP-2 which seems to be required for the cell growth. Despite for its unique structure, however, the function of SHPS-1 in cell growth remains largely unclear. in this study, we showed that cell transformation by v-src substantially suppresses the expression of SHPS-1 protein. In contrast, overexpression of exogenous SHIPS-1 in v-src-transformed cells virtually suppresses anchorage-independent growth of the cells.
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