| Project/Area Number |
18591006
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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 |
Metabolomics
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| Research Institution | Hyogo College of Medicine |
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Principal Investigator |
MIYAGAWA Jun-ichiro Hyogo College of Medicine, Faculty of Medicine, Associate Professor (00127721)
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| Co-Investigator(Kenkyū-buntansha) |
NAMBA Mitsuyoshi Hyogo College of Medicine, Faculty of Medicine, Professor (00183533)
HAMAGUCHI Tomoya Hyogo College of Medicine, Faculty of Medicine, Assistant Professor (60330461)
KONYA Hiroyuki Hyogo College of Medicine, Faculty of Medicine, Assistant Professor (50340956)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,410,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥210,000)
Fiscal Year 2007: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2006: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | NTAK / Pancreatic β cell / growth factor / proliferation / differentiation / development / regeneration / diabetes mellitus |
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| Research Abstract |
We have been studied on the mechanism of regeneration and differentiation, and apoptosis of pancreatic β cells to develop the new therapeutic approach to diabetes mellitus. In this research, we investigated the possible involvement of neural-and thymus-derived activator for ErbB kinases (NTAK), newly identified growth factor which belongs to the EGF family, and CD 9, one of the modulators of EGF family signal transduction. We demonstrated the adult and fetal pancreas produced NTAK which is localized in β cells and fetal pancreatic epithelial cells including endocrine precursor cells, respectively. CD-9 also expressed on islet cells. These results suggested that NTAK and CD-9 may be involved in the mechanism of differentiation and/or proliferation of pancreatic β cells in addition to the development of pancreas.
In vitro peptide study of NTAK revealed that partial sequence of peptides of NTAK showed the activity of proliferation, while some other part of peptide sequence inhibited the proliferation of β cell line, MIN6 cells, suggesting that NTAK signal transduction may be involved in both positive and negative (apoptotic?) regulatory pathways for β cell proliferation and/or differentiation. Further study is necessary to elucidate the detailed signal transduction pathway(s) of NTAK in pancreatic β cells.
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