| Project/Area Number |
14370335
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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 |
Metabolomics
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| Research Institution | Osaka University |
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Principal Investigator |
YAMASAKI Yoshimitsu Osaka University, Graduate School of Medicine, Associate Professor, 医学系研究科, 助教授 (40201834)
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| Co-Investigator(Kenkyū-buntansha) |
UMAYAHARA Yutaka Osaka University Hospital, Medical Staff, 医学部附属病院, 医員(臨床研究)
KAJIMOTO Yoshitaka Osaka University, Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (60301256)
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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 |
¥9,300,000 (Direct Cost: ¥9,300,000)
Fiscal Year 2003: ¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥5,700,000 (Direct Cost: ¥5,700,000)
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| Keywords | PAX4 / PAX6 / transcription factor / β-cell differentiation / pancreas / development / transdifferentiation / diabetes |
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| Research Abstract |
Pax4 is well known to play some important role in pancreas development. In our study, we showed that Pax4 overexpression induces differentiation from precursor cells to insulin-producing cells. Various β-cell-specific factors including GLUT2 were also induced by Pax4 overexpression, indicating that Pax4 facilitates p-cell differentiation. In addition, we showed that Pax4 functions as a transcriptional repressor and found several candidate molecules which binds to Pax4 and could function as a co-repressor of Pax4.
Also, we found that Pax6 plays some important role in maintaining β-cell function; we showed that in Pax6 (+/-) mice glucose-stimulated insulin secretion was impaired, although there was no difference in pancreas morphology and insulin content. These results indicate that Pax6 plays some important role in glucose-stimulated insulin secretion.
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