| Project/Area Number |
26460366
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General medical chemistry
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| Research Institution | Osaka University |
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Principal Investigator |
UEDA Hironori 大阪大学, 医学系研究科, 特任准教授 (90543463)
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| Co-Investigator(Kenkyū-buntansha) |
宮崎 早月 大阪大学, 医学系研究科, 助教 (60452439)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 新生児一過性糖尿病 / Zac1 / Plagl1 / MIN6 / CD4+ T cells / TNDM / conditional knockout / 糖尿病 / ZAC1 / インスリン / 膵ベータ細胞 / CD4陽性Tリンパ球 / 転写因子 |
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| Outline of Final Research Achievements |
Chromosome 6q24-related transient neonatal diabetes mellitus (6q24-TNDM) is defined as TNDM caused by genetic aberrations of the imprinted locus at 6q24. ZAC1 (also known as PLAGL1) is the gene which is located within the critical minimal 6q24-TNDM region. Zac1 has also been reported as a transcriptional factor to determine the characteristic CD4 (+) regulatory T cells signature. However, the function of Zac1 is still elusive. We generated Zac1 deficient pancreaticβ-cell lines (MIN6) and CD4 (+) T cells by using the Cre/loxP-induced conditional knockout system. The changes of cell functions were not largely different in both wild-type and Zac1-deficient MIN6 and CD4 (+) T cells. In MIN6 cells, Zac1 alters the expression of several genes and non-coding RNAs, including Egr1, Shh, cFos, and Sst. These data suggested that the redundancy of the Zac1 function existed in both mature cell types. Further studies to elucidate the Zac1 function in the development of these cells will be required.
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