Molecular mechanisms involved in zinc-deficiency mediated epigenetic regulation of gene expression
Project/Area Number |
25460179
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Environmental and hygienic pharmacy
|
Research Institution | Setsunan University |
Principal Investigator |
KIMURA Tomoki 摂南大学, 理工学部, 准教授 (70340859)
|
Co-Investigator(Kenkyū-buntansha) |
HOSAKA Takuomi 静岡県立大学, 薬学部, 助教 (30611579)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
|
Keywords | 亜鉛 / カドミウム / エピジェネティクス / メタロチオネイン / MTF1 / p300 / MTF-1 |
Outline of Final Research Achievements |
Zinc is an essential micronutrient. It is critically important to control intracellular zinc concentrations tightly. In mammals, metallothionein (MT), a small metal-binding protein, plays important roles in zinc homeostasis. Mouse MT1 gene transcription is regulated by metal response element-binding transcription factor-l (MTF-l), which is recruited to the promoter by zinc. Here, we showed that HAT domain of transactivation factor p300 was involved in MTF-1-DNA complex formation. It is not clear that the molecular mechanisms of zinc-mediated epigenetic modification of MT gene expression. But, MT induction in response to Cd in the 100 nM Cd, 1 week-treated mouse lymphoma P1798 cells was up-regulated compared to that in normal 1798 cells. Bisulfite sequence analysis reveals the demethylation of DNA in CpG island of MT1 promoter in the 100 nM Cd, 1 week-treated P1798 cells. The result suggests that 1 week Cd treatment affects epigenetic modification in MT gene.
|
Report
(4 results)
Research Products
(9 results)