2010 Fiscal Year Final Research Report
Changes in activity of the transcriptional regulator Id by toxic trace elements and redox signaling.
| Project/Area Number |
20570128
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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 |
Functional biochemistry
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| Research Institution | University of Fukui |
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Principal Investigator |
KUROOKA Hisanori University of Fukui, 医学部, 准教授 (00293879)
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| Co-Investigator(Renkei-kenkyūsha) |
SUGAI Manabu 京都大学, 医学(系)研究科(研究院), 講師 (90303891)
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| Research Collaborator |
MATSUI Yukie 福井大学, 医学部, 技術補佐員
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| Project Period (FY) |
2008 – 2010
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| Keywords | Id / 細胞内局在 / ヒ素 / ジスルフィド結合 / レドックスシグナル / システイン / 酸化ストレス / ホモ多量体 |
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| Research Abstract |
To understand the regulation of interaction between the transcriptional repressor Id and other transcription factors, we analyzed the subcellular localization of Id3 regulated by toxic trace elements such as arsenite and cadmium, and the intramolecular disulfide bonds formed in the HLH proteins by redox signaling. Although the involvement of cysteine residues has been shown in both cases, they differ in which residues are important, suggesting that there are various regulations for the interaction.
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[Journal Article] Glutathione S-transferase M1 inhibits dexamethasone-induced apoptosis in association with the suppression of Bim through dual mechanisms in a lymphoblastic leukemia cell line.2010
Author(s)
Hosono, N., Kishi, S., Iho, S., Urasaki, Y., Yoshida, A., Kurooka, H., Yokota, Y., Ueda, T.
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Journal Title
Cancer Sci. 第101巻
Pages: 767-773
Peer Reviewed
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