Analysis of the cell neoplastic transformation mechanism based on the molecular chaperone HSP90
| Project/Area Number |
24659357
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Akita University |
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Principal Investigator |
ITOH Hideaki 秋田大学, 工学(系)研究科(研究院), 教授 (80168369)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 分子シャペロン / DNAポリメラーゼη / DNA ポリメラーゼ |
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| Research Abstract |
Deficiency of DNA Pol eta in humans causes a variant form of the cancer predisposition syndrome xeroderma pigmentosum.
We will clarify the physiological significance of HSP90 and Pol eta interaction. We tried the construction and purification of full-length human Pol eta. Pol eta is a very unstable protein, but by the addition of a His-tag in the C-terminal, we have succeeded in purification of Pol eta. Also, we got specific polyclonal antibody against Pol eta. HSP effected on the stability of Pol eta. HSP90 and Pol eta were co-localized strongly near nuclear of glyoblastoma cells. Glyoblastoma is the most aggressive malignant primary brain tumor in humans. On the contrary, we couldn't clear interaction between HSP90 and Pol eta in the ependymoma cells. Ependymoma is a tumor that arises from the ependyma, a tissue of the central nervous system.
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Report
(3 results)
Research Products
(6 results)
