| Project/Area Number |
13671728
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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 |
Obstetrics and gynecology
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| Research Institution | Kyushu University |
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Principal Investigator |
MATSUDA Takao Medical Institute of Bioregulation Kyushu Univ. Research Associate, 生体防御医学研究所, 助手 (10304825)
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| Co-Investigator(Kenkyū-buntansha) |
WAKE Norio Medical Institute of Bioregulation Kyushu Univ. Professor, 生体防御医学研究所, 教授 (50158606)
ARIMA Takahiro Medical Institute of Bioregulation Kyushu Univ. Research Associate, 生体防御医学研究所, 助手 (80253532)
KATO Hidenori Medical Institute of Bioregulation Kyushu Univ. Lecturer, 生体防御医学研究所, 講師 (60214392)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2002: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2001: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Choriocarcinoma / HTF12 / KRAB domain / Zn finger domain / Deterioration / NECC1 / homeobox / HOP / KRAV / Kruppel / Zinc finger / choriocarcinoma / homeo domain / hPL |
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| Research Abstract |
For the isolation of the putative choriocarcinoma suppressor gene, we used 1) positional cloning and 2) subtraction technique. The delection site that it was regarded as 7q11.22 at first understood that it was 7q11.21 by comparison with bulletin of newly reported draft sequence. OS-4 gene regarded as a candidate important more at first was not included in this draft sequence. We gave priority to the 6-8 clone that draft sequence included array and analyzed it. Among ten kinds of gene which there is in common deletion region of 7q11.21 of choriocarcinoma, 6-8 clone is included in array given a presentation in draft sequence. This was gene having KRAB domain and Zn finger domain in human teratocarcinoma finger (HTF) 12 gene. HTF12 gene was conjugated by in full length vector plasmid and was introduced into choriocarcinoma cell strain. By induction, becoming gigantic of cell occurred, and cell mass culturing deteriorated. The syndesis ability of cell did not change very much. Cell fusion
… More
begins in induction cell. It was accompanied with deterioration with becoming gigantic of cell. Three kinds of splicing variants produced by a difference of promotor. By both induction, cell propagation was restrained. It was HTF12-2 that used for induction this time. It was each a thing on the basis of a difference of number of domain of Zn finger domain in HTF12-1 that appeared in normal placental villus. On this account it was estimated that the KRAV domain which there was in 5' site participated in cell fusion, propagation inhibition. We understood that there was a lot of similar gene in homology analysis. In particular concern area provided in linkage analysis of familial hydatidiform mole on the chromosome 19 has near by existing ZF1 gene and homology of 80%. The gene expression of ZF1 is recognized both in placenta and choriocarcinoma, and a difference of the work attracts attention.
NECC1 provided by subtraction technique was gene provided than human gingival cDNA library. It was thought with the gene which contributed to deterioration of cell, and I thought that I participated in the legalization of villous trophoblast cell. When villous cytotrophoblast cell became the syncytium cell which fused, marker such as HPL, CSH expressed, but it was immunohistochmestrical that marker of similar expressed, and it was proved, and what I produced in mechanism same as syncitionization was estimated. This NECC1 understood gene only for homeobox needed in case of incidence of mouse, a thing same as HOP. Retrieval in placenta is not considered to be it. Less
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