Research of RAD51B in the pathogenesis of ocular vascular occlusive disease
| Project/Area Number |
12671710
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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 |
Ophthalmology
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
MINAMOTO Atsushi Hiroshima University, Department of Opthalmology, Associate Professor, 医学部, 助教授 (10253072)
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| Co-Investigator(Kenkyū-buntansha) |
MISHIMA Hiromu Hiroshima University, Department of Opthalmology, Professor, 医学部, 教授 (20034100)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2001: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2000: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | RAD51B / Nervous system / recombinational repair / knockout mouse / embryonal stem cell / homologous recombination / Rad51B / ES細胞(胚性幹細胞) / 細胞周期 |
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| Research Abstract |
A targeting vector was transfected into the embryonal stem cell for developing conditional knockout mouse of RAD51B. Clones that developed homologous recombination were chosen, however, the occurrence of homologous recombination was poor. Therefore, this method was discontinued. To clarify the function of RAD51B, the knockout of RAD51B in human somatic cells were investigated. The knockout of XRCC2 was also investigated. Cell lines utilized were human retinal pigment epithelial cells and HCJ116 (human colon cancer) cells. Homologous recombinations were not observed in human retinal pigment epithelial cells, however, XRCC2 hetero knockout cells were derived in HCT116 cell lines. Frequency of targeted integration was investigated in HCT116 cells. The transfection procedure and analyses for the generation of homo knockout cell is now underway. Inactivation of RAD54B in a colon cancer cell line resulted in reduction of targeted integration in human cells.
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Report
(3 results)
Research Products
(3 results)
