Project/Area Number |
13670648
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Neurology
|
Research Institution | Okayama University |
Principal Investigator |
KAWABATA Masahiro Okayama University Graduate School of Medicine and Dentistry, Assistant, 大学院・医歯学総合研究科, 助手 (30204762)
|
Co-Investigator(Kenkyū-buntansha) |
AKIYAMA Kousuke Okayama University Graduate School of Medicine and Dentistry, Assistant, 大学院・医歯学総合研究科, 助手 (30222540)
KAWABATA Teruyuki Okayama University Graduate School of Medicine and Dentistry, Lecturer, 大学院・医歯学総合研究科, 講師 (60201448)
|
Project Period (FY) |
2001 – 2002
|
Project Status |
Completed (Fiscal Year 2002)
|
Budget Amount *help |
¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 2002: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 2001: ¥2,200,000 (Direct Cost: ¥2,200,000)
|
Keywords | Trad / Rad51d / RecA / Rad51 / recombination / repair / Rad51D |
Research Abstract |
One of the mechanisms of neurodegenerative disorders is accumulation of DNA deletion and/or mutation which cause mutated proteins leading to cell dysfunction and cell death. It is essential for long-term survival and normal function of neurons to repair DNA damage. Previously we have identified a novel DNA recombinational repair protein named Trad. In this project, we have aimed at fundamental research of the Trad protein in neuron to develop new treatments of neuronal disorders. Northern blot analysis and reverse transcriptase-polymerase chain reaction (RT-PCR) showed multiple transcript variants of mouse TRAD gene as the human previously reported by us. Complete genomic DNA sequence analysis confirmed that the exon-intron structures keep the GT/AG splicing rule and the multiplicity is due to alternative splicing. Western blot analysis with anti-polypeptide antibody against the mouse protein detected several bands. It remains unknown which band corresponds to the translated product of each transcript variant.
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