| Project/Area Number |
20591109
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Hematology
|
|---|
| Research Institution | Gunma University |
|---|
Principal Investigator |
YAMASHITA Takayuki Gunma University, 生体調節研究所, 教授 (10166671)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
ODA Tsukasa 群馬大学, 生体調節研究所, 助教 (10323643)
SEKIMOTO Takayuki 群馬大学, 生体調節研究所, 助教 (20436322)
大江 良秀 群馬大学, 生体調節研究所, 助教 (80125830)
|
|---|
| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2008: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
|---|
| Keywords | DNA複製 / 損傷乗越えDNA合成 / Yファミリー・ポリメラーゼ / Hsp90 / 造血不全 / 複製ストレス / ファンコニ貧血 / Yファミリーポリメラーゼ / 損傷乗り越えDNA合成 / DNAポリメラーゼη / モノユビキチン化PCNA / DNA損傷 / 突然変異 / 分子シャペロン |
|---|
| Research Abstract |
Fanconi anemia (FA) is genetically heterogeneous inherited bone marrow failure syndrome, characterized by cellular sensitivity to DNA crosslinkers and susceptibility to various types of malignant tumors including acute myeloid leukemia. Increasing evidence indicates that FA proteins protect against "replicative stress" induced by various genotoxic agents, cooperating with other machineries. Translesion DNA synthesis is one of such cellular protective mechanisms, using specialized DNA polymerases including Pol-eta and REV1.However, regulatory mechanism of these polymerases was largely unknown. We identified the molecular chaperone Hsp90 as an essential regulator of these polymerases. The present findings may lead to development of new therapy of hematopoietic diseases.
|
