| Project/Area Number |
24659459
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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 |
Hematology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
YAMAOKA Shoji 東京医科歯科大学, 医歯(薬)学総合研究科, 教授 (90263160)
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| Co-Investigator(Kenkyū-buntansha) |
SAITOH Yasunori 東京医科歯科大学, 大学院医歯学総合研究科, 助教 (00516312)
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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: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 血液腫瘍 / 細胞死 / カスパーゼ / A20 / 翻訳後修飾 / ユビキチン / 癌 / ATL |
|---|
| Research Abstract |
A20 is a ubiquitin-editing enzyme that regulates inflammation and cancer development. Our current studies revealed that A20 was abundantly expressed in several types of cancer cells such as HTLV-I infected cells in contrast to lymphomas of B-cell lineage that harbor somatic mutation or deletion. In HTLV-I infected cell lines, A20 was co-immunoprecipitated with caspase-8 or FADD independently of any death-ligand stimulation. RNA-interference mediated depletion of A20 induced activation of caspase-8 and its downstream effectors, caspase-3 and -7, and caused marked reduction in the cell viability. Taken together, these results suggest that A20 plays a pivotal role in the survival of HTLV-I-infected cells.
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