| Project/Area Number |
14570266
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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 |
Virology
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| Research Institution | Nagasaki University |
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Principal Investigator |
MORIUCHI Ryozo Nagasaki University, Graduate School of Biomedical Sciences, Department of Molecular Microbiology & immunology, Associate Professor, 大学院・医歯薬学総合研究科, 助教授 (60210142)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2002: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | oncogene / T get / ATL / RECK / Invasion activity / NF-κB / 成人T細胞白血病 / がん関連遺伝子 / RhoGEF / トランスフォーメーション / Tax |
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| Research Abstract |
We screened for ATL tumor cell-derived cDNAs with the potential to transform murine fibroblasts, NIH3T3, and succeeded in cloning a trio related transforming gene in ATL tumor cells (Tgat). Tgat was expressed exclusively in leukemic cells of acute or chronic ATL patients and cell lines originating from ATL cells, but the expression could not be detected in PBMCs of healthy volunteers, healthy HTLV-1 carriers, or HTLV-1 infected cell lines established in vitro. Comparison of the cDNA with the human. genome database revealed that Tgat is alternatively transcribed from the Trio-encoding gene (from exons 38 to 46) and spliced to a novel exon located downstream of exon 58. We found that both the Rho-GEF activity and the C-terminal region of Tgat were required for not only transforming but also invasion-inducing activity. These results indicate that Tgat expression contributes to the malignant profiles of ATL tumor cells.
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