| Project/Area Number |
15390150
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Virology
|
|---|
| Research Institution | National University Corporation Tottori University |
|---|
Principal Investigator |
SAIRENJI Takeshi National University Corporation Tottori University, Faculty of Medicine, Department of Biomedical Sciences, Professor, 医学部, 教授 (10117351)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SATOH Yukio National University Corporation Tottori University, Faculty of Medicine, Department of Biomedical Sciences, Research Associate, 医学部, 助手 (70144657)
|
|---|
| Project Period (FY) |
2003 – 2004
|
| Project Status |
Completed (Fiscal Year 2004)
|
| Budget Amount *help |
¥5,400,000 (Direct Cost: ¥5,400,000)
Fiscal Year 2004: ¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 2003: ¥2,800,000 (Direct Cost: ¥2,800,000)
|
|---|
| Keywords | Epstein-Barr virus (EBV) / TGF-β1 / TGF-β receptor / TGF-β1 signal / Burkitt's lymphoma / EBV oncogenesis / EBV reactivation / siRNA |
|---|
| Research Abstract |
(1).Loss of Functional Transforming Growth Factor(TGF)-β Type II Receptor Results in Insensitivity to TGF-β1 in Epstein-Barr Virus-positive Burkitt's Lymphoma Cell Line Akata (submitted).
We analyzed the effect of TGF-β1 on the cell growth and Epstein-Barr virus(EBV) reactivation in six Burkitt's lymphoma cell lines. TGF-β1 induced cell growth inhibition and EBV reactivation in these cell lines but did not in Akata cells. To elucidate the mechanism of TGF-β1 unresponsiveness in Akata cells, we studied the expression of TGF-β receptors and the intracellular signaling molecules Smads. All cell lines expressed TGF-β type I receptor, Smad2, Smad3 and Smad4. TGF-β type II receptor (R-II) was expressed in all cell lines except Akata cells. Introduction of the TGF-β R-II into Akata cells results in sensitivity to TGF-β1-mediated growth inhibition, and EBV reactivation. To test a possibility to the transcriptional repression of the TGF-β R-II gene in Akata cells, the effect of histone deacetyla
… More
tion (HDAC) inhibitor, trichostatin A(TSA) was examined. The expression of TGF-β R-II in Akata cells was induced by TSA treatment. These results suggest that the defect in the TGF-β1 response in Akata cells is caused by the lack of TGF-β R-II and the alteration of HDAC may be involved in the loss of TGF-β R-II in the cells.
(2).Mechanism for induction of hydroxyurea(HU) resistance and loss of latent EBV genome in HU-treated BL cell line Raji (J.Med.Virol.70: 224,2003;J.Med.Virol.73:589,2004).
(3).Inhibition of EBV reactivation by short interfering RNAs targeting p38 mitogen activated protein kinase or c-Myc in EBV-positive epithelial cells (J.Virol.78:11798,2004).
(4).Characterization of Epstein-Barr virus infection in a human signet ring cell gastric carcinoma cell line HSC-39. (Microbes and Infection 6:429,2004).
(5).Diagnostic evaluation of 2',5'-oligoadenylate synthetase activities and antibodies against Epatein-Barr virus and Coxiella burnetii in patients with choronic fatigue syndrome in Japan (Microbes and Infection 5:1096,(2003). Less
|
