Molecular piracy by Kaposis Sarcoma-Associated Herpesvirus: dysregulation of wnt signaling and the unfolded protein response
Project/Area Number |
15K07952
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Biological pharmacy
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Research Institution | Kyoto Pharmaceutical University |
Principal Investigator |
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Project Status |
Completed (Fiscal Year 2017)
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Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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Keywords | ウイルス / 小胞体ストレス / Wntシグナル / リンパ腫 / アポトーシス / ヘルペスウイルス / カポジ肉腫 / 小胞体ストレス応答 / ERKシグナル / Snail / がんウイルス / IRE1 / Nigericin / GSK3 |
Outline of Final Research Achievements |
Kaposi’s sarcoma associated herpesvirus (KSHV) is an oncogenic DNA virus and classified in the gamma-herpesvirus subfamily. Kaposi's sarcoma and AIDS-related primary effusion lymphoma (PEL) is caused by KSHV infection. We have demonstrated that LANA protein suppresses the phosphorylation ability of GSK-3beta and stabilizes the protein-X by binding to the GSK-3beta. In addition, KSHV encoded vCyclin and LANA suppressed the unfolded protein response (UPR) such as IRE1 and PERK transcription, suggesting that KSHV achieves anti-apoptosis through the suppression of pro-apoptotic UPR. Furthermore, we found that diallyl trisulfide, methylseleninic acid, and sodium selenite are the novel and effective drugs against PEL.
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Report
(4 results)
Research Products
(20 results)
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[Journal Article] Diallyl trisulfide induces apoptosis by suppressing NF-kappa B signaling through destabilization of TRAF6 in primary effusion lymphoma.2016
Author(s)
Shigemi Z, Furukawa Y, Hosokawa K, Minami S, Matsuhiro J, Nakata S, Watanabe T, Kagawa H, Nakagawa K, Takeda H, Fujimuro M.
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Journal Title
Int J Oncol.
Volume: 48
Issue: 1
Pages: 293-304
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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