| Project/Area Number |
12670282
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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 | Osaka University |
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Principal Investigator |
UEDA Keiji Osaka University, Graduate School of Medicine, Associate Professor, 医学系研究科, 助教授 (00221797)
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| Co-Investigator(Kenkyū-buntansha) |
YAMANISHI Koichi Osaka University, Graduate School of Medicine, Professor, 医学系研究科, 教授 (10029811)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2001: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2000: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Human Herpesvirus 8 / Kaposi's sarcoma-associated herpesvirus (KSHV) / Reactivation and transcription activator / ORF50(RTA) / latency / reactivation / γ-herpesvirus / OCT1 / K5 / ORF50 / OCT 1 / KSHV / MHLclassl / 転写因子 / 前初期遺伝子 |
|---|
| Research Abstract |
Human herpesvirus 8 (HHV8) or Kaposi's sarcoma-associated herpesvirus (KSHV) is a member of γ-herpesviridae and supposed to be a causative agent for Kapasi' s sarcoma (KS) and primary effusion lymphoma (PEL). We investigated the molecular mechanism of the onset of lytic replication. We identified lytic gene products, RTA, K5, K8, K9 etc. and generated monoclonal antibodies against such gene products. We also isolated TPA non-reactive cell clones infected with KSHV from the parental BCBL1. Using these, we clarified that RTA was a key transcriptional regulator for the reactivation, that RTA upregulated K9 gene through non-DNA binding mechanism, that RTA upregulated its own promoter through the interaction with OCT1 and hat K5 downregulated the MHC class I, which lead to the immune evasion during lytic replication.
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