Strategy for inhibition of HIV-1 replication without appearance of drug resistant virus and attenuation of the virus
Project/Area Number |
20790112
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Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Environmental pharmacy
|
Research Institution | Kumamoto University |
Principal Investigator |
TAKAMUNE Nobutoki Kumamoto University, 大学院・生命科学研究部, 助教 (60322749)
|
Project Period (FY) |
2008 – 2009
|
Project Status |
Completed (Fiscal Year 2009)
|
Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
|
Keywords | HIV-1 N-ミリストイル化 / NMT / 薬剤耐性 / HTV-1 / ウイルス / 薬学 / HIV-1 |
Research Abstract |
N-Myristoyltransferase (NMT) isozymes, NMT1 and NMT2, are essential host factors for human immunodeficiency virus type-1 (HIV-1), by which the viral proteins Pr55^(gag) and Nef are N-myristoylated. The study demonstrated that the N-terminal region of each NMT isozyme was required for the isozyme-specific binding to ribosome. The each isozyme specific binding to ribosome was associated with HIV-1 release, in which NMT1 and NMT2 in ribosome were respectively related to Pr55^(gag) and Nef. These results implicate that the N-terminal region mediated binding to ribosome could become target for NMT isozyme-specific inhibition, which could block HIV-1 release.
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Report
(3 results)
Research Products
(13 results)