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Titlebook: Aspartic Proteinases; Retroviral and Cellu Michael N. G. James Book 1998 The Editor(s) (if applicable) and The Author(s), under exclusive l

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發(fā)表于 2025-3-21 18:50:59 | 只看該作者 |倒序瀏覽 |閱讀模式
期刊全稱Aspartic Proteinases
期刊簡稱Retroviral and Cellu
影響因子2023Michael N. G. James
視頻videohttp://file.papertrans.cn/164/163036/163036.mp4
學(xué)科分類Advances in Experimental Medicine and Biology
圖書封面Titlebook: Aspartic Proteinases; Retroviral and Cellu Michael N. G. James Book 1998 The Editor(s) (if applicable) and The Author(s), under exclusive l
影響因子The VIIth International Conference on Aspartic Proteinases was held in Banff, Alberta, Canada, from October 22 to 27, 1996. The venue was the Banff Centre in the Canadian Rockies, a setting well known worldwide for the scenic beauty and mountain grandeur. It was perhaps presumptuous of the organizers to call this the seventh Aspartic Proteinase Conference but it was felt that the meeting in 1982, organized by Tom Blundell and John Kay, was of an international stature and covered topics sufficiently broad to constitute a conference. Thus, there is a discontinuity in that the Gifu Conference organized by Prof. Kenji Takahashi was the fifth International Conference on Aspartic Proteinases. Officially, there has not been a sixth Conference and if there is confusion, it is the result of my desire to recognize the importance of the London meeting. Banffhosted 106 scientists from 14 different countries. There were 26 invited speak- ers among the 44 oral presentations of the 7 main sessions. In addition, there were 53 con- tributed poster presentations that spanned the whole range of interest in aspartic proteinases.
Pindex Book 1998
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Matthias Pilz,Susanne Berger,Roy Canningtability and half-life; and 5) mutations that provide new substrate specificities with corresponding mutations in the gag—pol polyprotein precursor substrate. Since the binding modes of both the natural substrates for HIV protease and the substrate analog class of inhibitors are similar, amino acid
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https://doi.org/10.1007/978-3-658-03521-1ol viral polypeptide. The kinetic data were interpreted with the aid of molecular modeling to understand the effect of mutations on inhibitor binding and processing of the gag-pol polypeptide to generate infective virions.
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https://doi.org/10.1007/978-3-658-12181-5... They maintain the level of catalytic activity, allowing the virus to replicate, but they lower the affinity of the HIV-1 PR for the anti-viral drug, reducing the drug’s potential therapeutic power. At present, the molecular mechanisms that underlie drug resistance are not fully understood. Their
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Book 1998ountries. There were 26 invited speak- ers among the 44 oral presentations of the 7 main sessions. In addition, there were 53 con- tributed poster presentations that spanned the whole range of interest in aspartic proteinases.
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Optimization of a Macromolecular Inhibitor of HIV-1 Proteasetability and half-life; and 5) mutations that provide new substrate specificities with corresponding mutations in the gag—pol polyprotein precursor substrate. Since the binding modes of both the natural substrates for HIV protease and the substrate analog class of inhibitors are similar, amino acid
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