Aspartic Proteinases: Retroviral and Cellular Enzymes by Tom L. Blundell, Kunchur Guruprasad, Armando Albert, Mark

By Tom L. Blundell, Kunchur Guruprasad, Armando Albert, Mark Williams (auth.), Michael N. G. James (eds.)

The VIIth overseas convention on Aspartic Proteinases was once held in Banff, Alberta, Canada, from October 22 to 27, 1996. The venue was once the Banff Centre within the Canadian Rockies, a surroundings popular around the world for the scenic attractiveness and mountain grandeur. It was once maybe presumptuous of the organizers to name this the 7th Aspartic Proteinase convention however it was once felt that the assembly in 1982, geared up via Tom Blundell and John Kay, used to be of a global stature and lined subject matters sufficiently vast to represent a convention. therefore, there's a discontinuity in that the Gifu convention prepared by means of Prof. Kenji Takahashi was once the 5th overseas convention on Aspartic Proteinases. formally, there has no longer been a 6th convention and if there's confusion, it's the results of my wish to realize the significance of the London assembly. Banffhosted 106 scientists from 14 varied international locations. there have been 26 invited converse­ ers one of the forty four oral displays of the 7 major periods. furthermore, there have been fifty three con­ tributed poster displays that spanned the full diversity of curiosity in aspartic proteinases.

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1994). We examined whether the basic motif between the zinc fingers of NC functioned in the regulation of piS cleavage during Gag processing in the context of the virion. The P3BE and CS2 mutations were transferred to an infectious clone of viral DNA and characterized for their effects on viral release, NC-p 15 generation and cleavage, infectivity, and virion morphology. The CS2 mutation serves as a control, since that mutation creates a lesion in NC closer to the affected downstream processing sites than the P3BE mutations.

4. CONCLUSIONS The recent introduction of three new HIV pr inhibitors as antiviral treatments for AIDS is an important milestone in treating this catastrophic infectious disease. , the quantity of infectious virus in circulation. A separate option we are pursuing is to modify the gene A. NGF~ IL-1 0 SCF iFn-a B. j.. ~HiV PR -+~2 1 R8diDtiOnr -'> ---.... -. OTC. p53. t ~: E1 b / " EG' DEATH Figure 1. Scheme for regulation of HIV replication and apoptosis by bcl-2. Cellular Anti-Apoptosis Protein Cleaved by the HIV-I Protease 29 fgr bcl-2 so that the protein is less susceptible to cleavage by the HIV pro This is not comp1etely straightforward; altered bcl-2 must also retain its cytoprotective properties, and there are many amino acids in bcl-2 conserved throughout evolution from nematode to man, in particular in a portion of the molecule where the primary HIV cleavage site is located.

The term "dominant negative" was applied to describe the ability of defective (wt) gene products to interfere with the function of wild-type gene products in vivo [20]. The use of dominant negative inhibition has been proposed for a number of HIV proteins [21] and demonstrated for variants of gag [22] and rev [23]. The inhibition due to variant rev was shown to occur through the formation of inactive protein complexes [24]. More recently, T-Iymphocytes stably transfected with mutant rev [25] or gag genes [26] were shown to inhibit the growth of HIV-l following infection, A similar strategy may be more effective at a stage of the viral life cycle dependent upon a catalytic function such as proteolytic processing.

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