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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 513 (1987), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Archives of virology 79 (1984), S. 285-292 
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The addition of mouse interferon (IFN) to AKR murine leukemia virus (MuLV)-producing NIH3T3 cells inhibited the extracellular appearance of AKR MuLV when assayed for reverse transcriptase activity or infectious virus production. IFN treatment had no detectable effect on proviral DNA formation during infection nor on the level of viral RNA in virus-producing cells. However, addition of IFN did alter the level of cellular viral reverse transcriptase activity. Chromatography of extracts from virus-producing cells on poly(G)-Sepharose columns revealed two peaks of reverse transcriptase activity. Peaks I and II eluted at 0.45m and 0.65m NaCl, respectively, while the cellular DNA polymerase β eluted earlier at 0.3m NaCl. IFN treatment of these chronic virus producer cells resulted in a 5-fold increase in peak I whereas peak II and polymerase β remained essentially unchanged. When reverse transcriptase from purified virions was similarly chromatographed on poly(G)-Sepharose, all of the enzymatic activity eluted as peak I. Thus, the reverse transcriptase in peak I from cell extracts appears to be the form which is present in mature virions. Contrary to the results with chronic virus-producing cells, IFN treatment prior to exogenous infection with MuLV did not alter levels of reverse transcriptase peaks I and II or polymerase β. These results provide further evidence that the major effect of IFN occurs at the level of MuLV maturation and assembly.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Archives of virology 78 (1983), S. 255-266 
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Analyses of Hirt extracts from endogeneous murine leukemia virus (MuLV)-infected cells revealed the presence of 9-kbp linear DNA and two superhelical forms with one or two tandem copies of the long terminal repeat (LTR). In contrast, cells that were infected with AKR MCF247 MuLV yielded two major linear forms of 9.0 and 8.4 kbp and one discrete superhelical DNA. In addition, there was a heterogeneous population of superhelical DNAs that were larger and smaller than the major superhelical DNA species. Restriction endonuclease treatment of purified linear and superhelical DNAs have revealed that MCF247 MuLV unintegrated viral DNA is very heterogeneous. Evidence is presented that there are at least two linear DNAs; one is 9-kbp full-length linear DNA, whereas the other major form contains a 0.6 to 0.7-kbp deletion in the envelope gene adjecent to the right LTR. In addition, there are two size classes of the LTR in at least the full-length linear DNA. The major superhelical DNA species is a 8.4-kbp form which contains one copy of the LTR. Other heterogeneous superhelical DNAs appear to contain env-gene deletions or partially deleted copies of a tandem LTR region.
    Type of Medium: Electronic Resource
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