tailieunhanh - Retrovirology Commentary BioMed Central Open Access Inhibition of HIV-1 gene expression by

Retrovirology Commentary BioMed Central Open Access Inhibition of HIV-1 gene expression by Sam68ΔC: multiple targets but a common mechanism? Alan Cochrane Address: Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada Email: Alan Cochrane - Published: 2 March 2009 Retrovirology 2009, 6:22 doi: Received: 11 February 2009 Accepted: 2 March 2009 This article is available from: © 2009 Cochrane; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Two recent publications have explored the mechanisms by which a. | Retrovirology BioMed Central Commentary Inhibition of HIV-1 gene expression by Sam68AC multiple targets but a common mechanism Alan Cochrane Open Access Address Department of Molecular Genetics University of Toronto Toronto Ontario Canada Email Alan Cochrane - Published 2 March 2009 Received II February 2009 Accepted 2 March 2009 Retrovirology 2009 6 22 doi 1742-4690-6-22 This article is available from http content 6 1 22 2009 Cochrane licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Two recent publications have explored the mechanisms by which a mutant of the host protein Sam68 blocks HIV-1 structural protein synthesis and expands its activity to encompass Nef. Although the two studies propose different mechanisms for the responses observed it is possible that a common activity is responsible. Understanding how this Sam68 mutant discriminates among the multiple viral mRNAs promises to reveal unique properties of HIV-1 RNA metabolism. Commentary One of the principles underlying the use of any compound or factor as a therapeutic agent is its capacity to selectively affect the target with little or no off-target effects. With this concept in mind recent reports regarding the ability of a variant of the host factor Sam68 to selectively regulate the expression of several key components of HIV-1 take on particular interest. HIV-1 replication is critically dependent on the expression of its structural proteins Gag Gagpol and Env 1 . As a result any factor able to inhibit expression of these proteins would force the virus into a state akin to latency. In addition HIV-1 Nef has been implicated as a major player in the pathogenesis of this virus 2 3 expression of Nef .

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