The Experts below are selected from a list of 15009 Experts worldwide ranked by ideXlab platform
James C. Alwine - One of the best experts on this subject based on the ideXlab platform.
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The TORrid affairs of viruses: effects of mammalian DNA viruses on the PI3K–Akt–mTOR signalling pathway
Nature Reviews Microbiology, 2008Co-Authors: Nicholas J. Buchkovich, Carisa A. Zampieri, James C. AlwineAbstract:The Successful Replication of mammalian DNA viruses requires that they gain control of key cellular signalling pathways that affect broad aspects of cellular macromolecular synthesis, metabolism, growth and survival. The phosphatidylinositol 3′-kinase–Akt–mammalian target of rapamycin (PI3K–Akt–mTOR) pathway is one such pathway. Mammalian DNA viruses have evolved various mechanisms to activate this pathway to obtain the benefits of Akt activation, including the maintenance of translation through the activation of mTOR. In addition, viruses must overcome the inhibition of this pathway that results from the activation of cellular stress responses during viral infection. This Review will discuss the range of mechanisms that mammalian DNA viruses use to activate this pathway, as well as the multiple mechanisms these viruses have evolved to circumvent inhibitory stress signalling. The Successful Replication of mammalian DNA viruses requires viral adaptation of the host cell to establish an environment that can accommodate the increased demands for nutrients, energy and macromolecular synthesis that accompany viral infection. Therefore, the DNA viruses must gain control of key cellular signalling pathways that affect broad aspects of cellular macromolecular synthesis, metabolism, growth and survival, such as the phosphatidylinositol 3′-kinase–Akt–mammalian target of rapamycin (PI3K–Akt–mTOR) pathway. However, a viral mechanism for activating this pathway is not enough; to maintain control of this pathway, viruses must also overcome the many controls that cells use to inhibit this pathway when cellular stress responses are activated during viral infection. This Review discusses the normal activation and control of the PI3K–Akt–mTOR pathway, and why the activation and control of this pathway is important to mammalian DNA viruses. The authors also outline how the PI3K–Akt–mTOR pathway can be inhibited by signalling that is induced by the stress that is imposed on the cell by the viral lytic infection, for example, by the depletion of nutrients, energy, amino acids or oxygen. The range of mechanisms that mammalian DNA viruses use to activate the PI3K–Akt–mTOR pathway are discussed, as well as the multiple mechanisms that these viruses have evolved to circumvent the inhibitory stress signalling that would normally inhibit this pathway. This Review ends with a discussion of remaining questions about the viral control of the PI3K–Akt–mTOR pathway and how the manipulation of the pathway, and its downstream effectors, may contribute to viral pathogenesis. The Successful Replication of mammalian DNA viruses requires that they gain control of key cellular signalling pathways, including the phosphatidylinositol 3′-kinase–Akt–mammalian target of rapamycin (PI3K–Akt–mTOR) pathway. This Review discusses the range of mechanisms that mammalian DNA viruses use to activate this pathway, as well as the multiple mechanisms these viruses have evolved to circumvent inhibitory stress signalling.
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the torrid affairs of viruses effects of mammalian dna viruses on the pi3k akt mtor signalling pathway
Nature Reviews Microbiology, 2008Co-Authors: Nicholas J. Buchkovich, Carisa A. Zampieri, James C. AlwineAbstract:The Successful Replication of mammalian DNA viruses requires that they gain control of key cellular signalling pathways, including the phosphatidylinositol 3′-kinase–Akt–mammalian target of rapamycin (PI3K–Akt–mTOR) pathway. This Review discusses the range of mechanisms that mammalian DNA viruses use to activate this pathway, as well as the multiple mechanisms these viruses have evolved to circumvent inhibitory stress signalling.
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The TORrid affairs of viruses: effects of mammalian DNA viruses on the PI3K–Akt–mTOR signalling pathway
Nature Reviews Microbiology, 2008Co-Authors: Nicholas J. Buchkovich, Carisa A. Zampieri, James C. AlwineAbstract:The Successful Replication of mammalian DNA viruses requires that they gain control of key cellular signalling pathways, including the phosphatidylinositol 3′-kinase–Akt–mammalian target of rapamycin (PI3K–Akt–mTOR) pathway. This Review discusses the range of mechanisms that mammalian DNA viruses use to activate this pathway, as well as the multiple mechanisms these viruses have evolved to circumvent inhibitory stress signalling.
Nicholas J. Buchkovich - One of the best experts on this subject based on the ideXlab platform.
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The TORrid affairs of viruses: effects of mammalian DNA viruses on the PI3K–Akt–mTOR signalling pathway
Nature Reviews Microbiology, 2008Co-Authors: Nicholas J. Buchkovich, Carisa A. Zampieri, James C. AlwineAbstract:The Successful Replication of mammalian DNA viruses requires that they gain control of key cellular signalling pathways that affect broad aspects of cellular macromolecular synthesis, metabolism, growth and survival. The phosphatidylinositol 3′-kinase–Akt–mammalian target of rapamycin (PI3K–Akt–mTOR) pathway is one such pathway. Mammalian DNA viruses have evolved various mechanisms to activate this pathway to obtain the benefits of Akt activation, including the maintenance of translation through the activation of mTOR. In addition, viruses must overcome the inhibition of this pathway that results from the activation of cellular stress responses during viral infection. This Review will discuss the range of mechanisms that mammalian DNA viruses use to activate this pathway, as well as the multiple mechanisms these viruses have evolved to circumvent inhibitory stress signalling. The Successful Replication of mammalian DNA viruses requires viral adaptation of the host cell to establish an environment that can accommodate the increased demands for nutrients, energy and macromolecular synthesis that accompany viral infection. Therefore, the DNA viruses must gain control of key cellular signalling pathways that affect broad aspects of cellular macromolecular synthesis, metabolism, growth and survival, such as the phosphatidylinositol 3′-kinase–Akt–mammalian target of rapamycin (PI3K–Akt–mTOR) pathway. However, a viral mechanism for activating this pathway is not enough; to maintain control of this pathway, viruses must also overcome the many controls that cells use to inhibit this pathway when cellular stress responses are activated during viral infection. This Review discusses the normal activation and control of the PI3K–Akt–mTOR pathway, and why the activation and control of this pathway is important to mammalian DNA viruses. The authors also outline how the PI3K–Akt–mTOR pathway can be inhibited by signalling that is induced by the stress that is imposed on the cell by the viral lytic infection, for example, by the depletion of nutrients, energy, amino acids or oxygen. The range of mechanisms that mammalian DNA viruses use to activate the PI3K–Akt–mTOR pathway are discussed, as well as the multiple mechanisms that these viruses have evolved to circumvent the inhibitory stress signalling that would normally inhibit this pathway. This Review ends with a discussion of remaining questions about the viral control of the PI3K–Akt–mTOR pathway and how the manipulation of the pathway, and its downstream effectors, may contribute to viral pathogenesis. The Successful Replication of mammalian DNA viruses requires that they gain control of key cellular signalling pathways, including the phosphatidylinositol 3′-kinase–Akt–mammalian target of rapamycin (PI3K–Akt–mTOR) pathway. This Review discusses the range of mechanisms that mammalian DNA viruses use to activate this pathway, as well as the multiple mechanisms these viruses have evolved to circumvent inhibitory stress signalling.
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the torrid affairs of viruses effects of mammalian dna viruses on the pi3k akt mtor signalling pathway
Nature Reviews Microbiology, 2008Co-Authors: Nicholas J. Buchkovich, Carisa A. Zampieri, James C. AlwineAbstract:The Successful Replication of mammalian DNA viruses requires that they gain control of key cellular signalling pathways, including the phosphatidylinositol 3′-kinase–Akt–mammalian target of rapamycin (PI3K–Akt–mTOR) pathway. This Review discusses the range of mechanisms that mammalian DNA viruses use to activate this pathway, as well as the multiple mechanisms these viruses have evolved to circumvent inhibitory stress signalling.
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The TORrid affairs of viruses: effects of mammalian DNA viruses on the PI3K–Akt–mTOR signalling pathway
Nature Reviews Microbiology, 2008Co-Authors: Nicholas J. Buchkovich, Carisa A. Zampieri, James C. AlwineAbstract:The Successful Replication of mammalian DNA viruses requires that they gain control of key cellular signalling pathways, including the phosphatidylinositol 3′-kinase–Akt–mammalian target of rapamycin (PI3K–Akt–mTOR) pathway. This Review discusses the range of mechanisms that mammalian DNA viruses use to activate this pathway, as well as the multiple mechanisms these viruses have evolved to circumvent inhibitory stress signalling.
Carisa A. Zampieri - One of the best experts on this subject based on the ideXlab platform.
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The TORrid affairs of viruses: effects of mammalian DNA viruses on the PI3K–Akt–mTOR signalling pathway
Nature Reviews Microbiology, 2008Co-Authors: Nicholas J. Buchkovich, Carisa A. Zampieri, James C. AlwineAbstract:The Successful Replication of mammalian DNA viruses requires that they gain control of key cellular signalling pathways that affect broad aspects of cellular macromolecular synthesis, metabolism, growth and survival. The phosphatidylinositol 3′-kinase–Akt–mammalian target of rapamycin (PI3K–Akt–mTOR) pathway is one such pathway. Mammalian DNA viruses have evolved various mechanisms to activate this pathway to obtain the benefits of Akt activation, including the maintenance of translation through the activation of mTOR. In addition, viruses must overcome the inhibition of this pathway that results from the activation of cellular stress responses during viral infection. This Review will discuss the range of mechanisms that mammalian DNA viruses use to activate this pathway, as well as the multiple mechanisms these viruses have evolved to circumvent inhibitory stress signalling. The Successful Replication of mammalian DNA viruses requires viral adaptation of the host cell to establish an environment that can accommodate the increased demands for nutrients, energy and macromolecular synthesis that accompany viral infection. Therefore, the DNA viruses must gain control of key cellular signalling pathways that affect broad aspects of cellular macromolecular synthesis, metabolism, growth and survival, such as the phosphatidylinositol 3′-kinase–Akt–mammalian target of rapamycin (PI3K–Akt–mTOR) pathway. However, a viral mechanism for activating this pathway is not enough; to maintain control of this pathway, viruses must also overcome the many controls that cells use to inhibit this pathway when cellular stress responses are activated during viral infection. This Review discusses the normal activation and control of the PI3K–Akt–mTOR pathway, and why the activation and control of this pathway is important to mammalian DNA viruses. The authors also outline how the PI3K–Akt–mTOR pathway can be inhibited by signalling that is induced by the stress that is imposed on the cell by the viral lytic infection, for example, by the depletion of nutrients, energy, amino acids or oxygen. The range of mechanisms that mammalian DNA viruses use to activate the PI3K–Akt–mTOR pathway are discussed, as well as the multiple mechanisms that these viruses have evolved to circumvent the inhibitory stress signalling that would normally inhibit this pathway. This Review ends with a discussion of remaining questions about the viral control of the PI3K–Akt–mTOR pathway and how the manipulation of the pathway, and its downstream effectors, may contribute to viral pathogenesis. The Successful Replication of mammalian DNA viruses requires that they gain control of key cellular signalling pathways, including the phosphatidylinositol 3′-kinase–Akt–mammalian target of rapamycin (PI3K–Akt–mTOR) pathway. This Review discusses the range of mechanisms that mammalian DNA viruses use to activate this pathway, as well as the multiple mechanisms these viruses have evolved to circumvent inhibitory stress signalling.
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the torrid affairs of viruses effects of mammalian dna viruses on the pi3k akt mtor signalling pathway
Nature Reviews Microbiology, 2008Co-Authors: Nicholas J. Buchkovich, Carisa A. Zampieri, James C. AlwineAbstract:The Successful Replication of mammalian DNA viruses requires that they gain control of key cellular signalling pathways, including the phosphatidylinositol 3′-kinase–Akt–mammalian target of rapamycin (PI3K–Akt–mTOR) pathway. This Review discusses the range of mechanisms that mammalian DNA viruses use to activate this pathway, as well as the multiple mechanisms these viruses have evolved to circumvent inhibitory stress signalling.
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The TORrid affairs of viruses: effects of mammalian DNA viruses on the PI3K–Akt–mTOR signalling pathway
Nature Reviews Microbiology, 2008Co-Authors: Nicholas J. Buchkovich, Carisa A. Zampieri, James C. AlwineAbstract:The Successful Replication of mammalian DNA viruses requires that they gain control of key cellular signalling pathways, including the phosphatidylinositol 3′-kinase–Akt–mammalian target of rapamycin (PI3K–Akt–mTOR) pathway. This Review discusses the range of mechanisms that mammalian DNA viruses use to activate this pathway, as well as the multiple mechanisms these viruses have evolved to circumvent inhibitory stress signalling.
John H. Connor - One of the best experts on this subject based on the ideXlab platform.
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Translational control by negative-strand RNA viruses: methods for the study of a crucial virus/host interaction.
Methods, 2013Co-Authors: Erin Hodges, John H. ConnorAbstract:Protein synthesis is a vital step in the Successful Replication of negative-strand RNA viruses. Protein synthesis is also a critical step in the development of a Successful antiviral response from the host. This makes understanding the interplay between host and viral translation an important aspect of defining the virus/host interaction. For the negative-strand RNA viruses there are disparate mechanism of how viruses interact with the host protein synthesis apparatus, ranging from the complete takeover of all protein synthesis to the subtle insertion of viral mRNAs into an otherwise unchanged protein synthesis pattern. In this article, we discuss different ways to investigate protein synthesis in virus-infected cells, ranging from the use of metabolic labeling for the study of general translation changes to using fluorescence-coupled labeling techniques that allow the pinpointing of any subcellular localization of protein synthesis during virus Replication. We also discuss methods for analyzing the translation initiation factors that are frequently modified in virus-infected cells.
Maurizio Pellecchia - One of the best experts on this subject based on the ideXlab platform.
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Identification of Small Molecules that Interfere with H1N1 Influenza A Viral Replication
ChemMedChem, 2012Co-Authors: Angel Bottini, Bas J. G. Baaten, Elisa Barile, Stephen Soonthornvacharin, John L. Stebbins, Linda M. Bradley, Sumit K. Chanda, Maurizio PellecchiaAbstract:Successful Replication of the influenza A virus requires both viral proteins and host cellular factors. In this study we used a cellular assay to screen for small molecules capable of interfering with any of such necessary viral or cellular components. We used an established reporter assay to assess influenza viral Replication by monitoring the activity of co-expressed luciferase. We screened a diverse chemical compound library, resulting in the identification of compound 7, which inhibits a novel yet elusive target. Quantitative real-time PCR studies confirmed the dose-dependent inhibitory activity of compound 7 in a viral Replication assay. Furthermore, we showed that compound 7 is effective in rescuing high-dose influenza infection in an in vivo mouse model. As oseltamivir-resistant influenza strains emerge, compound 7 could be further investigated as a new and potentially suitable scaffold for the development of anti-influenza agents that act on novel targets.
