Herpes Simplex Virus 1 Recombinant Blocks the Shutoff of Protein Synthesis Induced by Activated Protein Kinase R and Partially Restores Neurovirulence
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چکیده
Second-Site Mutation Outside of the US10-12 Domain of 134.5 Herpes Simplex Virus 1 Recombinant Blocks the Shutoff of Protein Synthesis Induced by Activated Protein Kinase R and Partially Restores Neurovirulence Kevin A. Cassady, Martin Gross, G. Yancey Gillespie, and Bernard Roizman* The Marjorie B. Kovler Viral Oncology Laboratories and Department of Pathology, The University of Chicago, Chicago, Illinois 60637, and Division of Clinical Virology and Division of Neurosurgery, The University of Alabama at Birmingham, Birmingham, Alabama 35233
منابع مشابه
The herpes simplex virus type 1 U(S)11 protein interacts with protein kinase R in infected cells and requires a 30-amino-acid sequence adjacent to a kinase substrate domain.
The herpes simplex virus type 1 gamma(1)34.5 gene product precludes the host-mediated protein shutoff response induced by activated protein kinase R (PKR). Earlier studies demonstrated that recombinant viruses lacking the gamma(1)34.5 gene (Deltagamma(1)34.5) developed secondary mutations that allowed earlier U(S)11 expression and enabled continued protein synthesis. Further, in vitro studies d...
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تاریخ انتشار 2001