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September 1, 1998Journal of VirologyOpen Access

The Second-Site Mutation in the Herpes Simplex Virus Recombinants Lacking the γ 1 34.5 Genes Precludes Shutoff of Protein Synthesis by Blocking the Phosphorylation of eIF-2α

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Authors

KCKevin A. CassadyNationwide Children's HospitalMGMartin GrossDartmouth College
Bernard Roizman
Bernard RoizmanUniversity of Chicago

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Cite This Study

Cassady et al. (1998) studied this question.

synapsesocial.com/papers/6a7d633c7786afdcaca01490https://doi.org/10.1128/jvi.72.9.7005-7011.1998
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Also Consider

Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1The γ 1 34.5 protein of herpes simplex virus 1 complexes with protein phosphatase 1α to dephosphorylate the α subunit of the eukaryotic translation initiation factor 2 and preclude the shutoff of protein synthesis by double-stranded RNA-activated protein kinase1997 · 755 citations
  2. 2The carboxyl terminus of the murine MyD116 gene substitutes for the corresponding domain of the gamma(1)34.5 gene of herpes simplex virus to preclude the premature shutoff of total protein synthesis in infected human cells1996 · 141 citations
  3. 3Suppression of the phenotype of gamma(1)34.5- herpes simplex virus 1: failure of activated RNA-dependent protein kinase to shut off protein synthesis is associated with a deletion in the domain of the alpha47 gene1997 · 142 citations
  4. 4RNA synthesis in cells infected with herpes simplex virus. IX. Evidence for accumulation of abundant symmetric transcripts in nuclei1975 · 53 citations