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

Ítems similars

• The Herpes Simplex Virus U(S)11 Protein Effectively Compensates for the γ(1)34.5 Gene if Present before Activation of Protein Kinase R by Precluding Its Phosphorylation and That of the α Subunit of Eukaryotic Translation Initiation Factor 2
  per: Cassady, Kevin A., et al.
  Publicat: (1998)
• The 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 kinase
  per: He, Bin, et al.
  Publicat: (1997)
• Second-Site Mutation Outside of the U(S)10-12 Domain of Δγ(1)34.5 Herpes Simplex Virus 1 Recombinant Blocks the Shutoff of Protein Synthesis Induced by Activated Protein Kinase R and Partially Restores Neurovirulence
  per: Cassady, Kevin A., et al.
  Publicat: (2002)
• The gamma 1(34.5) gene of herpes simplex virus 1 precludes neuroblastoma cells from triggering total shutoff of protein synthesis characteristic of programed cell death in neuronal cells.
  per: Chou, J, et al.
  Publicat: (1992)
• The 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 cells.
  per: He, B, et al.
  Publicat: (1996)