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

Lignende værker

• 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
  af: Cassady, Kevin A., et al.
  Udgivet: (1998)
• Chimeric HCMV/HSV-1 and Δγ(1)34.5 oncolytic herpes simplex virus elicit immune mediated antigliomal effect and antitumor memory()()
  af: Ghonime, Mohammed G., et al.
  Udgivet: (2017)
• Preclinical Evaluation of Oncolytic Δγ (1)34.5 Herpes Simplex Virus Expressing Interleukin-12 for Therapy of Breast Cancer Brain Metastases
  af: Cody, James J., et al.
  Udgivet: (2012)
• 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
  af: He, Bin, et al.
  Udgivet: (1997)
• Activated MEK Suppresses Activation of PKR and Enables Efficient Replication and In Vivo Oncolysis by Δγ(1)34.5 Mutants of Herpes Simplex Virus 1
  af: Smith, Kerrington D., et al.
  Udgivet: (2006)