Peptide Initiation Factors

• 

  Subject Areas on Research

  • Adenovirus inhibition of cellular protein synthesis involves inactivation of cap-binding protein. 
  • Fractionation of transcription factors for RNA polymerase II from Drosophila Kc cell nuclear extracts. 
  • Herpes simplex virus proteins ICP27 and UL47 associate with polyadenylate-binding protein and control its subcellular distribution. 
  • High potency silencing by single-stranded boranophosphate siRNA. 
  • Identification of phosphorylation sites in the translational regulator, PHAS-I, that are controlled by insulin and rapamycin in rat adipocytes. 
  • Identifying mRNA subsets in messenger ribonucleoprotein complexes by using cDNA arrays. 
  • In vitro RNA selection identifies RNA ligands that specifically bind to eukaryotic translation initiation factor 4B: the role of the RNA remotif. 
  • Insulin and diabetes cause reciprocal changes in the association of eIF-4E and PHAS-I in rat skeletal muscle. 
  • Isolation and characterization of the replicon of a Thiobacillus intermedius plasmid. 
  • Multiple mechanisms control phosphorylation of PHAS-I in five (S/T)P sites that govern translational repression. 
  • PHAS proteins as mediators of the actions of insulin, growth factors and cAMP on protein synthesis and cell proliferation. 
  • PHAS-I as a link between mitogen-activated protein kinase and translation initiation. 
  • Participation of ATM in insulin signalling through phosphorylation of eIF-4E-binding protein 1. 
  • Phosphorylation of the translational regulator, PHAS-I, by protein kinase CK2. 
  • Poliovirus replicase stimulation by terminal uridylyl transferase. 
  • Recessive Rare Variants in Deoxyhypusine Synthase, an Enzyme Involved in the Synthesis of Hypusine, Are Associated with a Neurodevelopmental Disorder. 
  • Spermidine-mediated hypusination of translation factor EIF5A improves mitochondrial fatty acid oxidation and prevents non-alcoholic steatohepatitis progression. 
  • The eukaryotic translation initiation factor 4E is not modified during the course of vaccinia virus replication. 
  • XPO1/CRM1 Inhibition Causes Antitumor Effects by Mitochondrial Accumulation of eIF5A.