Phosphorylation of only serine-51 in protein synthesis initiation factor-2 is associated with inhibition of peptide-chain initiation in reticulocyte lysates

1991 ◽  
Vol 176 (3) ◽  
pp. 993-999 ◽  
Author(s):  
Nigel T. Price ◽  
Gavin I. Welsh ◽  
Christopher G. Proud
Keyword(s):  
Protein Synthesis ◽  
Peptide Chain ◽  
Initiation Factor ◽  
Chain Initiation ◽  
Initiation Factor 2 ◽  
Reticulocyte Lysates ◽  
Protein Synthesis Initiation

Regulation of peptide-chain initiation in muscle during sepsis by interleukin-1 receptor antagonist

1996 ◽  
Vol 271 (3) ◽  
pp. E513-E520 ◽  
Author(s):  
T. C. Vary ◽  
L. Voisin ◽  
R. N. Cooney
Keyword(s):  
Protein Synthesis ◽  
Receptor Antagonist ◽  
Interleukin 1 ◽  
Peptide Chain ◽  
Initiation Factor ◽  
Translational Efficiency ◽  
Ribosomal Subunits ◽  
Chain Initiation ◽  
Interleukin 1 Receptor Antagonist ◽  
Inhibition Of Protein Synthesis

The mechanism by which interleukin-1 (IL-1) regulates protein synthesis in skeletal muscle during hypermetabolic sepsis in rats was investigated. Treatment of septic rats with a specific interleukin-1 receptor antagonist (IL-1ra) prevented the sepsis-induced inhibition of protein synthesis and translational efficiency in gastrocnemius. Analysis of ribosomal subunits revealed that the increase in free 40S and 60S ribosomal subunits observed in septic rats was prevented by infusion of IL-1ra, indicating peptide-chain initiation was maintained at control values. The failure of sepsis to inhibit peptide-chain initiation after infusion of IL-1ra correlated with a maintenance of the epsilon-subunit of eukaryotic initiation factor (eIF) 2B (eIF-2B epsilon) protein at control values. The alterations in the eIF-2B epsilon protein content in gastrocnemius of septic rats treated with or without IL-1ra were associated with corresponding changes in the abundance of eIF 2B epsilon mRNA. The results provide evidence that infusion of IL-1ra attenuates the sepsis-induced inhibition of protein synthesis by preventing the inhibition of peptide-chain initiation and downregulation of eIF-2B expression during sepsis.

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