A recent report also showed that AMPK could regulate translation elongation via regulation of eEF2 kinase, in both C. elegans and mammalian cells (Leprivier et al., 2013).
The impact of codon usage on protein synthesis has been recognized for several decades, and it is now generally accepted that codon bias can regulate translation rates to facilitate co-translational protein folding and secretion [50], [51], [52].
The mTOR regulate translation of specific mRNAs and protein synthesis involved in cell cycle regulation and has been shown to influence tissue fibrosis [ 2].
Codon usage bias is a universal feature of eukaryotic and prokaryotic genomes and has been proposed to regulate translation efficiency, accuracy, and protein folding based on the assumption that codon usage affects translation dynamics.
Results from expression studies using trpE′-′lacZ translational fusions and RNA-directed cell-free translation experiments suggest that the Mg2+-dependent tertiary structure inhibits TRAP's ability to regulate translation of trpE.
This discovery of snoRNA U19 as a new downstream effector of the mTOR pathway suggests that cell engineering of snoRNAs can be used to regulate translation and improve cellular growth in CHO cell cultures in the future.
MicroRNAs (miRNAs) are small, noncoding RNAs (ribonucleic acids) that regulate translation.
Small, non-protein coding dendritic BC1 RNA is thought to regulate translation in dendritic microdomains.
MicroRNAs (miRNA) are small non-coding RNAs that regulate translation of mRNA and protein.
DAZ family proteins interact with several other RNA binding proteins to regulate translation in diverse organisms [12] [16].
These targets include ribosomal S6 kinase (S6K1) and eukaryotic translation initiation factor 4E (eIF4E) that regulate translation [27].
