A parsimonious biophysical model correctly predicts the conserved expression stoichiometry of core bacterial mRNA translation factors, providing intuitive and quantitative design principles for in vivo pathway construction.

The yeast mRNA decapping enzyme Dcp1/Dcp2 repressses many genes whose products are required on poor carbon or nitrogen sources in nutrient-replete cells by mRNA decapping and degradation or translational repression, adding post-transcriptional controls to the transcriptional repression of these functions.

Cryo-electron microscopy has been used to provide a structural interpretation of the complete action cycle of release factor 3 during translation termination, which includes a coordinated sequence of interactions with a class-I release factor and the ribosome.

Eukaryotic translation elongation factor 1A1 controls the process of heat shock response, from transcriptional activation of the HSP70 gene, to HSP70 mRNA stabilization, nuclear export, and translation.

The anticonvulsant drug lamotrigine inhibits bacterial ribosome biogenesis and reveals an unexplored role for initiation factor 2 (IF2) in ribosome assembly.

A mutant impaired for ribosome recycling exhibits translational reprogramming wherein strong mRNAs outcompete weak mRNAs, also observed when preinitiation complexes are diminished by eIF2α phosphorylation or 40S ribosomal subunit depletion.

Eukaryotic translation initiation factor 3 (eIF3) is required to stabilize the binding of mRNA at the exit channel of the small ribosomal subunit and acts at the entry channel to accelerate mRNA recruitment to the translation preinitiation complex.

During initiation factor-independent RNA structure-driven translation initiation, a flexible RNA element drives the movement of a viral IRES through the ribosome's tRNA binding sites and promotes tRNA binding.

The eukaryotic translation initiation factor eIF4E induces hyaluronic acid (HA) synthesis to drive cancer metastasis which can be reversed following eIF4E inhibition and HA degradation.

In mouse cardiomyocytes, (lymph)angiogenic growth factors are induced during early hypoxia by a translational mechanism involving a new IRES trans-acting factor, vasohibin-1.