Asc1/RACK1 promotes the translation of mRNAs associated with the translational closed loop complex, which have short open reading frames and encode proteins required for core metabolic processes.

Ribosome profiling has bridged the knowledge gap between transcription and translation during malaria blood stage development and provided a comprehensive gene expression resource for this parasite.

Activation of the integrated stress response by stalled translation elongation complexes attenuates neurodegeneration, and demonstrates a protective link between a decrease in the rate of translation initiation and defects in translation elongation.

Ribosomal profiling reveals that translational repression is an important mechanism for cell cycle control and can complement protein degradation.

An ensemble of cryo-EM structures reveals how eukaryotic elongation factor 2 positions the first codon of a viral mRNA for translation.

Operonic mRNAs in bacteria are comprised of ORF (open reading frame)-wide units of secondary structure, which are intrinsically distinct between adjacent ORFs and encode a rough blueprint for ORF-specific translation efficiency.

LARP1 turns off and on the translation of an essential class of mRNAs by acting as a key effecter and regulator for mTORC1.

Ribosome collisions along an mRNA are shown to recruit factors that prevent additional ribosomes from initiating translation on that mRNA, thereby providing time to resolve the collision.

Substitutions in general translation initiation factor eIF1A found as recurring somatic mutations in uveal melanoma destabilize the closed conformation of the preinitiation complex at the start codon and increase discrimination against suboptimal initiation codons genome-wide.

Disruption of quality control pathways that function at distinct steps to mitigate errors in translation evoke similar cellular responses and pathologies.