Ribosome profiling reveals genome-wide stimulation of stop codon readthrough by aminoglycosides that is influenced sequence context.

Ribosomes translate through stop codons far more often than previously thought, yielding C-terminally extended proteins in a variety of eukaryotes.

Whole-genome in silico screening for stop codon contexts that produce elevated translational readthrough and peroxisome targeting reveals that in mammals, the amount of lactate dehydrogenase in the peroxisome is controlled by translational readthrough.

Noncanonical usage of stop codons in ciliates expands structurally flexible Q-rich domains and coevolves with codon usage biases to avoid triplet repeat disorders mediated by CAG/GTC replication slippage.

Inhibition of bacterial protein synthesis by an antimicrobial peptide apidaecin triggers translation arrest at the stop codons, ribosome queuing and pervasive stop codon readthrough.

Nonstop mRNA decay degrades mRNAs with a premature stop codon after such mRNAs are targeted by the nonsense-mediated decay machinery.

Ribosomes undergo an unanticipated movement (‘sliding’) while translating homopolymeric A sequences, which provides a biochemical rationale for the observation that iterated AAA codons are under-represented in gene-coding sequences.

microRNAs can serve as a surveillance system to repress nonsense mRNAs by recognizing miRNA-responsive elements in the open reading frame region downstream of the premature termination codon.

Ensemble cryo-EM visualizes how structural rearrangements poise the newly made protein and release factor RF2 to dissociate in preparation for ribosome recycling.

The RNA-binding protein PTBP1 is recruited to sites near stop codons in retroviral and human mRNAs, shielding them from detection and degradation by the nonsense-mediated mRNA decay pathway.