Although puromycin staining is often used to examine subcellular translation, puromycin-labeled proteins are rapidly released from ribosomes even in the presence of elongation inhibitors, which may confound translation site localization.
Systematic CRISPR-based editing of tRNA genes revealed that different human cells that span a range of growth rates and different modes of proliferation states require diverse tRNA sets.
Inhibition of bacterial protein synthesis by an antimicrobial peptide apidaecin triggers translation arrest at the stop codons, ribosome queuing and pervasive stop codon readthrough.
RNAs enriched at cell protrusions are translated regardless of their location in the cytoplasm but are dynamically repressed in retracting protrusions and incorporated into heterogeneous RNA clusters.
The retarding effect of a ribosome-bound internal ribosome entry site on eukaryotic protein synthesis is largely overcome following translocation of tripeptidyl-tRNA.
In vitro culture of brain endothelial cells leads to a rapid loss of the blood-brain barrier transcriptional and accessible chromatin landscapes that is resistant to the effects of beta-catenin stabilization.
The tripartite drug efflux pump AcrA-AcrB-TolC, representative of a wide group of pumps from Gram-negative bacteria, enters a transport-competent state through long-distance conformational changes that switch the channel from a closed to an open state.
In neurons, inhibition of the proteasome results in feedback inhibition of protein synthesis, mediated by heme-regulated kinase 1, which is optimized to act as both a sensor and an effector.
