Reconstitution of interleukin-1β secretion in non-macrophage cells implicates how this pro-inflammatory cytokine enters into the unconventional pathway of secretion through autophagy.

Kasugamycin potentiates rifampicin killing of Mycobacterium tuberculosis by targeting adaptive mistranslation.

Structural analysis of translating human mitoribosome illustrates elemental steps of translation in mitochondria.

Multivariate data decomposition applied to local field potentials recorded from the primate amygdala revealed simultaneously active and functionally distinct networks, defined by anatomical boundaries between the nuclei.

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.

Hoxa3 and Hoxa11 translation inhibitory elements block cap-dependent translation by using upstream open reading frames with distinct modes of action.

The transcription factor Xrp1 mediates a previously unrecognized branch of stress-response signaling, specifically as a downstream effector of eIF2alpha kinases.

Under starvation conditions, anti-carD antisense RNA and Clp protease work together to decrease the CarD level to mediate the adaptation and survival of mycobacterial cells.

Thousands of novel open-reading frames (ORFs) are translated in the bacterium Mycobacterium tuberculosis, including many short ORFs that are likely to contribute to cell fitness.

Plasma membrane damage causes the release of exosomes from cultured human cells.