Shigella flexneri, globally the most frequent cause of bacterial dysentery, is far more diverse, and has caused disease around the world for far longer than other Shigella species by persisting in local environments over extended timescales.

The oral carbapenem 'Tebipenem' has high level antibacterial activity against highly drug-resistant Shigella, and its mode of action and pharmacokinetics make it suitable for the treatment of severe diarrhoea caused by highly drug-resistant bacteria.

Shigella infection induces a calpain-mediated loss of SUMO conjugates that promotes bacterial entry.

Multiplexed mass spectrometry shows how the autophagy gene Atg16l1 regulates macrophage innate immunity against intracellular bacterial pathogens by modulating basal oxidative stress responses.

Genetic analyses using a new oral infection mouse model demonstrate that cell death pathways protect against the gastrointestinal bacterial pathogen Shigella flexneri.

Multiple axonal guidance receptors control the local and selective translation of mRNAs by binding to ribosomes, specific mRNAs and RNA-binding proteins.

Post-translational modifications regulate transient protein-protein interactions to disrupt Ubiquitin enzyme/ligase complexes, a strategy used by Shigella to inactivate the host immune response.

The NAIP-NLRC4 inflammasome in intestinal epithelial cells protects mice from oral route Shigella infection.

Measurements of visual response to motion of different contrasts along with network modeling reveals a microcircuit in superficial layers of cortex that regulates the gain regime.

Discrepancies between functional responses measured with electrophysiology and calcium imaging can be largely reconciled by considering the spike-to-calcium transfer function, neuronal sampling bias, and cluster merging artifacts during spike sorting.