A chemical screen reveals that a compound used to treat a parasitic disease can trigger pluripotent stem cells to become neurons, uncovering a novel mechanism behind neuronal development.

Mechanisms that enable wild mice to survive infection with strains of the Toxoplasma gondii parasite virulent enough to kill laboratory mice offer an explanation for how these parasites have been able to persist in the mouse population.

A missing link between the AP complexes and COPI sheds light on the evolution of vesicle coat proteins and trafficking pathways in the earliest eukaryotes.

Two complexes that contain the histone acetyl transferase MOF engage in a two-pronged approach to ensure the repression of X inactivation in mouse embryonic stem cells.

Erastin and sorafenib inhibit system x_c^- and induce ER stress, suggesting these may be useful tools for probing the functions of system x_c^- and its role in inducing ER stress and ferroptosis.

Favipiravir, a novel nucleoside analogue, can clear a persistent norovirus infection in vivo through lethal mutagenesis.

Disrupting extrusion, a process that drives epithelial cell death, leads to increased cell survival, poor barrier function, and enhanced cell invasion and, thereby, promotes tumor initiation and progression.

Flow-dependent remodeling of blood vessels is critical for normal physiology and for recovery from arterial blockage in disease; understanding its cellular mechanisms may lead to the development of treatments for patients that are deficient in this process following myocardial infarction or other vascular diseases.

A new protein–protein interaction motif identified in the polarity protein and tumor suppressor Scribble, and other cortical proteins, controls their interaction with spectrins and is crucial for the localization and function of Scribble.

An attenuated Herpes simplex type 2 virus deleted in glycoprotein D can be used as an effective vaccine to provide robust transferable humoral immunity and complete protection in murine intravaginal and skin infection models.