A compound that prevents stressors such as UV light and viral infection from downregulating protein synthesis inside cells improves memory performance in mice.

Mutations in CHD7, which cause CHARGE syndrome, cause a reduction in FGF8 signalling and subsequent abnormalities in the cerebellar vermis in both mice and humans.

A deubiquitinase antagonizes the activity of an associated E3 ligase to prevent uncontrolled ubiquitination of a degradation machinery protein and thus maintain its functionality in protein quality control at the endoplasmic reticulum.

The repair of spontaneous DNA damage can introduce mutators that lead to further genetic changes, which could underlie evolutionary change, disease and aging.

Mammalian sperm subject to shear flow swim in upstream spirals along the walls bounding such flows, thereby demonstrating a robust mechanism for upstream navigation to the ovum.

The involvement of SETD2 in an important DNA repair pathway could explain the high frequency of SETD2 mutations in several cancers and may provide an alternative mechanism to evade the p53-mediated checkpoint.

Flow cytometric isolation and fate mapping shows that neurosphere-initiating cells are highly mitotically active and persist only transiently in vivo, and are distinct from quiescent, long-lived neural stem cells.

A novel master regulatory mechanism of cell proliferation and senscence employs the lncRNA UCA1 and a CAPERα/TBX3 corepressor.

An orphan TBP-associated factor, TAF9B, works in conjunction with the histone acetyl-transferase PCAF as transcriptional co-regulators of neuronal differentiation.

The RNA-binding protein MSI1, which is required for stem cell and cancer cell proliferation in the brain and epithelial tissues, also directly senses the concentration of long non-esterified omega-9 fatty acids.