The spider venom peptide Pn3a recognizes a pharmacophore unique to Ca_V3.3 amongst T-type calcium channels, underscoring its potential as a novel molecular tool for the study of Ca_V3.3-mediated currents in native cells.

Drosophila p53 protein isoforms function during oogenesis to ensure the integrity of the transmitted genome, a function that is conserved to humans.

Orbitofrontal cortex lesions impact the neural correlates of detection of auditory regularity violation at two hierarchical levels of rule abstraction, providing a novel perspective on the role of the orbitofrontal cortex in auditory predictive processing.

Somatically derived genomic mosaicism in the form of increased DNA content and APP copy number in single neurons plausibly has a function in sporadic Alzheimer’s disease and points to functions for single-neuron gene copy number changes.

Common mouse models of polycystic ovary syndrome (PCOS) have variable ability to recapitulate the increased GnRH pulse generator frequency thought to exist in women with PCOS.

E. coli that cause neonatal meningitis largely derive from two global clonal lineages that can additionally form intestinal reservoirs to seed recrudescent invasive infection even when appropriate antibiotics are used.

Genetically modified mouse model and comprehensive analysis reveal the molecular mechanisms regulating early T-cell development through intracellular TCRβ expression-mediated β-selection and independent cell survival signaling.

Covert visual attention modulates alpha-band traveling waves propagating from frontal to occipital regions in both hemispheres, yet it modulates waves propagating in the opposite direction (occipital to frontal) only in the presence of visual stimulation.

IL-1β release from macrophages might be responsible for the unexplained cone segment loss in retinal degenerative diseases that are associated with subretinal inflammation, such as retinitis pigmentosa or geographic atrophy.

While semantic symptoms in fronto-temporal dementia patients were mainly dependent on short-range white-matter fibre disruption, long-range white-matter fibres damage was the major contributor to executive dysfunction, highlighting the importance of controlling for risk factors associated with deep white-matter disease.