The appearance of NG2⁺ glial cells in the dorsal telencephalon of the embryo coincides with the establishment of the brain blood vessel network in mice.

Use of experimental manipulation demonstrates that social/solitary feeding behaviors are unrelated to the fitness gains conferred by causative alleles in two previously identified genes.

NG2 glial cells respond to synaptic input with calcium signals in the absence of action potentials and process synaptic depolarizations with somatic and dendritic voltage gated channels.

Tissue damage induces a reversible cell cycle arrest in G2, which promotes survival and mitogenic signals to facilitate tissue regeneration but drives senescence-like phenotypes under chronic stress conditions.

Wnts can act synergistically to affect G2 arrest via transcriptional upregulation of a Checkpoint Kinase in the absence of any detectable DNA damage.

Single cell knockout and overexpression reveal that the synaptic cell adhesion molecule NGL2 maintains synapses and axons, and can restore lost connections in the developing and mature retina.

Triggered by (long-duration) hippocampal ripples, spindles facilitate communication between the hipppocampus and neocortex during natural sleep.

A structural analysis of the transcription regulator Mot1 in complex with promoter DNA and the proteins TBP and NC2 provides a first structural framework for how a Swi2/Snf2 type remodeler interacts with a histone fold protein:DNA complex.

The ER membrane protein complex (EMC) facilitates the correct topology of the flavivirus non-structural proteins NS4A and NS4B at the ER membrane critical for viral replication.

The extrinsic cue NGF and the intrinsic signal Islet1 converge at the level of the Runx1/CBFβ transcription factor complex formation to promote differentiation of a major nociceptor subtype.