Trisomy 21, the genetic cause of Down syndrome, produces elevated centrosome protein levels reducing intracellular trafficking to and from the centrosome thereby delaying primary ciliogenesis, ciliary signaling, and mouse cerebellar development.

A new tumor suppressor function of p21, needed at each undamaged duplication cycle, ensures the adequate execution of the DNA replication program thereby protecting the genome integrity.

Influenza vaccination in humans stimulates novel B cell evolution that is detectable in germinal centers, but not the peripheral blood.

Senescent cells accumulate in the fracture callus and a reduction in the number of these cells accelerates fracture healing in mice.

The two most commonly used chemogenetic actuators, clozapine-N-oxide and compound 21, similarly modulate sleep in wild-type laboratory mice indicating that even designer drugs which do not convert to clozapine can elicit behavioural effects and require adequate controls.

Hyperactive interferon signaling is a hallmark of trisomy 21 and may contribute to many of the comorbidities associated with Down syndrome.

Interaction of cofactor Phactr1 with PP1 creates a composite substrate-binding surface that defines the sequence specificity of the Phactr1/PP1 holoenzyme.

The gating mechanism of trimeric ATP-gated P2X receptors has been explored using photo-switchable cross-linkers, via a versatile strategy that could be applied to other membrane proteins.

p27Kip1 directly controls invadopodia turnover by promoting the interaction of PAK1 with Cortactin, which induces Cortactin phosphorylation, invadopodia disassembly and facilitates invasion through extracellular matrix.

Neutrophil-dependent innate immune responses to the human pathogen, methicillin-resistant Staphylococcus aureus, are modulated by an interplay between interleukin-21 and type 1 interferons.