A systems level reconstitution of H-Ras GTPase signaling reveals a rich space of tunable dynamic outputs and clarifies the consequences of oncogenic perturbations to signaling.

A key activator of Ras signaling adopts an autoinhibited, dimeric conformation that is activated by membrane and calcium binding.

The ability of tumors to respond to nutritional signals is mediated by Salt-inducible kinases, which ensure tumor growth under nutrient-rich conditions including obesity.

Libraries of patient-derived tumor organoids are a reliable and scalable model system that can help identify and optimize targeted therapies in a pre-clinical setting.

The combination of intraneural microstimulation and 7T fMRI makes it possible to bridge the gap between first-order mechanoreceptive afferent input codes and their spatial, dynamic and perceptual representations in human cortex.

Rare mutations in the switch III region of Ras can increase its nanoscale clustering, which enhances effector recruitment and downstream signaling.

Several key functional features of jawed vertebrate rods are also present in lamprey photoreceptors, indicating that our Cambrian ancestors possessed dim light vision.

A biosensor resource has been developed to monitor the intracellular interactions of RAS family proteins with effector molecules and the effects of inhibitors as an aid to drug development.

The oncogenic Ras^V12 keeps cells mutant for the tumor suppressor scribble in an undead-like condition, which is required for an amplification loop that promotes tumorigenesis.

The higher amount of cortical immature neurons in brains with expanded neocortices may represent a reservoir of young cells for mammals with reduced neurogenesis.