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.

Inhibition of microRNA-203 by oncogenic HRas mutations promotes skin cancer initiation.

Identifying the translational targets of the shuttling protein, SRSF1, reveals that it is needed for normal cell division, and suggests that it couples pre-mRNA splicing and translation.

The impact of phosphorylation on the dynamics of RAS is considered to find allosteric binding sites on the flat surface of the protein, to which small molecules could bind and perturb the RAS-RAF interaction interface.

Genetic analyses reveal that the tropism towards specific Kras driver mutations during urethane carcinogenesis appears to arise from the selection of an oncogenic mutation in normal cells that imparts a narrow window of signaling conducive for tumorigenesis.

Altering the level of different oncogenic mutants of Kras induces unique tumor patterns in mice, suggesting that tissue-specific responses mold the sensitivity of normal tissues to different oncogenic RAS mutations.

Optogenetic and electrical low-frequency stimulation in the sclerotic hippocampus prevents the emergence of spontaneous focal and evoked generalized seizures in a mouse epilepsy model.

Local sensory signals in visual and frontal cortex play a causal role in task performance, while widespread dorsal cortical signals correlating with movement reflect processes that do not.

Compared to other isoforms of RAS, KRAS4b has unique membrane diffusion behavior related to its biology, and the two major domains of the protein both contribute to this diffusion behavior.

Senescent cells release an arachidonic acid-derived electrophilic oxylipin that inhibits myoblast differentiation by covalent modification and activation of HRas.