Salt-inducible kinase 3 (SIK3) is an essential component of the mammalian circadian clock machinery, which governs robust circadian behavioral and other rhythms by destabilization of a core clock protein PER2 in a phosphorylation-dependent manner.

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.

Simultaneous inhibition of two distinct kinase targets stimulates bone formation without concurrently increasing bone resorption, therefore representing a promising new treatment strategy for osteoporosis.

Protein kinase A-driven increases in c-MYC protein expression and tumor cell proliferation can be blocked by eIF4A inhibitors, suggesting a potential new treatment option for patients with oncogenic PKA activation.

A neuromodulatory circuit bidirectionally regulates the glial capacity to buffer ions and water in response to changes in neuronal excitation in order to balance glial versus neuronal protection.

Partial copy loss of spliceosome genes are common non-driver gene dependencies in cancer.

Targeting aberrant CRTC-CREB activation blocks the growth of LKB1-inactivated lung cancer.

TRPV4 channels in brain capillaries are suppressed by the phosphoinositide PIP2 and activated by receptor agonists implicated in neurovascular coupling.

A comprehensive, quantitative, protein-protein interaction screen maps the network of interactions between human MIT domains and ESCRT-III C-terminal tails, and reveals MIT domain-containing protein cofactors for abscission and the 'No Cut' abscission checkpoint.