The catalytic activity of a Drosophila neprilysin is critical to proper insulin expression and food intake by regulating homeostasis of distinct signaling peptides.

By controlling the SUMOylation of the protein CAR-1, the aging-regulating pathways downstream of the Insulin/IGF signaling cascade and of the germ cells of the nematode Caenorhabditis elegans are integrated.

By regulating protein translation within the neuron, insulin signaling can control neuronal activity by altering the release of neurotransmitter molecules.

Yeast specific lipids promote the transport of lipid transfer protein (LTP) across the blood brain barrier to the neurons that regulate systemic insulin signaling.

Hermaphroditic Caenorhabditis elegans slow the onset of mating-induced death through self-sperm-regulated insulin-like gene expression, which regulates the activity of the IIS/FOXO pathway, mTOR signaling, and the TFEB/HLH-30 transcription factor.

Feedback signaling between the synapse and nucleus via FGF22 and IGF2 directs the activity-dependent stabilization of presynaptic terminals in the mouse hippocampus.

Two functionally antagonizing groups of hormones directly regulate starvation-induced increase in locomotion via a common neural target in fruit flies.

Young Caenorhabditis elegans hermaphrodites use their own sperm to protect against the negative consequences of mating.

In Drosophila melanogaster, nutrition controls body size by acting through the Forkhead Box class O (FoxO)/Ultraspiracle complex to regulate nutrition-sensitive ecdysone biosynthesis, thereby controlling the switch to stop growth.

Nutrient limitation elicits differential responses in cells lacking the tumor suppressor PTEN and in normal cells, resulting in hyperplastic overgrowth of PTEN mutant tissue independent of additional mutations.