Genetic manipulation demonstrates the costs and benefits of detoxifying glucosinolate plant defenses in a pest insect and its predator.

Sulforaphane through NRF2-dependent and -independent cellular and molecular pathways alleviates leptin resistance to reverse the diet-induced obesity.

Fruit flies can taste and avoid food contaminated with a bacterial toxin using the same channel protein that functions in humans as sensor of noxious chemical stimuli.

Electrophysiological experiments, Ca²⁺ imaging, and behavioral studies in mice identify the TRPM3 ion channel as a novel target of G-protein βγ subunits.

Two natural cooling agents activate the cold-activated channel TRPM8 via two opposite mechanisms, evoking distinct electrical responses in cold-sensitive neurons.

A pain-relaying ion channel on a hypersensitive population of sensory neurons can instead elicit sensations of itch in both fish and mice when directly activated, providing a novel model of itch transduction.

The activation and membrane localization of the broadly-tuned noxious chemosensory cation channel TRPA1 are regulated by direct interactions with cholesterol via CRAC motifs in transmembane segments 2 and 4.

Young defense metabolites are often believed to be solely outputs but evidence suggests that they can regulate ancient signaling pathways.

Cold detecting thermoreceptor TRPM8's signalling is diminished with ageing which leads to an impaired response to cold observed in ageing.

A gain-of-function in a new chemical defense resulted in no trade-offs and and independent evolution between novel and ancestral defenses, suggesting low redundancy among different defensive chemicals.