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Novel drug-binding sites of TRPC6 could potentially facilitate future design of drugs to treat TRPC6-mediated diseases.

A dual-color TIRFM study reveals a new form of inflammatory regulation, in which a lipid kinase and ion channel reciprocally regulate each other to amplify the response to painful stimuli.

High-resolution structures of human TRPM2 in different functional states provided the mechanism underlying ligand recognition, channel activation and inhibition.

TRPM2 is simply a ligand gated channel and does not to possess enzymatic activity, even though it shows sequence similarity to Nudix hydrolases.

Molecular and genetics approaches reveal a dual regulatory role of neuronal G-protein-coupled receptor NPR-15 in both immunity and avoidance behavior, independent of aerotaxis, mediated by amphid sensory neurons, ASJ.

PKD2 (polycystin-2) channels are a major component of a flow-sensing signaling mechanism in endothelial cells that stimulates vasodilation and reduces blood pressure.

Disease-associated mutants of the TRPM3 ion channel are overactive, and they are inhibited by the antiepileptic medication primidone, offering a potential therapeutic intervention to treat this channelopathy.

Hedgehog signaling plays a role in regulating glia gene expression in planarians, pointing to a candidate ancestral and broadly used role for the Hedgehog pathway.

The TRPM4 ion channel has been identified as an important component in the causation of mechanical pressure overload-induced pathological left ventricular hypertrophy, which is a powerful predictor of cardiovascular mortality.

Arterial myocyte PKD2 channels are activated by vasoconstrictor stimuli, which increases blood pressure, are upregulated during hypertension and cell-specific knockout in vivo reduces both physiological blood pressure and hypertension.