Genetics, in vivo imaging, and unbiased chemical biology screens reveal that Trpv6 functions as a cellular quiescence regulator and delineates a Trpv6-mediated Ca2+ signaling pathway maintaining the quiescent state.
Temperature-activated TRPV1 ion channels respond to increased temperatures by opening and then entering an inactivated state from which they cannot recover, suggesting that this form of irreversible gating results from partial unfolding during heat absorption.
In response to tissue damage, reactive oxygen species can be sensed by cation channels TRPA1/RyR to cause increases of cytosolic Ca2+ in intestinal stem cells, activating Ras/MAPK activity and stimulating stem cell proliferation in Drosophila.
The structure of a bivalent double-knot tarantula toxin bound to the outer pore of the capsaicin receptor reveals a novel mode of toxin-channel recognition that has important implications for thermosensation.
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.