The rotation of the β11-12 linker is a crucial control point for acid-sensing ion channel gating and motion of this linker is required for the channel to desensitize.
Three residues work together as a valve-like mechanism to control desensitization from pre-open and open states in the ion channels ASIC1a, ASIC2a, and ASIC3.
The loss of calcium-dependent D2 autoreceptor desensitization caused by prior in vivo cocaine exposure may be conferred by an unexpected role of the D2L splice variant as an autoreceptor.
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.
Chronic exposure to a potent chemical contact sensitizer drives a self-limiting expansion of a polyclonal population of T cells recognizing a small number of dominant antigens.
Structural and functional analysis of the OTOP3 channel from Xenopus tropicalis offers insights into the mechanism of ion transport and regulation in the otopetrin proton channel family.