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The Platynereis startle circuit links polycystin-dependent hydrodynamic sensors to muscle and ciliary effector cells.

A zebrafish model for a particular form of human deafness (DFNB63) changes our view of this disease by revealing a defect in the localization of Transmembrane channel-like proteins that are essential for mechanotransduction in sensory cells.

MCTP is a novel presynaptic calcium sensor, resident within the endoplasmic reticulum, that is required for normal baseline neurotransmission, short-term synaptic plasticity and presynaptic homeostatic plasticity.

Engineered E3 ubiquitin ligases are utilized to elucidate mechanisms underlying ubiquitin regulation of membrane proteins, and to achieve robust post-translational functional knockdown of ion channels.

Signaling by TAM receptor tyrosine kinases requires the coincident engagement of a TAM ligand with both its receptor and the phospholipid phosphatidylserine.

The voltage-gated sodium channel Na_v1.1 is identified as an essential component of the proprioceptive transmission machinery that is required in vivo for normal motor behavior.

ORAI1 ion channel lipid modification is required for a proper immune synapse formation and T cell activation.

Ecdysone-mediated repression of the TMEM16 channel subdued initiates a sensory switch in peripheral nociceptors during Drosophila larval development, increasing thermal nociceptive behavior and reducing responsiveness to ultraviolet light.

Electrophysiological and structural characterizations reveal that a previously proposed ion channel responsible for sensing mechanical pain is insensitive to poking or stretching stimuli for conducting ions and may serve as a coenzyme A-binding protein instead.

Neural crest cells differentiated from patient-derived cells with mutations in the chromatin remodeler CHD7 show defective delamination, migration and motility in vitro, and defective migration in chick embryos.