Elena B. Riel

This paper genetically engineers K2P channels to be activated by rapamycin or its analogs, enabling chemogenetic control of cellular membrane potential.

The paper identifies the down-to-up state transition as the primary activation pathway for TREK K2P channels, showing it does not involve lipid occlusion of the pore.

This paper identifies a lower cytoplasmic gate in TALK-2 channels and demonstrates bidirectional coupling between this gate and the selectivity filter gate, showing that ion occupancy and stimuli can influence both gates.

The paper identifies de novo gain-of-function mutations in KCNK3 causing a developmental disorder with sleep apnea by disrupting X-gating of TASK-1 channels.