Excited to share our new paper in Science Advances @science.org
In this work, we uncover how a disease-linked TRPC3 mutation, together with a cerebellum-specific splice isoform, stabilizes the channel in an open state, drives Calcium overload, and promotes neurodegeneration. (1/4)
www.science.org
Structural snapshots capture an ataxia-linked overactive ion channel in its open state and reveal a druggable site for inhibition.
