| Literature DB >> 32084332 |
Lou Beaulieu-Laroche1, Marine Christin1, Annmarie Donoghue2, Francina Agosti3, Noosha Yousefpour4, Hugues Petitjean1, Albena Davidova1, Craig Stanton1, Uzair Khan5, Connor Dietz5, Elise Faure6, Tarheen Fatima1, Amanda MacPherson5, Stephanie Mouchbahani-Constance1, Daniel G Bisson7, Lisbet Haglund7, Jean A Ouellet8, Laura S Stone9, Jonathan Samson10, Mary-Jo Smith11, Kjetil Ask12, Alfredo Ribeiro-da-Silva4, Rikard Blunck13, Kate Poole14, Emmanuel Bourinet3, Reza Sharif-Naeini15.
Abstract
Mechanotransduction, the conversion of mechanical stimuli into electrical signals, is a fundamental process underlying essential physiological functions such as touch and pain sensing, hearing, and proprioception. Although the mechanisms for some of these functions have been identified, the molecules essential to the sense of pain have remained elusive. Here we report identification of TACAN (Tmem120A), an ion channel involved in sensing mechanical pain. TACAN is expressed in a subset of nociceptors, and its heterologous expression increases mechanically evoked currents in cell lines. Purification and reconstitution of TACAN in synthetic lipids generates a functional ion channel. Finally, a nociceptor-specific inducible knockout of TACAN decreases the mechanosensitivity of nociceptors and reduces behavioral responses to painful mechanical stimuli but not to thermal or touch stimuli. We propose that TACAN is an ion channel that contributes to sensing mechanical pain.Entities:
Keywords: TACAN; bilayer; ion channel; mechanosensitive; mechanotransduction; nociceptor; pain; patch clamp; pillar
Year: 2020 PMID: 32084332 DOI: 10.1016/j.cell.2020.01.033
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 41.582