English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

TMEM120A (TACAN) is an enigmatic protein with several seemingly unconnected functions. It was proposed to be an ion channel involved in sensing mechanical stimuli, and knockdown/knockout experiments have implicated that TMEM120A may be necessary for sensing mechanical pain. TMEM120A’s ion channel function has subsequently been challenged, as attempts to replicate electrophysiological experiments have largely been unsuccessful. Several cryo-EM structures revealed TMEM120A is structurally homologous to a lipid modifying enzyme called Elongation of Very Long Chain Fatty Acids 7 (ELOVL7). Although TMEM120A’s channel function is debated, it still seems to affect mechanosensation by inhibiting PIEZO2 channels and by modifying tactile pain responses in animal models. TMEM120A was also shown to inhibit polycystin-2 (PKD2) channels through direct physical interaction. Additionally, TMEM120A has been implicated in adipocyte regulation and in innate immune response against Zika virus. The way TMEM120A is proposed to alter each of these processes ranges from regulating gene expression, acting as a lipid modifying enzyme, and controlling subcellular localization of other proteins through direct binding. Here, we examine TMEM120A’s structure and proposed functions in diverse physiological contexts.

TMEM120A/TACAN: A putative regulator of ion channels, mechanosensation, and lipid metabolism