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The Excelsatoxin A-Receptor TMEM233 Modulates Nav1.8.

George Oprita1,2,3, Marvin J A Meyer1, Daniel Rudolf1

  • 1Department of Anesthesiology and Intensive Care Medicine, Hannover Medical School, Hannover, Lower Saxony, Germany.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|March 19, 2026
PubMed
Summary
This summary is machine-generated.

Transmembrane protein 233 (TMEM233) regulates sodium channel Nav1.8, potentially mediating Excelsatoxin A (ExTxA)-induced pain. This interaction alters Nav1.8 channel function, suggesting a new target for pain relief.

Keywords:
Nav1.8TMEM233excelsatoxinpainsensory neurons

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Transmembrane protein 233 (TMEM233) is implicated in Excelsatoxin A (ExTxA)-induced pain via modulation of the sodium channel Nav1.7.
  • ExTxA-induced dorsal root ganglion (DRG) neuron activation is partially resistant to tetrodotoxin (TTX), suggesting involvement of TTX-resistant sodium channels like Nav1.8.

Purpose of the Study:

  • To investigate the role of TMEM233 and its interaction with the sodium channel Nav1.8 in ExTxA-induced pain.
  • To characterize the functional and pharmacological consequences of TMEM233 co-expression with Nav1.8.

Main Methods:

  • Patch clamp electrophysiology and calcium imaging were performed on mouse DRG neurons and heterologous cell systems (ND7/23, CHO) expressing Nav1.8 and TMEM233.
  • Pharmacological agents including TTX and the selective Nav1.8 inhibitor suzetrigine (VX-548) were used to dissect channel contributions.

Main Results:

  • ExTxA-induced calcium influx in DRG neurons was significantly reduced by combined TTX and suzetrigine, confirming Nav1.8 involvement.
  • Co-expression of Nav1.8 and TMEM233 resulted in ExTxA-induced removal of fast inactivation in TTX-resistant sodium currents.
  • TMEM233 co-expression with Nav1.8 led to altered channel gating, impaired recovery from inactivation, and increased sensitivity to lidocaine, independent of ExTxA stimulation.

Conclusions:

  • TMEM233 plays a significant role in ExTxA-induced pain by modulating the Nav1.8 sodium channel.
  • TMEM233 is a key interacting protein that alters the functional and pharmacological properties of Nav1.8.
  • These findings highlight TMEM233 as a potential therapeutic target for managing pain associated with Nav1.8 channel activity.