Rise of palmitoylation: A new trick to tune NCX1 activity

Biochim Biophys Acta Mol Cell Res. 2024 Jun;1871(5):119719. doi: 10.1016/j.bbamcr.2024.119719. Epub 2024 Apr 3.

Abstract

The cardiac Na+/Ca2+ Exchanger (NCX1) controls transmembrane calcium flux in numerous tissues. The only reversible post-translational modification established to regulate NCX1 is palmitoylation, which alters the ability of the exchanger to inactivate. Palmitoylation creates a binding site for the endogenous XIP domain, a region of the NCX1 intracellular loop established to inactivate NCX1. The binding site created by NCX1 palmitoylation sensitizes the transporter to XIP. Herein we summarize our recent knowledge on NCX1 palmitoylation and its association with cardiac pathologies, and discuss these findings in the light of the recent cryo-EM structures of human NCX1.

Keywords: Ca2+ handling; Cardiac pathologies; Depalmitoylation; NCX1 inactivation; Palmitoylation.

Publication types

  • Review

MeSH terms

  • Animals
  • Binding Sites
  • Calcium / metabolism
  • Humans
  • Lipoylation*
  • Myocardium / metabolism
  • Protein Processing, Post-Translational*
  • Sodium-Calcium Exchanger* / chemistry
  • Sodium-Calcium Exchanger* / genetics
  • Sodium-Calcium Exchanger* / metabolism

Substances

  • Sodium-Calcium Exchanger
  • sodium-calcium exchanger 1
  • Calcium