AI Article Synopsis

  • Hypokalemic periodic paralysis (HypoPP) is a genetic disorder linked to mutations in specific genes (CACNA1S and SCN4A) affecting certain voltage-gated ion channels.
  • These mutations disrupt the channel's ability to maintain a hydrophobic seal, leading to abnormal leak currents known as gating pore currents, which are believed to cause the symptoms of HypoPP.
  • Researchers created model cell lines for HypoPP and developed a new method to measure gating pore currents, offering a potential platform for testing new drugs for HypoPP and other related disorders.

Article Abstract

Hypokalemic periodic paralysis (HypoPP) is a rare genetic disease associated with mutations in CACNA1S or SCN4A encoding the voltage-gated Ca2+ channel Cav1.1 or the voltage-gated Na+ channel Nav1.4, respectively. Most HypoPP-associated missense changes occur at the arginine residues within the voltage-sensing domain (VSD) of these channels. It is established that such mutations destroy the hydrophobic seal that separates external fluid and the internal cytosolic crevices, resulting in the generation of aberrant leak currents called gating pore currents. Presently, the gating pore currents are thought to underlie HypoPP. Here, based on HEK293T cells and by using the Sleeping Beauty transposon system, we generated HypoPP-model cell lines that co-express the mouse inward-rectifier K+ channel (mKir2.1) and HypoPP2-associated Nav1.4 channel. Whole-cell patch-clamp measurements confirmed that mKir2.1 successfully hyperpolarizes the membrane potential to levels comparable to those of myofibers, and that some Nav1.4 variants induce notable proton-based gating pore currents. Importantly, we succeeded in fluorometrically measuring the gating pore currents in these variants by using a ratiometric pH indicator. Our optical method provides a potential in vitro platform for high-throughput drug screening, not only for HypoPP but also for other channelopathies caused by VSD mutations.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10320719PMC
http://dx.doi.org/10.1242/dmm.049704DOI Listing

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