| Literature DB >> 25240195 |
Zhi-Yong Tan1, Birgit T Priest2, Jeffrey L Krajewski2, Kelly L Knopp2, Eric S Nisenbaum2, Theodore R Cummins3.
Abstract
Resurgent sodium currents likely play a role in modulating neuronal excitability. Here we studied whether protein kinase C (PKC) activation can increase resurgent currents produced by the human sodium channel hNav1.7. We found that a PKC agonist significantly enhanced hNav1.7-mediated resurgent currents and this was prevented by PKC antagonists. The enhancing effects were replicated by two phosphorylation-mimicking mutations and were prevented by a phosphorylation-deficient mutation at a conserved PKC phosphorylation site (Serine 1479). Our results suggest that PKC can increase sodium resurgent currents through phosphorylation of a conserved Serine residue located in the domain III-IV linker of sodium channels.Entities:
Keywords: Mutation; Protein kinase C; Resurgent current; Sodium channel; Voltage clamp; hNav1.7
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Year: 2014 PMID: 25240195 PMCID: PMC4451938 DOI: 10.1016/j.febslet.2014.09.011
Source DB: PubMed Journal: FEBS Lett ISSN: 0014-5793 Impact factor: 4.124