蛋白激酶C通过结构域III-IV连接区中的一个丝氨酸残基增强人钠通道hNav1.7的复苏电流。
Protein kinase C enhances human sodium channel hNav1.7 resurgent currents via a serine residue in the domain III-IV linker.
作者信息
Tan Zhi-Yong, Priest Birgit T, Krajewski Jeffrey L, Knopp Kelly L, Nisenbaum Eric S, Cummins Theodore R
机构信息
Department of Pharmacology and Toxicology and Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Lilly Research Laboratories, Indianapolis, IN 46285, USA.
出版信息
FEBS Lett. 2014 Nov 3;588(21):3964-9. doi: 10.1016/j.febslet.2014.09.011. Epub 2014 Sep 19.
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.
摘要
复苏钠电流可能在调节神经元兴奋性中发挥作用。在此，我们研究了蛋白激酶C（PKC）激活是否能增加人钠通道hNav1.7产生的复苏电流。我们发现PKC激动剂显著增强了hNav1.7介导的复苏电流，而PKC拮抗剂可阻止这种增强。两种模拟磷酸化的突变复制了增强作用，而在保守的PKC磷酸化位点（丝氨酸1479）的磷酸化缺陷突变则阻止了这种增强。我们的结果表明，PKC可通过磷酸化位于钠通道结构域III-IV连接区的保守丝氨酸残基来增加钠复苏电流。
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J Neurosci. 2014 May 21;34(21):7190-7. doi: 10.1523/JNEUROSCI.5011-13.2014.
2
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J Gen Physiol. 2013 Sep;142(3):191-206. doi: 10.1085/jgp.201310984. Epub 2013 Aug 12.
3
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4
Anticancer drug oxaliplatin induces acute cooling-aggravated neuropathy via sodium channel subtype Na(V)1.6-resurgent and persistent current.
Proc Natl Acad Sci U S A. 2012 Apr 24;109(17):6704-9. doi: 10.1073/pnas.1118058109. Epub 2012 Apr 9.
5
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6
Effects of the PKC inhibitors chelerythrine and bisindolylmaleimide I (GF 109203X) on delayed rectifier K+ currents.
Naunyn Schmiedebergs Arch Pharmacol. 2011 Feb;383(2):141-8. doi: 10.1007/s00210-010-0584-8. Epub 2010 Dec 1.
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8
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9
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10
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