ArticlePflugers Archiv : European journal of physiology2006
Electrophysiological characterization of three non-synonymous single nucleotide polymorphisms (R87Q, A251T, and P307S) found in hKv1.5.
Article in Pflugers Archiv : European journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Cellular context and multiple channel domains determine cAMP sensitivity of HCN4 channels: ligand-independent relief of autoinhibition in HCN4.The Journal of general physiology · 2012Article
- Tetramerization domain mutations in KCNA5 affect channel kinetics and cause abnormal trafficking patterns.American journal of physiology. Cell physiology · 2010Article
- A pilot study to estimate the feasibility of assessing the relationships between polymorphisms in hKv1.5 and atrial fibrillation in patients following coronary artery bypass graft surgery.The Canadian journal of cardiology · 2008Article
- Ischemic, genetic and pharmacological origins of cardiac arrhythmias: the contribution of the Quebec Heart Institute.The Canadian journal of cardiology · 2007Review
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9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-synonymous single nucleotide polymorphisms (SNPs) in the KCNA5/hKv1.5 gene, which encodes for a voltage-gated K+ channel responsible for the I (Kur) current in the human atria, have been recently reported. To gain further knowledge on potential influence of hKv1.5 SNPs, we searched for their presence in a specific population of 96 French-Canadians and characterized electrophysiological properties of the variants in two cell lines. The presumed promoter (-83 bp) and coding regions were sequenced. We found three heterozygous SNPs: R87Q, A251T, and P307S. Functional analysis of SNPs transfected in Chinese hamster ovary (CHO) cells showed that both R87Q and P307S diminished the inactivation amplitude (e.g., at +60 mV, amplitudes were 89+/-26, 23+/-4, and 22+/-7 pA/pF for the wild type, R87Q and P307S, respectively; n=8, 6, and 8, respectively). Inactivation was slowed with these variants (e.g., tau (fast) at +50 mV were 270+/-48, 490+/-66, and 340+/-45 ms for the wild type, R87Q, and P307S, respectively) while R87Q additionally accelerated the rate of hKv1.5 channel opening. A dominant-negative effect was observed for R87Q but not for P307S. SNPs properties were not reproduced when expressed in the HEK293 cell line, suggesting that the regulatory beta-subunit present in CHO cells (and the human heart) is essential for the SNPs effects that we have observed.
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