ArticleBiophysical journal2011
KCNE1 and KCNE2 provide a checkpoint governing voltage-gated potassium channel α-subunit composition.
Article in Biophysical journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Functions of the KCNE Gene Family in Ion Channels.Biochemical genetics · 2026Review
- Ion channel traffic jams: the significance of trafficking deficiency in long QT syndrome.Cell discovery · 2025Review
- Kv Channel Ancillary Subunits: Where Do We Go from Here?Physiology (Bethesda, Md.) · 2022Review
- The focal adhesion protein Testin modulates KCNE2 potassium channel β subunit activity.Channels (Austin, Tex.) · 2021Article
- Control of Biophysical and Pharmacological Properties of Potassium Channels by Ancillary Subunits.Handbook of experimental pharmacology · 2021Article
- Hypochlorhydria reduces mortality in heart failure caused by Kcne2 gene deletion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Disease-linked mutations alter the stoichiometries of HCN-KCNE2 complexes.Scientific reports · 2019Article
- AKT and ERK1/2 activation via remote ischemic preconditioning prevents Kcne2-dependent sudden cardiac death.Physiological reports · 2019Article
- A-Type KFrontiers in molecular neuroscience · 2018Review
- Article
- β Subunits Functionally Differentiate Human Kv4.3 Potassium Channel Splice Variants.Frontiers in physiology · 2017Article
- Dysbindin Deficiency Modifies the Expression of GABA Neuron and Ion Permeation Transcripts in the Developing Hippocampus.Frontiers in genetics · 2017Article
- Review
- Novel exon 1 protein-coding regions N-terminally extend human KCNE3 and KCNE4.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Review
- Review
- Dysregulation of Kv3.4 channels in dorsal root ganglia following spinal cord injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Domain structure and function of matrix metalloprotease 23 (MMP23): role in potassium channel trafficking.Cellular and molecular life sciences : CMLS · 2014Review
- An evolutionarily conserved mode of modulation of Shaw-like K⁺ channels.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Intracellular trafficking of the KV1.3 potassium channel is regulated by the prodomain of a matrix metalloprotease.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Voltage-gated potassium (Kv) currents generated by N-type α-subunit homotetramers inactivate rapidly because an N-terminal ball domain blocks the channel pore after activation. Hence, the inactivation rate of heterotetrameric channels comprising both N-type and non-N-type (delayed rectifier) α-subunits depends upon the number of N-type α-subunits in the complex. As Kv channel inactivation and inactivation recovery rates regulate cellular excitability, the composition and expression of these heterotetrameric complexes are expected to be tightly regulated. In a companion article, we showed that the single transmembrane segment ancillary (β) subunits KCNE1 and KCNE2 suppress currents generated by homomeric Kv1.4, Kv3.3, and Kv3.4 channels, by trapping them early in the secretory pathway. Here, we show that this trapping is prevented by coassembly of the N-type α-subunits with intra-subfamily delayed rectifier α-subunits. Extra-subfamily delayed rectifier α-subunits, regardless of their capacity to interact with KCNE1 and KCNE2, cannot rescue Kv1.4 or Kv3.4 surface expression unless engineered to interact with them using N-terminal A and B domain swapping. The KCNE1/2-enforced checkpoint ensures N-type α-subunits only reach the cell surface as part of intra-subfamily mixed-α complexes, thereby governing channel composition, inactivation rate, and-by extension-cellular excitability.
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