ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2007
Regulation of Kv1 channel trafficking by the mamba snake neurotoxin dendrotoxin K.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- Comparison of KHandbook of experimental pharmacology · 2021Article
- Article
- Auditory Input Shapes Tonotopic Differentiation of Kv1.1 Expression in Avian Cochlear Nucleus during Late Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- mTORC1 Is a Local, Postsynaptic Voltage Sensor Regulated by Positive and Negative Feedback Pathways.Frontiers in cellular neuroscience · 2017Article
- A novel epileptic encephalopathy mutation in KCNB1 disrupts Kv2.1 ion selectivity, expression, and localization.The Journal of general physiology · 2015Article
- Domain structure and function of matrix metalloprotease 23 (MMP23): role in potassium channel trafficking.Cellular and molecular life sciences : CMLS · 2014Review
- Heterogeneous intrinsic excitability of murine spiral ganglion neurons is determined by Kv1 and HCN channels.Neuroscience · 2014Article
- Trafficking mechanisms underlying neuronal voltage-gated ion channel localization at the axon initial segment.Epilepsia · 2012Review
- Kv2.1 cell surface clusters are insertion platforms for ion channel delivery to the plasma membrane.Molecular biology of the cell · 2012Article
- Subunit-dependent axonal trafficking of distinct alpha heteromeric potassium channel complexes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Cdk-mediated phosphorylation of the Kvβ2 auxiliary subunit regulates Kv1 channel axonal targeting.The Journal of cell biology · 2011Article
- Transmembrane segments prevent surface expression of sodium channel Nav1.8 and promote calnexin-dependent channel degradation.The Journal of biological chemistry · 2010Article
- Localization of Kv1.3 channels in presynaptic terminals of brainstem auditory neurons.The Journal of comparative neurology · 2010Article
- Potassium channel modulation by a toxin domain in matrix metalloprotease 23.The Journal of biological chemistry · 2010Article
- Tetramerization domain mutations in KCNA5 affect channel kinetics and cause abnormal trafficking patterns.American journal of physiology. Cell physiology · 2010Article
- SLEEPLESS, a Ly-6/neurotoxin family member, regulates the levels, localization and activity of Shaker.Nature neuroscience · 2010Article
- An endoplasmic reticulum retention signal located in the extracellular amino-terminal domain of the NR2A subunit of N-Methyl-D-aspartate receptors.The Journal of biological chemistry · 2009Article
- Trafficking-dependent phosphorylation of Kv1.2 regulates voltage-gated potassium channel cell surface expression.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Modulation of voltage-gated potassium (Kv) channel surface expression can profoundly affect neuronal excitability. Some, but not all, mammalian Shaker or Kv1 alpha subunits contain a dominant endoplasmic reticulum (ER) retention signal in their pore region, preventing surface expression of Kv1.1 homotetrameric channels and of heteromeric Kv1 channels containing more than one Kv1.1 subunit. The critical amino acid residues within this ER pore-region retention signal are also critical for high-affinity binding of snake dendrotoxins (DTX). This suggests that ER retention may be mediated by an ER protein with a domain structurally similar to that of DTX. One facet of such a model is that expression of soluble DTX in the ER lumen should compete for binding to the retention protein and allow for surface expression of retained Kv1.1. Here, we show that luminal DTX expression dramatically increased both the level of cell surface Kv1.1 immunofluorescence staining and the proportion of Kv1.1 with processed N-linked oligosaccharides. Electrophysiological analyses showed that luminal DTX expression led to significant increases in Kv1.1 currents. Together, these data showed that luminal DTX expression increases surface expression of functional Kv1.1 homotetrameric channels and support a model whereby a DTX-like ER protein regulates abundance of cell surface Kv1 channels.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.