ArticleNature neuroscience2009
Oxidation of a potassium channel causes progressive sensory function loss during aging.
Article in Nature neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 73 citations in OpenAlex.
- Physiological oxygen levels reset KRedox biology · 2026Article
- Loss of Cisd2 Exacerbates the Progression of Age-Related Hearing Loss.Aging and disease · 2024Article
- Non-conducting functions of ion channels: The case of integrin-ion channel complexes.Channels (Austin, Tex.) · 2022Review
- Ageing induces tissue-specific transcriptomic changes in Caenorhabditis elegans.The EMBO journal · 2022Article
- Modelling learning in Caenorhabditis elegans chemosensory and locomotive circuitry for T-maze navigation.The European journal of neuroscience · 2022Article
- Modulation of sensory perception by hydrogen peroxide enables Caenorhabditis elegans to find a niche that provides both food and protection from hydrogen peroxide.PLoS pathogens · 2021Article
- Age-related hearing loss pertaining to potassium ion channels in the cochlea and auditory pathway.Pflugers Archiv : European journal of physiology · 2021Review
- The decrease of intraflagellar transport impairs sensory perception and metabolism in ageing.Nature communications · 2021Article
- Age-related changes in Kv4/Shal and Kv1/Shaker expression in Drosophila and a role for reactive oxygen species.PloS one · 2021Article
- Auditory Threshold Variability in the SAMP8 Mouse Model of Age-Related Hearing Loss: Functional Loss and Phenotypic Change Precede Outer Hair Cell Loss.Frontiers in aging neuroscience · 2021Article
- Oxidation of KCNB1 potassium channels in the murine brain during aging is associated with cognitive impairment.Biochemical and biophysical research communications · 2019Article
- Biophysical modeling of C. elegans neurons: Single ion currents and whole-cell dynamics of AWCon and RMD.PloS one · 2019Article
- Oxidation of KCNB1 channels in the human brain and in mouse model of Alzheimer's disease.Cell death & disease · 2018Article
- Redox Signaling in Neurotransmission and Cognition During Aging.Antioxidants & redox signaling · 2018Review
- Membrane ion Channels and Receptors in Animal lifespan Modulation.Journal of cellular physiology · 2017Review
- Oxidation of KCNB1 Potassium Channels Causes Neurotoxicity and Cognitive Impairment in a Mouse Model of Traumatic Brain Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- The neurotoxic effects of hydrogen peroxide and copper in Retzius nerve cells of the leech Haemopis sanguisuga.Biology open · 2016Article
- Oxidation of K(+) Channels in Aging and Neurodegeneration.Aging and disease · 2016Review
- KChIP-like auxiliary subunits of Kv4 channels regulate excitability of muscle cells and control male turning behavior during mating in Caenorhabditis elegans.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Guanine nucleotide exchange factor OSG-1 confers functional aging via dysregulated Rho signaling in Caenorhabditis elegans neurons.Genetics · 2015Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Potassium channels are key regulators of neuronal excitability. Here we show that oxidation of the K(+) channel KVS-1 during aging causes sensory function loss in Caenorhabditis elegans and that protection of this channel from oxidation preserves neuronal function. Chemotaxis, a function controlled by KVS-1, was significantly impaired in worms exposed to oxidizing agents, but only moderately affected in worms harboring an oxidation-resistant KVS-1 mutant (C113S). In aging C113S transgenic worms, the effects of free radical accumulation were significantly attenuated compared to those in wild type. Electrophysiological analyses showed that both reactive oxygen species (ROS) accumulation during aging and acute exposure to oxidizing agents acted primarily to alter the excitability of the neurons that mediate chemotaxis. Together, these findings establish a pivotal role for ROS-mediated oxidation of voltage-gated K(+) channels in sensorial decline during aging in invertebrates.
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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.