ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Toxic role of K+ channel oxidation in mammalian brain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 50 papers.
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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
50 citing papers in PubMed, 72 citations in OpenAlex.
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- Therapeutic role of voltage-gated potassium channels in age-related neurodegenerative diseases.Frontiers in cellular neuroscience · 2024Review
- Distinct cellular expression and subcellular localization of Kv2 voltage-gated KbioRxiv : the preprint server for biology · 2023Article
- Non-conducting functions of potassium channels in cancer and neurological disease.Current topics in membranes · 2023Review
- Non-conducting functions of ion channels: The case of integrin-ion channel complexes.Channels (Austin, Tex.) · 2022Review
- Antagonistic roles of Ras-MAPK and Akt signaling in integrin-KFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Alzheimer's disease therapy based on acetylcholinesterase inhibitor/blocker effects on voltage-gated potassium channels.Metabolic brain disease · 2022Review
- Hydrogen sulfide regulates hippocampal neuron excitability via S-sulfhydration of Kv2.1.Scientific reports · 2021Article
- Voltage-gated potassium channels are involved in oxymatrine-regulated islet function in rat islet β cells and INS-1 cells.Iranian journal of basic medical sciences · 2021Article
- Age-related changes in Kv4/Shal and Kv1/Shaker expression in Drosophila and a role for reactive oxygen species.PloS one · 2021Article
- Dopamine-Dependent QR2 Pathway Activation in CA1 Interneurons Enhances Novel Memory Formation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Vasoconstrictor Mechanisms in Chronic Hypoxia-Induced Pulmonary Hypertension: Role of Oxidant Signaling.Antioxidants (Basel, Switzerland) · 2020Review
- Voltage-Gated Potassium Channels as Regulators of Cell Death.Frontiers in cell and developmental biology · 2020Review
- Complexes formed with integrin-α5 and KCNB1 potassium channel wild type or epilepsy-susceptibility variants modulate cellular plasticityFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Oxidation of KCNB1 potassium channels in the murine brain during aging is associated with cognitive impairment.Biochemical and biophysical research communications · 2019Article
- Clustered Kv2.1 decreases dopamine transporter activity and internalization.The Journal of biological chemistry · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Potassium (K(+)) channels are essential to neuronal signaling and survival. Here we show that these proteins are targets of reactive oxygen species in mammalian brain and that their oxidation contributes to neuropathy. Thus, the KCNB1 (Kv2.1) channel, which is abundantly expressed in cortex and hippocampus, formed oligomers upon exposure to oxidizing agents. These oligomers were ∼10-fold more abundant in the brain of old than young mice. Oxidant-induced oligomerization of wild-type KCNB1 enhanced apoptosis in neuronal cells subject to oxidative insults. Consequently, a KCNB1 variant resistant to oxidation, obtained by mutating a conserved cysteine to alanine, (C73A), was neuroprotective. The fact that oxidation of KCNB1 is toxic, argues that this mechanism may contribute to neuropathy in conditions characterized by high levels of oxidative stress, such as Alzheimer's disease (AD). Accordingly, oxidation of KCNB1 channels was exacerbated in the brain of a triple transgenic mouse model of AD (3xTg-AD). The C73A variant protected neuronal cells from apoptosis induced by incubation with β-amyloid peptide (Aβ(1-42)). In an invertebrate model (Caenorhabditis elegans) that mimics aspects of AD, a C73A-KCNB1 homolog (C113S-KVS-1) protected specific neurons from apoptotic death induced by ectopic expression of human Aβ(1-42). Together, these data underscore a novel mechanism of toxicity in neurodegenerative disease.
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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.