ArticleNeuron2014
Hyper-SUMOylation of the Kv7 potassium channel diminishes the M-current leading to seizures and sudden death.
Article in Neuron, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
62 citing papers in PubMed, 94 citations in OpenAlex.
- Identification of Key Genes Related to SUMOylation and Potassium Channels and Their Mechanism of Influence on Pulmonary Arterial Hypertension.Biochemical genetics · 2026Article
- SUMO Regulation of Ion Channels in Health and Disease.Physiology (Bethesda, Md.) · 2025Review
- SUMOylation balance: a key determinant in synapse physiology.Frontiers in physiology · 2025Review
- Unveiling the role of histone deacetylases in neurological diseases: focus on epilepsy.Biomarker research · 2024Review
- Autocrine VEGF-B signaling maintains lipid synthesis and mitochondrial fitness to support T cell immune responses.The Journal of clinical investigation · 2024Article
- Post translational modifications of connexin 43 in ventricular arrhythmias after myocardial infarction.Molecular biology reports · 2024Review
- SUMOylation of the cardiac sodium channel NaHeart rhythm · 2023Article
- Seizure enhances SUMOylation and zinc-finger transcriptional repression in neuronal nuclei.iScience · 2023Article
- Involvement of CaCellular and molecular neurobiology · 2023Article
- SUMOylation of NaeLife · 2023Article
- Possible molecular mechanisms underlying the development of atherosclerosis in cancer survivors.Frontiers in cardiovascular medicine · 2023Review
- Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation in mice.Nature communications · 2022Article
- SUMOylation of Kir7.1 participates in neuropathic pain through regulating its membrane expression in spinal cord neurons.CNS neuroscience & therapeutics · 2022Article
- KIF17 Modulates Epileptic Seizures and Membrane Expression of the NMDA Receptor Subunit NR2B.Neuroscience bulletin · 2022Article
- SUMOylation and Major Depressive Disorder.International journal of molecular sciences · 2022Review
- Signaling pathways involved in NMDA-induced suppression of M-channels in corticotropin-releasing hormone neurons in central amygdala.Journal of neurochemistry · 2022Article
- KCNQ Channels Enable Reliable Presynaptic Spiking and Synaptic Transmission at High Frequency.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- The protease SENP2 controls hepatic gluconeogenesis by regulating the SUMOylation of the fuel sensor AMPKα.The Journal of biological chemistry · 2022Article
- SENP2-PLCβ4 signaling regulates neurogenesis through the maintenance of calcium homeostasis.Cell death and differentiation · 2022Article
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension.Cardiovascular research · 2022Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Sudden unexplained death in epilepsy (SUDEP) is the most common cause of premature mortality in epilepsy and was linked to mutations in ion channels; however, genes within the channel protein interactome might also represent pathogenic candidates. Here we show that mice with partial deficiency of Sentrin/SUMO-specific protease 2 (SENP2) develop spontaneous seizures and sudden death. SENP2 is highly enriched in the hippocampus, often the focus of epileptic seizures. SENP2 deficiency results in hyper-SUMOylation of multiple potassium channels known to regulate neuronal excitability. We demonstrate that the depolarizing M-current conducted by Kv7 channel is significantly diminished in SENP2-deficient hippocampal CA3 neurons, primarily responsible for neuronal hyperexcitability. Following seizures, SENP2-deficient mice develop atrioventricular conduction blocks and cardiac asystole. Both seizures and cardiac conduction blocks can be prevented by retigabine, a Kv7 channel opener. Thus, we uncover a disease-causing role for hyper-SUMOylation in the nervous system and establish an animal model for SUDEP.
Indexed as
Identifiers
What OpenQuestion holds
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.