ArticleFrontiers in molecular neuroscience2021
Activation of SGK1.1 Upregulates the M-current in the Presence of Epilepsy Mutations.
Article in Frontiers in molecular neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 3 citations in OpenAlex.
- Identification of Sodium/Myo-Inositol Transporter 1 as a Major Determinant of Arterial Contractility.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Serum/glucocorticoid regulated kinase 1 (SGK1) in neurological disorders: pain or gain.Experimental neurology · 2024Review
- The role of SGK1 in neurologic diseases: A friend or foe?IBRO neuroscience reports · 2024Review
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
In the central nervous system, the M-current plays a critical role in regulating subthreshold electrical excitability of neurons, determining their firing properties and responsiveness to synaptic input. The M-channel is mainly formed by subunits Kv7.2 and Kv7.3 that co-assemble to form a heterotetrametric channel. Mutations in Kv7.2 and Kv7.3 are associated with hyperexcitability phenotypes including benign familial neonatal epilepsy (BFNE) and neonatal epileptic encephalopathy (NEE). SGK1.1, the neuronal isoform of the serum and glucocorticoids-regulated kinase 1 (SGK1), increases M-current density in neurons, leading to reduced excitability and protection against seizures. Herein, using two-electrode voltage clamp on
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