ReviewAdvances in experimental medicine and biology2021
The Functional Properties, Physiological Roles, Channelopathy and Pharmacological Characteristics of the Slack (KCNT1) Channel.
Review in Advances in experimental medicine and biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 5 citations in OpenAlex.
- Antisense oligonucleotide-mediated knockdown therapy in two infants with severe KCNT1 epileptic encephalopathy.Nature medicine · 2026Article
- KCNT1 gene variant-associated epilepsy: genetic insights, functional mechanisms, and emerging therapies.Journal of neurology · 2025Review
- Electrophysiological characterization of human KCNT1 channel modulators and the therapeutic potential of hydroquinine and tipepidine in KCNT1 mutation-associated epilepsy mouse model.Acta pharmacologica Sinica · 2025Article
- Autosomal dominant sleep-related hypermotor epilepsy associated with a novel mutation ofTranslational neuroscience · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The KCNT1 gene encodes the sodium-activated potassium channel that is abundantly expressed in the central nervous system of mammalians and plays an important role in reducing neuronal excitability. Structurally, the KCNT1 channel is absent of voltage sensor but possesses a long C-terminus including RCK1 and RCK2domain, to which the intracellular sodium and chloride bind to activate the channel. Recent publications using electron cryo-microscopy (cryo-EM) revealed the open and closed structural characteristics of the KCNT1 channel and co-assembly of functional domains. The activation of the KCNT1 channel regulates various physiological processes including nociceptive behavior, itch, spatial learning. Meanwhile, malfunction of this channel causes important pathophysiological consequences, including Fragile X syndrome and a wide spectrum of seizure disorders. This review comprehensively describes the structure, expression patterns, physiological functions of the KCNT1 channel and emphasizes the channelopathy of gain-of-function KCNT1 mutations in epilepsy.
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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.