Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

KNa1.1 gain-of-function preferentially dampens excitability of murine parvalbumin-positive interneurons.

Neurobiology of disease - 15 Jun 2022

Gertler Tracy S, Cherian Suraj, DeKeyser Jean-Marc, Kearney Jennifer A, George Alfred L

Abstract excerpt

KCNT1 encodes the sodium-activated potassium channel KNa1.1, expressed preferentially in the frontal cortex, hippocampus, cerebellum, and brainstem. Pathogenic missense variants in KCNT1 are associated with intractable epilepsy, namely epilepsy of infancy with migrating focal seizures (EIMFS), and sleep-related hypermotor epilepsy (SHE). In vitro studies of pathogenic KCNT1 variants support predominantly a...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Epilepsy
Share to Gain of Function Mutation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Interneurons

Share to Nerve Tissue Proteins

Share to Parvalbumins

Share to Potassium Channels, Sodium-Activated

Share to Seizures

Share to Sodium Channels

Source

Open in PubMed Open full text

Identifiers

PMID: 35346832
DOI: 10.1016/j.nbd.2022.105713
PMCID: PMC9169414

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

KNa1.1 gain-of-function preferentially dampens excitability of murine parvalbumin-positive interneurons.PMID 35346832Read ↗

Impaired motor skill learning and altered seizure susceptibility in mice with loss or gain of function of the Kcnt1 gene encoding Slack (KNa1.1) Na+-activated K+ channels.Semantic proximity Read ↗

The paradoxical effects of K <sup>+</sup> channel gain-of-function are mediated by GABAergic neuron hypoexcitability and hyperconnectivitySemantic proximity Read ↗

Novel Gain of Function Mouse Model of KCNT1-Related EpilepsySemantic proximity Read ↗

Interneuron dysfunction in a new knock-in mouse model of SCN1A GEFS+Semantic proximity Read ↗

Nav1.1 localizes to axons of parvalbumin-positive inhibitory interneurons: a circuit basis for epileptic seizures in mice carrying an Scn1a gene mutation.Semantic proximity Read ↗

Impaired excitability of fast-spiking neurons in a novel mouse model of <i>KCNC1</i> epileptic encephalopathySemantic proximity Read ↗

Durable suppression of seizures in a preclinical model of KCNT1 genetic epilepsy with divalent small interfering RNASemantic proximity Read ↗

Interneuron Dysfunction in a New Mouse Model of SCN1A GEFS.Semantic proximity Read ↗

Targeting KNa1.1 channels in KCNT1-associated epilepsy.Semantic proximity Read ↗

Gene therapy for targeting a prenatally enriched potassium channel associated with severe childhood epilepsy and premature deathSemantic proximity Read ↗

Functional Effects of Epilepsy Associated KCNT1 Mutations Suggest Pathogenesis via Aberrant Inhibitory Neuronal Activity.Semantic proximity Read ↗

KCNT1 mutations in seizure disorders: the phenotypic spectrum and functional effects.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.