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

Opening the KV3.1 gates: A therapeutic strategy for progressive myoclonus epilepsy type 7?

Cell reports. Medicine - 20 Feb 2024

Gandini Maria A, Zamponi Gerald W

Abstract excerpt

Progressive myoclonus epilepsy type 7, a debilitating neurological disorder, is caused by a loss-of-function mutation in the KV3.1 channel. Exciting work by Feng et al.1 utilizes a new knockin mouse model to identify a potential therapeutic intervention.

Read the complete abstract on PubMed

Topics

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

Share to Mice
Share to Mutation
Share to Myoclonic Epilepsies, Progressive

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Open in PubMed Open full text

Identifiers

PMID: 38382469
DOI: 10.1016/j.xcrm.2024.101425
PMCID: PMC10897601

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Opening the KV3.1 gates: A therapeutic strategy for progressive myoclonus epilepsy type 7?PMID 38382469Read ↗

Progressive Myoclonic Epilepsy-Associated Gene KCTD7 is a Regulator of Potassium Conductance in NeuronsSemantic proximity Read ↗

The best evidence for progressive myoclonic epilepsy: A pathway to precision therapySemantic proximity Read ↗

KCNQ-Encoded Potassium Channels as Therapeutic Targets.Semantic proximity Read ↗

KV7 channelopathies.Semantic proximity Read ↗

Progressive myoclonus epilepsy caused by a gain-of-function KCNA2 mutationSemantic proximity Read ↗

Progressive myoclonus epilepsy KCNC1 variant causes a developmental dendritopathy.Semantic proximity Read ↗

Discovery of Kv3.1 channel inhibitors reveals VU0521426 as a state-dependent inactivator preferentially active against pathogenic gain-of-function mutants.Semantic proximity Read ↗

Novel E815K knock-in mouse model of alternating hemiplegia of childhood.Semantic proximity Read ↗

Early-onset epileptic encephalopathy caused by gain-of-function mutations in the voltage sensor of Kv7.2 and Kv7.3 potassium channel subunits.Semantic proximity Read ↗

Site and Mechanism of ML252 Inhibition of Kv7 Voltage-Gated Potassium Channels.Semantic proximity Read ↗

Targeting the Voltage-Dependent K+ Channels Kv1.3 and Kv1.5 as Tumor Biomarkers for Cancer Detection and PreventionSemantic proximity Read ↗

Kv1.3 K<sup>+</sup>Channel Physiology Assessed by Genetic and Pharmacological ModulationSemantic proximity Read ↗

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