Evidence map›Paper›PMID 36047730›Full record

ReviewEpilepsia2022

Mouse models of Kcnq2 dysfunction.

Lucile Brun, Jean-Charles Viemari, Laurent Villard

Abstract readReview
In one paragraph

Review in Epilepsia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Constitutive opening of the Kv7.2 pore activation gate causesProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Article
  8. Article
  9. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Lucile BrunAix Marseille Univ, Inserm, MMG, Marseille, France.
Jean-Charles ViemariAix Marseille Univ, CNRS, INT, Marseille, France.
Laurent VillardAix Marseille Univ, Inserm, MMG, Marseille, France.ORCID 0000-0001-6657-5008

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Variants in the Kv7.2 channel subunit encoded by the KCNQ2 gene cause epileptic disorders ranging from a benign form with self-limited epileptic seizures and normal development to severe forms with intractable epileptic seizures and encephalopathy. The biological mechanisms involved in these neurological diseases are still unclear. The disease remains intractable in patients affected by the severe form. Over the past 20 years, KCNQ2 models have been developed to elucidate pathological mechanisms and to identify new therapeutic targets. The diversity of Kcnq2 mouse models has proven invaluable to access neuronal networks and evaluate the associated cognitive deficits. This review summarizes the available models and their contribution to our current understanding of KCNQ2 epileptic disorders.

Indexed as

Brain DiseasesKCNQ2 Potassium ChannelAnimalsDisease Models, AnimalMiceMutationNerve Tissue ProteinsSeizuresKCNQ2 Potassium ChannelKcnq2 protein, mouseNerve Tissue Proteinsdevelopmental and epileptic encephalopathyM currentmouse modelsself-limited familial neonatal-infantile epilepsy

Identifiers

PMID36047730
PMCPMC9828481

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.