Evidence map›Paper›PMID 37321992›Full record

ArticleNature communications2023

Kv7/KCNQ potassium channels in cortical hyperexcitability and juvenile seizure-related death in Ank2-mutant mice.

Hyoseon Oh, Suho Lee, Yusang Oh, Seongbin Kim, Young Seo Kim, Yeji Yang, Woochul Choi, Ye-Eun Yoo, Heejin Cho, Seungjoon Lee and 11 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.0field-weighted citation impact, top 6% of its field
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

18 citing papers in PubMed, 26 citations in OpenAlex.

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  14. Evaluation of Small-Molecule Candidates as Modulators of M-Type KInternational journal of molecular sciences · 2025
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  18. Pathogenic gating pore current conducted by autism-related mutations in the NaProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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

21 authors at 5 institutions in 1 country.

Hyoseon OhDepartment of Biological Sciences, Korea Advanced Institute for Science and Technology (KAIST), Daejeon, 34141, Korea.ORCID 0000-0003-1713-2707
Suho LeeCenter for Synaptic Brain Dysfunctions, Institute for Basic Science (IBS), Daejeon, 34141, Korea.ORCID 0000-0002-5956-9985
Yusang OhDepartment of Biological Sciences, Korea Advanced Institute for Science and Technology (KAIST), Daejeon, 34141, Korea.
Seongbin KimDepartment of Biological Sciences, Korea Advanced Institute for Science and Technology (KAIST), Daejeon, 34141, Korea.ORCID 0009-0000-1105-5558
Young Seo KimGraduate School of Medical Science and Engineering, KAIST, Daejeon, 34141, Korea.
Yeji YangDepartment of Biological Sciences, Korea Advanced Institute for Science and Technology (KAIST), Daejeon, 34141, Korea.
Woochul ChoiDepartment of Bio and Brain Engineering, KAIST, Daejeon, 34141, Korea.ORCID 0000-0002-9937-1404
Ye-Eun YooCenter for Synaptic Brain Dysfunctions, Institute for Basic Science (IBS), Daejeon, 34141, Korea.
Heejin ChoCenter for Synaptic Brain Dysfunctions, Institute for Basic Science (IBS), Daejeon, 34141, Korea.
Seungjoon LeeCenter for Synaptic Brain Dysfunctions, Institute for Basic Science (IBS), Daejeon, 34141, Korea.ORCID 0000-0002-8583-528X
Esther YangDepartment of Anatomy and Brain Korea 21 Graduate Program, Biomedical Science, College of Medicine, Korea University, Seoul, 02841, Korea.
Wuhyun KohCenter for Cognition and Sociality, IBS, Daejeon, 34126, Korea.ORCID 0000-0002-4398-1094
Woojin WonCenter for Cognition and Sociality, IBS, Daejeon, 34126, Korea.
Ryunhee KimCenter for Synaptic Brain Dysfunctions, Institute for Basic Science (IBS), Daejeon, 34141, Korea.
C Justin LeeCenter for Cognition and Sociality, IBS, Daejeon, 34126, Korea.ORCID 0000-0002-3555-0980
Hyun KimDepartment of Anatomy and Brain Korea 21 Graduate Program, Biomedical Science, College of Medicine, Korea University, Seoul, 02841, Korea.ORCID 0000-0002-7210-5798
Hyojin KangDivision of National Supercomputing, Korea Institute of Science and Technology Information, Daejeon, 34141, Korea.
Jin Young KimResearch Center for Bioconvergence Analysis, Korea Basic Science Institute, 162 Yeongudanjiro, Ochang, Cheongju, Chungbuk, 28119, Korea.ORCID 0000-0002-0656-1269
Taeyun KuGraduate School of Medical Science and Engineering, KAIST, Daejeon, 34141, Korea.ORCID 0000-0001-9447-7579
Se-Bum PaikDepartment of Bio and Brain Engineering, KAIST, Daejeon, 34141, Korea.ORCID 0000-0002-4078-305X
Eunjoon KimDepartment of Biological Sciences, Korea Advanced Institute for Science and Technology (KAIST), Daejeon, 34141, Korea. kime@kaist.ac.kr.ORCID 0000-0001-5518-6584
Korea Advanced Institute of Science and Technology · KRInstitute for Basic Science · KRKorea University · KRKorea Basic Science Institute · KRKorea Institute of Science & Technology Information · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorders (ASD) represent neurodevelopmental disorders characterized by social deficits, repetitive behaviors, and various comorbidities, including epilepsy. ANK2, which encodes a neuronal scaffolding protein, is frequently mutated in ASD, but its in vivo functions and disease-related mechanisms are largely unknown. Here, we report that mice with Ank2 knockout restricted to cortical and hippocampal excitatory neurons (Ank2-cKO mice) show ASD-related behavioral abnormalities and juvenile seizure-related death. Ank2-cKO cortical neurons show abnormally increased excitability and firing rate. These changes accompanied decreases in the total level and function of the Kv7.2/KCNQ2 and Kv7.3/KCNQ3 potassium channels and the density of these channels in the enlengthened axon initial segment. Importantly, the Kv7 agonist, retigabine, rescued neuronal excitability, juvenile seizure-related death, and hyperactivity in Ank2-cKO mice. These results suggest that Ank2 regulates neuronal excitability by regulating the length of and Kv7 density in the AIS and that Kv7 channelopathy is involved in Ank2-related brain dysfunctions.

Indexed as

EpilepsyKCNQ Potassium ChannelsAnimalsAnkyrinsKCNQ2 Potassium ChannelKCNQ3 Potassium ChannelMiceNerve Tissue ProteinsNeuronsSeizuresAnk2 protein, mouseAnkyrinsKCNQ2 Potassium ChannelKcnq2 protein, mouseKCNQ3 Potassium ChannelKCNQ Potassium ChannelsNerve Tissue Proteins

Identifiers

PMID37321992
PMCPMC10272139
OpenAlexW4380853643

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.