Evidence map›Paper›PMID 41053028›Full record

ArticleCell death discovery2025

A knock-in mouse model for GABRG2-related epileptic encephalopathy displays spontaneous generalized seizures and cognitive impairment.

Dingding Shen, Jiali Wan, Xin Zhang, Jiahui Sui, Longwu Zhan, Yuqin Zheng, Yaohui Ni, Qi Zhang

Abstract read
In one paragraph

Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

8 authors.

Dingding Shen *Department of Neurology in Affiliated Hospital of Nantong University, Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Medical School, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China.
Jiali Wan *Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, China.
Xin ZhangKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, China.
Jiahui SuiKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, China.
Longwu ZhanKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, China.
Yuqin ZhengDepartment of Pediatrics, Affiliated Hospital of Nantong University, Medical School, Nantong University, Nantong, China.
Yaohui NiDepartment of Neurology in Affiliated Hospital of Nantong University, Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Medical School, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China. niyaohui200688@126.com.ORCID http://orcid.org/0000-0001-6944-5081
Qi ZhangDepartment of Neurology in Affiliated Hospital of Nantong University, Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Medical School, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China. zhangqi@ntu.edu.cn.ORCID http://orcid.org/0000-0001-7599-6533

Funding

Nantong Science and Technology Bureau MS2024038National Natural Science Foundation of China (National Science Foundation of China) 82271487National Natural Science Foundation of China (National Science Foundation of China) 82371460
6 · The paper itself

Abstract

De novo mutations in voltage- and ligand-gated ion channels have been associated with an increasing number of cases of developmental and epileptic encephalopathies (DEEs), which often fail to respond to classic antiseizure medications. A de novo mutation (c.C316G > A, p.A106T) in the human GABA type-A receptor γ2 subunit gene (GABRG2) has been recurrently identified in patients with DEE. In this study, we generated a knock-in mouse model replicating the human GABRG2(A106T) variation (Gabrg2

Identifiers

PMID41053028
PMCPMC12501280

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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.