Evidence map›Paper›PMID 40716012›Full record

ArticleNeuroscience bulletin2025

USP47 Regulates Excitatory Synaptic Plasticity and Modulates Seizures in Murine Models by Blocking Ubiquitinated AMPAR Degradation.

Juan Yang, Haiqing Zhang, You Wang, Yuemei Luo, Weijin Zheng, Yong Liu, Qian Jiang, Jing Deng, Qiankun Liu, Peng Zhang and 4 more

Abstract read
In one paragraph

Article in Neuroscience bulletin, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

14 authors.

Juan Yang *Department of Neurology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Haiqing Zhang *Department of Neurology, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, China.
You WangDepartment of Neurology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Yuemei LuoDepartment of Neurology, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, China.
Weijin ZhengDepartment of Health Management, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, China.
Yong LiuDepartment of Neurology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Qian JiangDepartment of Neurology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Jing DengDepartment of Neurology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Qiankun LiuDepartment of Neurology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Peng ZhangDepartment of Neurology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Hao HuangDepartment of Neurology, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, China.
Changyin YuDepartment of Neurology, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, China. yuchangyin68@163.com.ORCID http://orcid.org/0000-0002-4529-9750
Zucai XuDepartment of Neurology, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, China. docxzc@zmu.edu.cn.ORCID http://orcid.org/0000-0002-6849-7928
Yangmei ChenDepartment of Neurology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China. 300249@cqmu.edu.cn.ORCID http://orcid.org/0000-0003-4475-3883

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epilepsy is a chronic neurological disorder affecting ~65 million individuals worldwide. Abnormal synaptic plasticity is one of the most important pathological features of this condition. We investigated how ubiquitin-specific peptidase 47 (USP47) influences synaptic plasticity and its link to epilepsy. We found that USP47 enhanced excitatory postsynaptic transmission and increased the density of total dendritic spines and the proportion of mature dendritic spines. Furthermore, USP47 inhibited the degradation of the ubiquitinated α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) subunit glutamate receptor 1 (GluR1), which is associated with synaptic plasticity. In addition, elevated levels of USP47 were found in epileptic mice, and USP47 knockdown reduced the frequency and duration of seizure-like events and alleviated epileptic seizures. To summarize, we present a new mechanism whereby USP47 regulates excitatory postsynaptic plasticity through the inhibition of ubiquitinated GluR1 degradation. Modulating USP47 may offer a potential approach for controlling seizures and modifying disease progression in future therapeutic strategies.

Indexed as

Neuronal PlasticityReceptors, AMPASeizuresUbiquitin ThiolesteraseAnimalsDendritic SpinesDisease Models, AnimalExcitatory Postsynaptic PotentialsHippocampusMaleMiceMice, Inbred C57BLUbiquitinationReceptors, AMPAUbiquitin ThiolesteraseEpilepsyGlutamate receptor 1Protein degradationSynaptic plasticityUbiquitin-specific protease 47

Identifiers

PMID40716012
PMCPMC12494536

What Socratic holds

Textmetadata
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.