Evidence map›Paper›PMID 40571781›Full record

ArticleActa pharmacologica Sinica2025

A rat Satb1 truncation causes neurodevelopmental abnormalities recapitulating the symptoms of patients with SATB1 mutations.

Zhi-Bin Hu, Wei-Tang Liu, Yi-Wei Li, Ling Hu, Ying Huang, Xi-Yue Liu, Qiong Zhang, Yu-Bing Wang, Jia-Yin Chen, Ze-Xuan Li and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta pharmacologica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

15 authors.

Zhi-Bin HuState Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, 200032, China. 20111520014@fudan.edu.cn.
Wei-Tang LiuState Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Yi-Wei LiLaboratory Animal Center, Fudan University, Shanghai, 200032, China.
Ling HuLaboratory Animal Center, Fudan University, Shanghai, 200032, China.
Ying HuangLaboratory Animal Center, Fudan University, Shanghai, 200032, China.
Xi-Yue LiuState Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Qiong ZhangLaboratory Animal Center, Fudan University, Shanghai, 200032, China.
Yu-Bing WangKey Laboratory of Arrhythmias, Ministry of Education, East Hospital, and Department of Anatomy and Neurobiology, Tongji University School of Medicine, Shanghai, 200092, China.
Jia-Yin ChenLaboratory Animal Center, Fudan University, Shanghai, 200032, China.
Ze-Xuan LiLaboratory Animal Center, Fudan University, Shanghai, 200032, China.
Si-Xin TuLaboratory Animal Center, Fudan University, Shanghai, 200032, China.
Li ZhaoState Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Ning-Ning SongLaboratory Animal Center, Fudan University, Shanghai, 200032, China.
Oded KlavirSchool of Psychological Sciences, The University of Haifa, Haifa, 3103301, Israel.
Yu-Qiang DingState Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, 200032, China. dingyuqiang@vip.163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The special AT-rich sequence binding protein 1 (SATB1) has been linked to neurodevelopmental disorders (NDDs) including developmental delay, intellectual disabilities (ID) and autism spectrum disorder (ASD). But the underlying biological mechanisms are still not fully understood. In this study we generated a rat model with a truncated Satb1 protein. We showed that Satb1 mutant caused growth retardation, microcephaly, altered ultrasonic vocalization and delayed neurobehavioral development in mutant pups as well as social and cognitive behavior deficits in adult mutants, mimicking the typical clinical characteristics of SATB1-associated NDDs. Injection of a GABAergic enhancer clonazepam (0.04 mg/kg, i.p.) effectively alleviated the abnormal social and cognitive behaviors in Satb1 mutant rats. Finally, RNA sequencing analysis further revealed a potential role of Satb1 in a cortical transcriptional regulatory network associated with NDDs including ID and ASD. Our results confirm the crucial roles of SATB1 in the pathogenesis of NDDs and provide insights into treatment strategies for SATB1-associated NDDs.

Indexed as

Matrix Attachment Region Binding ProteinsNeurodevelopmental DisordersAnimalsBehavior, AnimalDisease Models, AnimalFemaleHumansMaleMutationRatsRats, Sprague-DawleyMatrix Attachment Region Binding Proteinsintellectual disabilitymicrocephalyneurodevelopmental disordersSATB1 syndrome

Identifiers

PMID40571781
PMCPMC12644705

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.