Evidence map›Paper›PMID 26621702›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

Synaptic P-Rex1 signaling regulates hippocampal long-term depression and autism-like social behavior.

Jun Li, Anping Chai, Lifang Wang, Yuanlin Ma, Zhiliu Wu, Hao Yu, Liwei Mei, Lin Lu, Chen Zhang, Weihua Yue and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing 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

49 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
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  5. Science advances · 2025
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  15. Roles of AMPA receptors in social behaviors.Frontiers in synaptic neuroscience · 2024
    Review
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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

13 authors at 5 institutions in 1 country.

Jun LiInstitute of Mental Health, Sixth Hospital of Peking University, Beijing 100191, China; National Clinical Research Center for Mental Disorders, Ministry of Health (Peking University), Beijing 100191, China; Key Laboratory for Mental Health, Ministry of Health (Peking University), Beijing 100191, China;
Anping ChaiKey Laboratory of Animal Models and Human Disease Mechanisms, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, Yunnan, China; Kunming Institute of Zoology/The Chinese University of Hong Kong Joint Laboratory of Bioresources and Molecular Research in Common Disease, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, Yunnan, China; Laboratory of Learning and Memory, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, Yunnan, China;
Lifang WangInstitute of Mental Health, Sixth Hospital of Peking University, Beijing 100191, China; National Clinical Research Center for Mental Disorders, Ministry of Health (Peking University), Beijing 100191, China; Key Laboratory for Mental Health, Ministry of Health (Peking University), Beijing 100191, China;
Yuanlin MaInstitute of Mental Health, Sixth Hospital of Peking University, Beijing 100191, China; National Clinical Research Center for Mental Disorders, Ministry of Health (Peking University), Beijing 100191, China; Key Laboratory for Mental Health, Ministry of Health (Peking University), Beijing 100191, China;
Zhiliu WuInstitute of Mental Health, Sixth Hospital of Peking University, Beijing 100191, China; National Clinical Research Center for Mental Disorders, Ministry of Health (Peking University), Beijing 100191, China; Key Laboratory for Mental Health, Ministry of Health (Peking University), Beijing 100191, China;
Hao YuInstitute of Mental Health, Sixth Hospital of Peking University, Beijing 100191, China; National Clinical Research Center for Mental Disorders, Ministry of Health (Peking University), Beijing 100191, China; Key Laboratory for Mental Health, Ministry of Health (Peking University), Beijing 100191, China;
Liwei MeiInstitute of Mental Health, Sixth Hospital of Peking University, Beijing 100191, China; National Clinical Research Center for Mental Disorders, Ministry of Health (Peking University), Beijing 100191, China; Key Laboratory for Mental Health, Ministry of Health (Peking University), Beijing 100191, China;
Lin LuInstitute of Mental Health, Sixth Hospital of Peking University, Beijing 100191, China; National Clinical Research Center for Mental Disorders, Ministry of Health (Peking University), Beijing 100191, China; Key Laboratory for Mental Health, Ministry of Health (Peking University), Beijing 100191, China;
Chen ZhangSchool of Life Sciences, Peking University, Beijing 100871, China; Peking University-International Data Group/McGovern Institute for Brain Research, Peking University, Beijing 100871, China;
Weihua YueInstitute of Mental Health, Sixth Hospital of Peking University, Beijing 100191, China; National Clinical Research Center for Mental Disorders, Ministry of Health (Peking University), Beijing 100191, China; Key Laboratory for Mental Health, Ministry of Health (Peking University), Beijing 100191, China;
Lin XuKey Laboratory of Animal Models and Human Disease Mechanisms, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, Yunnan, China; Kunming Institute of Zoology/The Chinese University of Hong Kong Joint Laboratory of Bioresources and Molecular Research in Common Disease, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, Yunnan, China; Laboratory of Learning and Memory, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, Yunnan, China; daizhang@bjmu.edu.cn lxu@vip.163.com.
Yi RaoSchool of Life Sciences, Peking University, Beijing 100871, China; Peking University-International Data Group/McGovern Institute for Brain Research, Peking University, Beijing 100871, China; Peking-Tsinghua Center for Life Sciences, Peking University, Beijing 100871, China;
Dai ZhangInstitute of Mental Health, Sixth Hospital of Peking University, Beijing 100191, China; National Clinical Research Center for Mental Disorders, Ministry of Health (Peking University), Beijing 100191, China; Key Laboratory for Mental Health, Ministry of Health (Peking University), Beijing 100191, China; Peking University-International Data Group/McGovern Institute for Brain Research, Peking University, Beijing 100871, China; Peking-Tsinghua Center for Life Sciences, Peking University, Beijing 100871, China; Shenzhen Key Laboratory for Neuronal Structural Biology, Shenzhen Peking University-Hong Kong University of Science and Technology Medical Center, Shenzhen, 518035, China daizhang@bjmu.edu.cn lxu@vip.163.com.
Peking University · CNPeking University Sixth Hospital · CNChinese Academy of Sciences · CNCenter for Life Sciences · CNChinese Institute for Brain Research · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorders (ASDs) are a group of highly inheritable mental disorders associated with synaptic dysfunction, but the underlying cellular and molecular mechanisms remain to be clarified. Here we report that autism in Chinese Han population is associated with genetic variations and copy number deletion of P-Rex1 (phosphatidylinositol-3,4,5-trisphosphate-dependent Rac exchange factor 1). Genetic deletion or knockdown of P-Rex1 in the CA1 region of the hippocampus in mice resulted in autism-like social behavior that was specifically linked to the defect of long-term depression (LTD) in the CA1 region through alteration of AMPA receptor endocytosis mediated by the postsynaptic PP1α (protein phosphase 1α)-P-Rex1-Rac1 (Ras-related C3 botulinum toxin substrate 1) signaling pathway. Rescue of the LTD in the CA1 region markedly alleviated autism-like social behavior. Together, our findings suggest a vital role of P-Rex1 signaling in CA1 LTD that is critical for social behavior and cognitive function and offer new insight into the etiology of ASDs.

Indexed as

Long-Term Synaptic DepressionSignal TransductionSocial BehaviorAnimalsAutistic DisorderCA1 Region, HippocampalDNA Copy Number VariationsGuanine Nucleotide Exchange FactorsHumansMiceMice, KnockoutReceptors, N-Methyl-D-AspartateSynapsesGuanine Nucleotide Exchange FactorsPREX1 protein, humanReceptors, N-Methyl-D-AspartateAMPA receptor endocytosisautismlong-term depressionP-Rex1social recognition

Identifiers

PMID26621702
PMCPMC4687539
OpenAlexW2188820648

What OpenQuestion 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 OpenQuestion graph.