Evidence map›Paper›PMID 40277210›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025

Dietary Intake of Octanoic Acid Restores UBE3A Expression and Improves the Behavioral Phenotypes in a Mouse Model of Angelman Syndrome.

Song Qu, Xingying Guan, Hongyan Li, Jian Yang, Pu Sun, Cui Song, Natalia Surzenko, Yanyan Wang

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. 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

8 authors.

Song QuDepartment of Medical Genetics, College of Basic Medical Science, Army Medical University (Third Military Medical University), Chongqing, China.
Xingying GuanDepartment of Medical Genetics, College of Basic Medical Science, Army Medical University (Third Military Medical University), Chongqing, China.
Hongyan LiDepartment of Medical Genetics, College of Basic Medical Science, Army Medical University (Third Military Medical University), Chongqing, China.
Jian YangUndergraduate Student Brigade, College of Basic Medical Science, Army Medical University (Third Military Medical University), Chongqing, China.
Pu SunMaternal and Child Health Hospital of Yongchuan District, Chongqing, China.
Cui SongDepartment of Endocrinology and Genetic Metabolism Disease, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatrics, Children's Hospital of Chongqing Medical University, Chongqing, China.
Natalia SurzenkoStandard Process Inc., Kannapolis, North Carolina, USA.ORCID https://orcid.org/0009-0004-5816-7425
Yanyan WangDepartment of Medical Genetics, College of Basic Medical Science, Army Medical University (Third Military Medical University), Chongqing, China.ORCID https://orcid.org/0000-0002-6312-206X

Funding

Chongqing Municipal Education Commission Foundation CYS23764CSTC | Chongqing Science and Technology Foundation cstc2021jcyj-msxmX0329MOST | National Natural Science Foundation of China (NSFC) 82171852
6 · The paper itself

Abstract

Angelman syndrome (AS) is a severe neurodevelopmental disorder with no effective therapies. Most of the behavioral deficits observed in AS patients arise from the absence of ubiquitin protein ligase E3A (UBE3A) in the brain during development, driven by the loss of maternally expressed UBE3A and silencing of the paternal copy of this gene through imprinting. Safe and effective therapies aiming at restoring the expression of the paternal UBE3A gene early in human life are currently lacking. In this study, we investigated whether octanoic acid (OA), a medium-chain fatty acid, could unsilence the paternal Ube3a allele in neurons and ameliorate the behavioral defects in a murine model of AS. To this end, Ube3a

Indexed as

Angelman SyndromeBehavior, AnimalCaprylatesUbiquitin-Protein LigasesAnimalsDisease Models, AnimalFemaleMaleMiceMice, Inbred C57BLNeuronsPhenotypeCaprylatesoctanoic acidUbe3a protein, mouseUbiquitin-Protein LigasesAngelman syndromedendritic spineimprintingoctanoic acidUbe3a

Identifiers

PMID40277210
PMCPMC12023718

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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.