Evidence map›Paper›PMID 39265888›Full record

ArticleJournal of advanced research2025

Haploinsufficiency of intraflagellar transport protein 172 causes autism-like behavioral phenotypes in mice through BDNF.

Nanxi Zheng, Shilin Luo, Xin Zhang, Ling Hu, Muzhi Huang, Mingyu Li, Colin McCaig, Yu-Qiang Ding, Bing Lang

Abstract read
In one paragraph

Article in Journal of advanced research, 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. 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

9 authors.

Nanxi ZhengDepartment of Psychiatry, National Clinical Research Center for Mental Disorders and National Center for Mental Disorders, The Second Xiangya Hospital, Central South University, Changsha 410011, China; Department of Psychiatry, Fujian Medical University Affiliated Fuzhou Neuropsychiatric Hospital, Fuzhou 350005, China.
Shilin LuoDepartment of Neurology, Xiangya Hospital of Central South University, Changsha 410008, China; National Clinical Research Center for Geriatric Disorder, Central South University, Changsha, China; Engineering Research Center of Human Province in Cognitive Impairment Disorders, Changsha 410008, China.
Xin ZhangCollege of Pharmaceutical Science, Zhejiang University of Technology, Hangzhou 310014, China.
Ling HuState Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, 200433 Shanghai, China.
Muzhi HuangDepartment of Psychiatry, National Clinical Research Center for Mental Disorders and National Center for Mental Disorders, The Second Xiangya Hospital, Central South University, Changsha 410011, China.
Mingyu LiDepartment of Psychiatry, National Clinical Research Center for Mental Disorders and National Center for Mental Disorders, The Second Xiangya Hospital, Central South University, Changsha 410011, China.
Colin McCaigSchool of Medicine, Medical Sciences & Nutrition, Institute of Medical Sciences, University of Aberdeen, Foresterhill, AB25 2ZD Aberdeen, Scotland, UK.
Yu-Qiang DingState Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, 200433 Shanghai, China.
Bing LangDepartment of Psychiatry, National Clinical Research Center for Mental Disorders and National Center for Mental Disorders, The Second Xiangya Hospital, Central South University, Changsha 410011, China. Electronic address: bing.lang@csu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionPrimary cilia are hair-like solitary organelles growing on most mammalian cells that play fundamental roles in embryonic patterning and organogenesis. Defective cilia often cause a suite of inherited diseases called ciliopathies with multifaceted manifestations. Intraflagellar transport (IFT), a bidirectional protein trafficking along the cilium, actively facilitates the formation and absorption of primary cilia. IFT172 is the largest component of the IFT-B complex, and its roles in Bardet-Biedl Syndrome (BBS) have been appreciated with unclear mechanisms.

objectivesWe performed a battery of behavioral tests with Ift172 haploinsufficiency (Ift172

resultsIft172

conclusionsOur data suggest that Ift172 per se drives neurotrophic effects and, when defective, could cause neurodevelopmental disorders reminiscent of autism-like disorders.

Indexed as

Autistic DisorderBrain-Derived Neurotrophic FactorHaploinsufficiencyAnimalsBehavior, AnimalCiliaDisease Models, AnimalHippocampusMaleMiceMice, Inbred C57BLPhenotypeSignal TransductionBdnf protein, mouseBrain-Derived Neurotrophic FactorAutism spectrum disordersBardet Biedl SyndromeBDNFIntraflagellar transport protein 172Primary ciliaSonic Hedgehog

Identifiers

PMID39265888
PMCPMC12225924

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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.