Evidence map›Paper›PMID 41217685›Full record

ArticleMolecular neurobiology2025

Gcm1 Orchestrates Lef1 Expression in Folate Deficiency-Induced Neural Tube Defects.

Zhihua Cao, Lu Li, Xiaolong Gu, Baolian Li, Qi Xie, Xuefen Wu, Xinhuan Zhang, Guohua Zhang, Ke Wu, Wenbing Ren and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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.

Zhihua Cao *Department of Biochemistry and Molecular Biology, College of Basic Medicine, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan, 030001, PR China.
Lu Li *Department of Biochemistry and Molecular Biology, College of Basic Medicine, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan, 030001, PR China.
Xiaolong Gu *Department of Biochemistry and Molecular Biology, College of Basic Medicine, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan, 030001, PR China.
Baolian LiDepartment of Gynecology, Lvliang People's Hospital, Lvliang, 033000, PR China.
Qi XieDepartment of Biochemistry and Molecular Biology, College of Basic Medicine, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan, 030001, PR China.
Xuefen WuDepartment of Biochemistry and Molecular Biology, College of Basic Medicine, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan, 030001, PR China.
Xinhuan ZhangDepartment of Obstetrics, First Clinical College of Shanxi Medical University, Taiyuan, 030001, PR China.
Guohua ZhangDepartment of Obstetrics, First Clinical College of Shanxi Medical University, Taiyuan, 030001, PR China.
Ke WuAcademy of Medical Sciences, Shanxi Medical University, Taiyuan, 030001, PR China.
Wenbing RenDepartment of Biochemistry and Molecular Biology, College of Basic Medicine, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan, 030001, PR China.
Zhizhen LiuDepartment of Biochemistry and Molecular Biology, College of Basic Medicine, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan, 030001, PR China.
Aili FangDepartment of Anesthesiology, Bethune Hospital of Shanxi Medical University, Taiyuan, 030001, PR China.
Shenghui LuDepartment of Obstetrics, First Clinical College of Shanxi Medical University, Taiyuan, 030001, PR China. lushenghui90028@163.com.
Qiu XieState Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100850, China. xieqiu1999@126.com.
Jianting LiDepartment of Biochemistry and Molecular Biology, College of Basic Medicine, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan, 030001, PR China. lijianting2021@sxmu.edu.cn.

Funding

Education Graduate Research and Innovation Project of Shanxi Provincial Department 2024KY354National Natural Science Foundation of China 82201841Open Project Fund from Key Laboratory of Coal Environmental Pathogenicity and Prevention (Shanxi Medical University) Ministy of Education, China CEPPOPF 202407Open Research Fund of National Health Commission Key Laboratory of Birth Defects Prevention NHCKLBDP202501Shanxi Basic Research Program 202203021212369Shanxi Basic Research Program 202203021221245Shanxi Basic Research Program 202403021221156Shanxi Province Higher Education"Billion Project" Science and Technology Guidance Project BYBLD006
6 · The paper itself

Abstract

Neural tube defects (NTDs) are severe congenital anomalies with limited therapeutic options. Increased expression of the transcription factor glial cell missing 1 (Gcm1) has been linked to NTDs, yet the mechanisms underlying this association remain elusive. Herein, folate deficiency upregulated Gcm1 expression through H4 acetylation (H4ac) enrichment in the promoter. ChIP-qPCR and Co-IP experiments revealed that folate deficiency enhanced H4 acetylation at the Gcm1 promoter via CREB-binding protein (CBP), subsequently resulting in increased Gcm1 transcription. Furthermore, Gcm1-ChIP-seq revealed lymphoid enhancer binding factor 1 (Lef1) as a potential downstream target of Gcm1 in mESCs without folate supplementation and the likely activator of the Wnt/β-catenin pathway for aberrant neurodevelopment. Immunohistochemistry and immunofluorescence analyses revealed significantly higher Gcm1 and Lef1 expression in a low-folate NTD mouse model than in controls. Finally, NanoString analysis of human low-folate NTD samples confirmed a positive correlation between upregulated Gcm1 expression and Lef1 expression. Collectively, these findings indicate that the CBP-dependent Gcm1 regulation of Lef1 expression is crucial in folate-deficient NTDs, revealing the potential mechanism by which NTDs are induced by low folate concentrations and providing a promising target for therapeutic intervention.

Indexed as

Folic Acid DeficiencyLymphoid Enhancer-Binding Factor 1Neural Tube DefectsNuclear ProteinsTranscription FactorsAcetylationAnimalsDNA-Binding ProteinsHumansMicePromoter Regions, GeneticUp-RegulationDNA-Binding ProteinsLef1 protein, mouseLymphoid Enhancer-Binding Factor 1Nuclear ProteinsTranscription FactorsAcetylationCREB-binding proteinGlial cell missing 1Lymphoid enhancer binding factor 1Neural tube defects

Identifiers

PMID41217685
PMCPMC12605484

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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.