失去KDM5A介导的H3K4me3脱甲基化,通过Wnt/β-catenin通路激活促进异常的神经发育

Jianting Li1, Yuxiang Liang1,2, Zhihua Cao1

  • 1Department 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, China.

Cell death & disease
|November 20, 2025
PubMed
概括

叶酸缺乏会增加Wnt目标基因的表观遗传标记,激活Wnt信号,并导致神经管缺陷 (NTD). 减少KDM5A的表达是这一过程的关键,这表明KDM5A是NTD的治疗点.

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