Jove
Visualize
联系我们
JoVE
x logofacebook logolinkedin logoyoutube logo
关于 JoVE
概览领导团队博客JoVE 帮助中心
作者
出版流程编辑委员会范围与政策同行评审常见问题投稿
图书馆员
用户评价订阅访问资源图书馆顾问委员会常见问题
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experiments存档
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教师资源中心教师网站
使用条款与条件
隐私政策
政策

相关概念视频

您也可能阅读

相关文章

通过共同作者、期刊和引用图与本文相关的文章。

排序
Same author

ARID1A loss drives gastric signet ring cell carcinoma by regulating mucin production and secretion.

Nature communications·2026
Same author

Glioblastoma-Secreted C1QL1 Orchestrates Tumor Microtube Expansion and Neural Synaptic Pruning to Drive Malignant Synapse Formation and Recurrence.

Cancer discovery·2026
Same author

Glioblastoma exploits ATP from leading-edge astrocytes to fuel its infiltrative growth revealed by spatially resolved chimeric analysis.

Science advances·2025
Same author

EZH2 loss promotes gastric squamous cell carcinoma.

Nature communications·2025
Same author

Acquired resistance to immunotherapy by physical barriers with cancer cell-expressing collagens in non-small cell lung cancer.

Proceedings of the National Academy of Sciences of the United States of America·2025
Same author

The Immunomechanical Checkpoint PYK2 Governs Monocyte-to-Macrophage Differentiation in Pancreatic Cancer.

Cancer discovery·2025

相关实验视频

Updated: Sep 19, 2025

The Mouse Hindbrain As a Model for Studying Embryonic Neurogenesis
11:39

The Mouse Hindbrain As a Model for Studying Embryonic Neurogenesis

Published on: January 29, 2018

10.1K

胚胎神经发生所需的表观遗传阅读器PHF23

Yue Wen1,2,3, Ping He1, Zongyao Huang1

  • 1Department of Neurosurgery, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu 610041, China.

The Journal of neuroscience : the official journal of the Society for Neuroscience
|May 30, 2025
PubMed
概括

PHF23对胚胎大脑发育至关重要,通过与HDAC2.2相互作用来调节神经发生. 它的缺失导致皮质缺陷,由于阻断了放射性质细胞分化.

关键词:
在PHD指的蛋白质.在 PHF2323 中.表观遗传学是指表观遗传学.神经干细胞的神经干细胞神经发生神经发生.

更多相关视频

Induction of Protein Deletion Through In Utero Electroporation to Define Deficits in Neuronal Migration in Transgenic Models
12:01

Induction of Protein Deletion Through In Utero Electroporation to Define Deficits in Neuronal Migration in Transgenic Models

Published on: January 12, 2015

10.3K
Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells NPCs
10:47

Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells NPCs

Published on: March 2, 2018

10.1K

相关实验视频

Last Updated: Sep 19, 2025

The Mouse Hindbrain As a Model for Studying Embryonic Neurogenesis
11:39

The Mouse Hindbrain As a Model for Studying Embryonic Neurogenesis

Published on: January 29, 2018

10.1K
Induction of Protein Deletion Through In Utero Electroporation to Define Deficits in Neuronal Migration in Transgenic Models
12:01

Induction of Protein Deletion Through In Utero Electroporation to Define Deficits in Neuronal Migration in Transgenic Models

Published on: January 12, 2015

10.3K
Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells NPCs
10:47

Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells NPCs

Published on: March 2, 2018

10.1K

科学领域:

  • 神经科学是一个神经科学.
  • 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
  • 发展生物学 发展生物学

背景情况:

  • 在胚胎发育过程中,表观遗传机制对神经发生至关重要.
  • 植物宿主群 (PHD) 指蛋白是参与发育的表观遗传读者,但它们在胚胎神经生成中的作用尚不清楚.

研究的目的:

  • 研究PHF23的作用,一个PHD指蛋白,在胚胎神经发生.
  • 确定PHF23调节神经元分化的分子机制.

主要方法:

  • 在神经发生过程中对PHD手指蛋白的差异表达分析.
  • 利用小鼠模型 (Phf23淘汰) 来研究神经发生.
  • 研究了蛋白质与蛋白质的相互作用 (PHF23-HDAC2) 和组织蛋白修饰 (H3K27ac).

主要成果:

  • PHF23在辐射质细胞 (RGC) 和中间原生细胞 (IPC) 中表达很高,但不是神经元.
  • Phf23淘汰小鼠表现出与RGC分化阻塞相关的皮质发育缺陷.
  • PHF23抑制了HDAC2的活性,防止了H3K27ac的脱乙化,并促进了神经元基因表达 (例如,Tcf4,Eya1).
  • Tcf4过度表达在Phf23-knockout神经干细胞中挽救了分化缺陷.

结论:

  • PHF23是胚胎神经发生和皮质发育的关键调节者.
  • PHF23通过调节HDAC2活性来控制素乙化和基因表达而起作用.
  • 这些发现突显了PHD指蛋白在神经发生过程中的细胞类型特异性功能.