KDM4A作为α-tubulin去甲基酶,调节微管聚合和细胞分裂
Suhao Cao1,2, Shaogang Wang2,3, Xuan Xie2
1Key Laboratory of Systems Health Science of Zhejiang Province, School of Life Science, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Hangzhou 310024, China.
歇斯脱甲基酶KDM4A从α-tubulin (α-TubK40me3) 中去除三甲基化,调节微管聚合和细胞分裂. 它的缺失导致缺陷,突出了α-TubK40me3平衡的重要性.
科学领域:
- 细胞生物学 细胞生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 分子生物学分子生物学
背景情况:
- 蛋白的翻译后修饰调节了微管的功能.
- 在lysine-40 (α-TubK40me3) 中对α-tubulin的三甲基化影响细胞分裂和神经元发育.
- 负责添加 (SETD2) 和读取 (PBRM1) α-TubK40me3 的酶已知,但"擦除器"仍未确定.
研究的目的:
- 为了确定去除α-TubK40me3.3的酶.
- 研究α-TubK40me3在细胞过程中的动态平衡的作用.
- 了解α-TubK40me3调节对微管子动态和线粒分裂的影响.
主要方法:
- 生物化学试验测试KDM4A对α-tubulin的脱甲基酶活性.
- KDM4A淘汰细胞模型研究其缺失的影响.
- 过度表达的α-tubulin突变体 (α-tubulinK40A) 和诺可达治疗来拯救缺陷.
主要成果:
- KDM4A直接与α-tubulin结合,并作为α-tubulin脱甲基酶起作用.
- KDM4A淘汰导致α-TubK40me3增加,增强微管聚合,以及线粒缺陷.
- 过度表达α-tubulinK40A或诺可达治疗可以挽救KDM4A淘汰诱导的表型.
结论:
- KDM4A被确定为α-TubK40me3.3的擦拭器.
- 通过KDM4A介导的脱甲基化对于维持微管聚合和细胞分裂至关重要.
- α-TubK40me3的动态调节对于正常的细胞功能至关重要.
更多相关视频
07:54Purification of Tubulin with Controlled Posttranslational Modifications and Isotypes from Limited Sources by Polymerization-Depolymerization Cycles
Published on: November 5, 2020
08:33Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis
Published on: December 5, 2017
相关概念视频
Destabilization of Microtubules
Drugs that Stabilize Microtubules
Microtubule Instability
Microtubule Associated Proteins (MAPs)
Drugs that Destabilize Microtubules
M-Cdk Drives Transition Into Mitosis
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
