基因素H2B的阿波性酸化是由哺乳动物无菌二十基因酶介导的
Wang L Cheung1, Kozo Ajiro, Kumiko Samejima
1Department of Microbiology, University of Virginia Health System, Charlottesville 22908, USA.
Cell
|May 22, 2003
概括
编程细胞死亡涉及质子的修饰. 研究人员发现,基素H2B在氨酸14的酸化与亡有关,由酶分裂的Mst1激酶调节.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 细胞DNA与基因素蛋白结合,影响染色体结构.
- 亡的标志,如染色体凝聚,可以通过翻译后的基因组修饰来调节.
研究的目的:
- 为了研究基因组修饰在亡中的作用.
- 在编程细胞死亡过程中识别特定的质子修饰和对其负责的激酶.
主要方法:
- 在14 (S14) 中对基因素H2B酸化与脊椎动物细胞中亡的相关分析.
- 鉴定和表征H2B S14激酶活性在亡细胞中.
- 在体外和体外的酸化试验中,使用Mst1激酶和 histone H2B.
主要成果:
- 在各种脊椎动物物种中,在经历了细胞亡的细胞中观察到S14处的组合素H2B的酸化.
- 发现一种34 kDa的激酶,被识别为caspase-cleaved哺乳动物无菌20 (Mst1) 激酶,可在S14处诱导H2B酸化.
- H2B S14酸化取决于Mst1被酶-3分裂,这表明与亡途径有直接联系.
结论:
- 在S14处的histon H2B酸化是一种与apoptotic染色体相关的保存修饰.
- 卡斯巴酶分离的Mst1激酶是亡过程中这种特定基因素修饰的关键调节者.
- 这些发现表明了编程细胞死亡的新机制,并提出了潜在的"核突组织细胞代码".
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