通过mSin3A进行完全的转录抑制,所需的基因组脱乙酶活性是mSin3A
C A Hassig1, T C Fleischer, A N Billin
1Howard Hughes Medical Institute, Department of Chemistry and Chemical Biology, Harvard University, Cambridge, Massachusetts 02138, USA.
Cell
|May 2, 1997
概括
马德:马克斯蛋白通过mSin3A核心压缩器抑制转录. 这些复合物表现出基因组脱乙酶活性,这表明基因组脱乙化是Mad-Max-mSin3A介导的转录抑制的关键.
科学领域:
- 分子生物学分子生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 蛋白质生物化学 蛋白质生物化学
背景情况:
- 疯狂家族蛋白质与马克斯异构,以抑制转录.
- 通过Mad:Max的转录抑制涉及核心压缩器mSin3A或mSin3B.
- 已知mSin3A是多蛋白质复合体的一部分.
研究的目的:
- 为了研究mSin3A含有复合物的体内成分.
- 为了确定mSin3A复合体是否具有基因素脱乙酶活性.
- 为了阐明基因素脱乙烯化在Mad-Max-mSin3A中介的转录抑制中的作用.
主要方法:
- 从细胞提取物中 mSin3A 的免疫沉.
- 通过蛋白质凝电泳分析对相关的多的分析.
- 在mSin3A免疫复合体中测定基因组脱乙酶活性.
- 记者基因测定用于评估转录抑制.
主要成果:
- mSin3A存在于体内,作为大型异质多蛋白质复合体的一部分.
- 至少有七种多与mSin3A.密切和特定相关.
- 两个mSin3A相关的蛋白质 (p50,p55) 与基因素脱乙酶HDAC1.1有关.
- mSin3A 免疫复合体表现出显著的 ヒ斯脱乙酶活性,对素敏感.
- 素治疗减少了mSin3A介导的记者基因的抑制.
结论:
- mSin3A是大型多蛋白质复合体的组成部分,具有基因素脱乙酶活性.
- 歇斯脱乙烯化被认为是通过Mad-Max-mSin3A复合体进行转录抑制的机制.
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