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本文引用的文献

1
Role of Bmi-1 and Ring1A in H2A ubiquitylation and Hox gene silencing.Bmi-1和Ring1A在H2A泛素化及Hox基因沉默中的作用。
Mol Cell. 2005 Dec 22;20(6):845-54. doi: 10.1016/j.molcel.2005.12.002.
2
Mammalian polyhomeotic homologues Phc2 and Phc1 act in synergy to mediate polycomb repression of Hox genes.哺乳动物多同源异型蛋白同源物Phc2和Phc1协同作用，介导对Hox基因的多梳抑制。
Mol Cell Biol. 2005 Aug;25(15):6694-706. doi: 10.1128/MCB.25.15.6694-6706.2005.
3
Ink4a and Arf differentially affect cell proliferation and neural stem cell self-renewal in Bmi1-deficient mice.Ink4a和Arf对Bmi1基因缺陷小鼠的细胞增殖和神经干细胞自我更新有不同影响。
Genes Dev. 2005 Jun 15;19(12):1438-43. doi: 10.1101/gad.1299305.
4
Bmi-1 promotes neural stem cell self-renewal and neural development but not mouse growth and survival by repressing the p16Ink4a and p19Arf senescence pathways.Bmi-1通过抑制p16Ink4a和p19Arf衰老途径来促进神经干细胞自我更新和神经发育，但不影响小鼠的生长和存活。
Genes Dev. 2005 Jun 15;19(12):1432-7. doi: 10.1101/gad.1299505.
5
Pocket proteins and cell cycle control.口袋蛋白与细胞周期调控。
Oncogene. 2005 Apr 18;24(17):2796-809. doi: 10.1038/sj.onc.1208619.
6
Biochemical and cellular mechanisms of mammalian CDK inhibitors: a few unresolved issues.哺乳动物细胞周期蛋白依赖性激酶抑制剂的生化与细胞机制：一些未解决的问题
Oncogene. 2005 Apr 18;24(17):2787-95. doi: 10.1038/sj.onc.1208611.
7
Role of histone H2A ubiquitination in Polycomb silencing.组蛋白H2A泛素化在多梳蛋白介导的基因沉默中的作用。
Nature. 2004 Oct 14;431(7010):873-8. doi: 10.1038/nature02985. Epub 2004 Sep 22.
8
Hierarchical recruitment of polycomb group silencing complexes.多梳蛋白组沉默复合体的分层募集
Mol Cell. 2004 Jun 4;14(5):637-46. doi: 10.1016/j.molcel.2004.05.009.
9
Polycomb complexes and silencing mechanisms.多梳复合体与沉默机制。
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10
Bmi-1 regulation of INK4A-ARF is a downstream requirement for transformation of hematopoietic progenitors by E2a-Pbx1.Bmi-1对INK4A-ARF的调控是E2a-Pbx1转化造血祖细胞的下游必要条件。
Mol Cell. 2003 Aug;12(2):393-400. doi: 10.1016/s1097-2765(03)00277-6.

pRB家族蛋白是H3K27三甲基化以及多梳抑制复合物结合并沉默p16INK4α肿瘤抑制基因所必需的。

pRB family proteins are required for H3K27 trimethylation and Polycomb repression complexes binding to and silencing p16INK4alpha tumor suppressor gene.

作者信息

Kotake Yojiro, Cao Ru, Viatour Patrick, Sage Julien, Zhang Yi, Xiong Yue

机构信息

Department of Biochemistry and Biophysics, Lineberger Comprehensive Cancer Center, Program in Molecular Biology and Biotechnology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.

出版信息

Genes Dev. 2007 Jan 1;21(1):49-54. doi: 10.1101/gad.1499407.

DOI:10.1101/gad.1499407
PMID:17210787
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1759899/
Abstract

Genetic studies have demonstrated that Bmi1 promotes cell proliferation and stem cell self-renewal with a correlative decrease of p16(INK4a) expression. Here, we demonstrate that Polycomb genes EZH2 and BMI1 repress p16 expression in human and mouse primary cells, but not in cells deficient for pRB protein function. The p16 locus is H3K27-methylated and bound by BMI1, RING2, and SUZ12. Inactivation of pRB family proteins abolishes H3K27 methylation and disrupts BMI1, RING2, and SUZ12 binding to the p16 locus. These results suggest a model in which pRB proteins recruit PRC2 to trimethylate p16, priming the BMI1-containing PRC1L ubiquitin ligase complex to silence p16.

摘要

基因研究表明，Bmi1可促进细胞增殖和干细胞自我更新，同时p16(INK4a)表达相应降低。在此，我们证明多梳基因EZH2和BMI1在人和小鼠原代细胞中抑制p16表达，但在pRB蛋白功能缺陷的细胞中则不然。p16基因座发生H3K27甲基化，并与BMI1、RING2和SUZ12结合。pRB家族蛋白的失活消除了H3K27甲基化，并破坏了BMI1、RING2和SUZ12与p16基因座的结合。这些结果提示了一种模型，即pRB蛋白招募PRC2使p16发生三甲基化，从而启动含BMI1的PRC1L泛素连接酶复合体使p16沉默。