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2
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本文引用的文献

1
TRIM28 mediates primer binding site-targeted silencing of murine leukemia virus in embryonic cells.TRIM28介导胚胎细胞中小鼠白血病病毒的引物结合位点靶向沉默。
Cell. 2007 Oct 5;131(1):46-57. doi: 10.1016/j.cell.2007.07.026.
2
The KAP1 corepressor functions to coordinate the assembly of de novo HP1-demarcated microenvironments of heterochromatin required for KRAB zinc finger protein-mediated transcriptional repression.KAP1 共抑制因子发挥作用，协调从头组装由 HP1 划定的异染色质微环境，这是 KRAB 锌指蛋白介导的转录抑制所必需的。
Mol Cell Biol. 2006 Nov;26(22):8623-38. doi: 10.1128/MCB.00487-06. Epub 2006 Sep 5.
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Association of the transcriptional corepressor TIF1beta with heterochromatin protein 1 (HP1): an essential role for progression through differentiation.转录共抑制因子TIF1β与异染色质蛋白1（HP1）的关联：在分化进程中的关键作用
Genes Dev. 2004 Sep 1;18(17):2147-60. doi: 10.1101/gad.302904.
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SETDB1: a novel KAP-1-associated histone H3, lysine 9-specific methyltransferase that contributes to HP1-mediated silencing of euchromatic genes by KRAB zinc-finger proteins.SETDB1：一种新型的与KAP-1相关的组蛋白H3赖氨酸9特异性甲基转移酶，它通过KRAB锌指蛋白促进HP1介导的常染色质基因沉默。
Genes Dev. 2002 Apr 15;16(8):919-32. doi: 10.1101/gad.973302.
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Targeting histone deacetylase complexes via KRAB-zinc finger proteins: the PHD and bromodomains of KAP-1 form a cooperative unit that recruits a novel isoform of the Mi-2alpha subunit of NuRD.通过KRAB锌指蛋白靶向组蛋白去乙酰化酶复合物：KAP-1的PHD和溴结构域形成一个协同单元，招募NuRD的Mi-2α亚基的一种新型异构体。
Genes Dev. 2001 Feb 15;15(4):428-43. doi: 10.1101/gad.869501.
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Lack of shielding of primer binding site silencer-mediated repression of an internal promoter in a retrovirus vector by the putative insulators scs, BEAD-1, and HS4.假定的绝缘子scs、BEAD-1和HS4对逆转录病毒载体中内部启动子的引物结合位点沉默子介导的抑制作用缺乏屏蔽。
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Molecular determinants for targeting heterochromatin protein 1-mediated gene silencing: direct chromoshadow domain-KAP-1 corepressor interaction is essential.靶向异染色质蛋白1介导的基因沉默的分子决定因素：直接的染色质阴影结构域与KAP-1共抑制因子相互作用至关重要。
Mol Cell Biol. 2000 Sep;20(17):6449-65. doi: 10.1128/MCB.20.17.6449-6465.2000.
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EMBO J. 1996 Dec 2;15(23):6701-15.
9
KAP-1, a novel corepressor for the highly conserved KRAB repression domain.KAP-1，一种用于高度保守的KRAB抑制结构域的新型共抑制因子。
Genes Dev. 1996 Aug 15;10(16):2067-78. doi: 10.1101/gad.10.16.2067.
10
Non-function of a Moloney murine leukaemia virus regulatory sequence in F9 embryonal carcinoma cells.莫洛尼鼠白血病病毒调控序列在F9胚胎癌细胞中的无功能状态
Nature. 1984;308(5958):470-2. doi: 10.1038/308470a0.

鼠白血病病毒的引物结合位点依赖性限制需要TRIM28与HP1结合。

Primer binding site-dependent restriction of murine leukemia virus requires HP1 binding by TRIM28.

作者信息

Wolf Daniel, Cammas Florence, Losson Régine, Goff Stephen P

机构信息

Department of Biochemistry and Molecular Biophysics, Howard Hughes Medical Institute, Columbia University, HHSC 1310, 701 West 168th Street, New York, NY 10032, USA.

出版信息

J Virol. 2008 May;82(9):4675-9. doi: 10.1128/JVI.02445-07. Epub 2008 Feb 20.

DOI:10.1128/JVI.02445-07
PMID:18287239
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2293057/
Abstract

TRIM28 is a transcriptional corepressor which is required for primer binding site (PBS)-dependent restriction of murine leukemia virus (MLV) replication in embryonic stem and embryonic carcinoma (EC) cells. PBS-dependent restriction of MLV leads to transcriptional silencing of the integrated provirus and has been shown to correlate with TRIM28-mediated recruitment of HP1 to the silenced loci. Here we show, using a cell line with a point mutation in the HP1 binding domain of TRIM28, that interaction with HP1 is absolutely required for the PBS-dependent restriction of MLV in the F9 EC cell line.

摘要

TRIM28是一种转录共抑制因子，它是胚胎干细胞和胚胎癌细胞（EC）中鼠白血病病毒（MLV）复制的引物结合位点（PBS）依赖性限制所必需的。MLV的PBS依赖性限制导致整合前病毒的转录沉默，并且已证明与TRIM28介导的HP1募集到沉默位点相关。在这里，我们使用在TRIM28的HP1结合域中具有点突变的细胞系表明，在F9 EC细胞系中，与HP1的相互作用对于MLV的PBS依赖性限制是绝对必需的。