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1
Association of p107 with Sp1: genetically separable regions of p107 are involved in regulation of E2F- and Sp1-dependent transcription.p107与Sp1的关联:p107的基因可分离区域参与E2F和Sp1依赖性转录的调控。
Mol Cell Biol. 1995 Oct;15(10):5444-52. doi: 10.1128/MCB.15.10.5444.
2
Differential roles of two tandem E2F sites in repression of the human p107 promoter by retinoblastoma and p107 proteins.视网膜母细胞瘤蛋白和p107蛋白通过两个串联E2F位点对人p107启动子的抑制作用中的差异作用
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3
E2F4-RB and E2F4-p107 complexes suppress gene expression by transforming growth factor beta through E2F binding sites.E2F4-RB和E2F4-p107复合物通过E2F结合位点转化生长因子β来抑制基因表达。
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4
Transcription factors of the Sp1 family: interaction with E2F and regulation of the murine thymidine kinase promoter.Sp1家族转录因子:与E2F的相互作用及对小鼠胸苷激酶启动子的调控
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Cell Growth Differ. 1995 Oct;6(10):1287-98.
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The p107 tumor suppressor induces stable E2F DNA binding to repress target promoters.p107肿瘤抑制因子诱导E2F与DNA稳定结合,从而抑制靶启动子。
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E2F-independent transcriptional repression by p107, a member of the retinoblastoma family of proteins.视网膜母细胞瘤蛋白家族成员p107的E2F非依赖性转录抑制作用。
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C/EBPalpha regulates formation of S-phase-specific E2F-p107 complexes in livers of newborn mice.C/EBPα调节新生小鼠肝脏中S期特异性E2F-p107复合物的形成。
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CDP/cut is the DNA-binding subunit of histone gene transcription factor HiNF-D: a mechanism for gene regulation at the G1/S phase cell cycle transition point independent of transcription factor E2F.CDP/cut是组蛋白基因转录因子HiNF-D的DNA结合亚基:一种在G1/S期细胞周期转换点独立于转录因子E2F进行基因调控的机制。
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10
E2F binding is required but not sufficient for repression of B-myb transcription in quiescent fibroblasts.在静止的成纤维细胞中,E2F结合对于抑制B-myb转录是必需的,但并不充分。
Oncogene. 1996 Sep 5;13(5):1073-82.

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Next-generation sequencing reveals regional differences of the α-synuclein methylation state independent of Lewy body disease.下一代测序揭示了α-突触核蛋白甲基化状态的区域差异,与路易体病无关。
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The papillomavirus E7 oncoprotein is ubiquitinated by UbcH7 and Cullin 1- and Skp2-containing E3 ligase.乳头瘤病毒E7癌蛋白被UbcH7以及含Cullin 1和Skp2的E3连接酶进行泛素化修饰。
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Stability of the Sp3-DNA complex is promoter-specific: Sp3 efficiently competes with Sp1 for binding to promoters containing multiple Sp-sites.Sp3-DNA复合物的稳定性具有启动子特异性:Sp3能有效地与Sp1竞争,以结合含有多个Sp位点的启动子。
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RelA-associated inhibitor blocks transcription of human immunodeficiency virus type 1 by inhibiting NF-kappaB and Sp1 actions.RelA相关抑制剂通过抑制核因子κB(NF-κB)和Sp1的作用来阻断1型人类免疫缺陷病毒的转录。
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10
E2F mediates induction of the Sp1-controlled promoter of the human DNA polymerase epsilon B-subunit gene POLE2.E2F介导人DNA聚合酶ε B亚基基因POLE2的Sp1调控启动子的诱导。
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本文引用的文献

1
Sp-1 binds promoter elements regulated by the RB protein and Sp-1-mediated transcription is stimulated by RB coexpression.Sp-1结合由RB蛋白调控的启动子元件,并且RB共表达可刺激Sp-1介导的转录。
Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3265-9. doi: 10.1073/pnas.90.8.3265.
2
Interactions of the p107 and Rb proteins with E2F during the cell proliferation response.细胞增殖反应过程中p107和Rb蛋白与E2F的相互作用。
EMBO J. 1993 Mar;12(3):1013-20. doi: 10.1002/j.1460-2075.1993.tb05742.x.
3
Human papillomavirus type 16 E7 associates with a histone H1 kinase and with p107 through sequences necessary for transformation.16型人乳头瘤病毒E7通过转化所需的序列与组蛋白H1激酶和p107相关联。
J Virol. 1993 May;67(5):2521-8. doi: 10.1128/JVI.67.5.2521-2528.1993.
4
The v-Rel oncoprotein increases expression from Sp1 site-containing promoters in chicken embryo fibroblasts.v-Rel癌蛋白可增加鸡胚成纤维细胞中含Sp1位点启动子的表达。
Oncogene. 1993 Sep;8(9):2501-9.
5
Evidence for physical interaction between the zinc-finger transcription factors YY1 and Sp1.锌指转录因子YY1和Sp1之间存在物理相互作用的证据。
Proc Natl Acad Sci U S A. 1993 Jul 1;90(13):6145-9. doi: 10.1073/pnas.90.13.6145.
6
Inhibition of cell proliferation by p107, a relative of the retinoblastoma protein.视网膜母细胞瘤蛋白相关蛋白p107对细胞增殖的抑制作用。
Genes Dev. 1993 Jul;7(7A):1111-25. doi: 10.1101/gad.7.7a.1111.
7
Transcription from TATA-less promoters: dihydrofolate reductase as a model.无TATA框启动子的转录:以二氢叶酸还原酶作为模型
Crit Rev Eukaryot Gene Expr. 1993;3(4):229-54.
8
Cell cycle-specific association of E2F with the p130 E1A-binding protein.E2F与p130 E1A结合蛋白的细胞周期特异性关联。
Genes Dev. 1993 Dec;7(12A):2392-404. doi: 10.1101/gad.7.12a.2392.
9
Isolation of the Rb-related p130 through its interaction with CDK2 and cyclins.通过Rb相关蛋白p130与细胞周期蛋白依赖性激酶2(CDK2)及细胞周期蛋白的相互作用对其进行分离。
Genes Dev. 1993 Dec;7(12A):2378-91. doi: 10.1101/gad.7.12a.2378.
10
The adenovirus E1A-associated 130-kD protein is encoded by a member of the retinoblastoma gene family and physically interacts with cyclins A and E.腺病毒E1A相关的130-kD蛋白由视网膜母细胞瘤基因家族的一个成员编码,并与细胞周期蛋白A和E发生物理相互作用。
Genes Dev. 1993 Dec;7(12A):2366-77. doi: 10.1101/gad.7.12a.2366.

p107与Sp1的关联:p107的基因可分离区域参与E2F和Sp1依赖性转录的调控。

Association of p107 with Sp1: genetically separable regions of p107 are involved in regulation of E2F- and Sp1-dependent transcription.

作者信息

Datta P K, Raychaudhuri P, Bagchi S

机构信息

Center for Molecular Biology of Oral Diseases, College of Dentistry, University of Illinois at Chicago 60612, USA.

出版信息

Mol Cell Biol. 1995 Oct;15(10):5444-52. doi: 10.1128/MCB.15.10.5444.

DOI:10.1128/MCB.15.10.5444
PMID:7565695
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC230794/
Abstract

The retinoblastoma-related protein p107 has been shown to be a regulator of the transcription factor E2F. p107 associates with E2F via its pocket region and represses E2F-dependent transcription. In this study, we provide evidence for a novel interaction between p107 and the transcription factor Sp1. We show that p107 can be found endogenously associated with Sp1 in the extracts of several different cell lines. Moreover, in transient transfection assays, expression of p107 represses Sp1-dependent transcription. This repression of Sp1-dependent transcription does not require the DNA-binding domain of Sp1. Transcription driven by a chimeric protein containing the Ga14 DNA-binding domain and the Sp1 activation domains is inhibited by p107. Interestingly, unlike the repression of E2F-dependent transcription, the repression of Sp1-dependent transcription does not depend on an intact pocket region. We show that distinct regions of p107 are involved in the control of Sp1 and E2F.

摘要

视网膜母细胞瘤相关蛋白p107已被证明是转录因子E2F的一种调节因子。p107通过其口袋区域与E2F结合,并抑制E2F依赖的转录。在本研究中,我们提供了p107与转录因子Sp1之间存在新型相互作用的证据。我们发现,在几种不同细胞系的提取物中,p107可内源性地与Sp1结合。此外,在瞬时转染实验中,p107的表达可抑制Sp1依赖的转录。这种对Sp1依赖转录的抑制并不需要Sp1的DNA结合结构域。由包含Gal4 DNA结合结构域和Sp1激活结构域的嵌合蛋白驱动的转录受到p107的抑制。有趣的是,与对E2F依赖转录的抑制不同,对Sp1依赖转录的抑制并不依赖于完整的口袋区域。我们表明,p107的不同区域参与对Sp1和E2F的调控。