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1
Intranuclear localization of human papillomavirus 16 E7 during transformation and preferential binding of E7 to the Rb family member p130.人乳头瘤病毒16 E7在转化过程中的核内定位以及E7与Rb家族成员p130的优先结合
Proc Natl Acad Sci U S A. 1999 Jun 8;96(12):6999-7004. doi: 10.1073/pnas.96.12.6999.
2
Destabilization of the retinoblastoma tumor suppressor by human papillomavirus type 16 E7 is not sufficient to overcome cell cycle arrest in human keratinocytes.人乳头瘤病毒16型E7蛋白导致的视网膜母细胞瘤肿瘤抑制因子失稳不足以克服人角质形成细胞中的细胞周期停滞。
J Virol. 2001 Aug;75(15):6737-47. doi: 10.1128/JVI.75.15.6737-6747.2001.
3
Repression of human papillomavirus oncogenes in HeLa cervical carcinoma cells causes the orderly reactivation of dormant tumor suppressor pathways.人乳头瘤病毒致癌基因在HeLa宫颈癌细胞中的抑制会导致休眠的肿瘤抑制途径有序重新激活。
Proc Natl Acad Sci U S A. 2000 Nov 7;97(23):12513-8. doi: 10.1073/pnas.97.23.12513.
4
The E7 proteins of low- and high-risk human papillomaviruses share the ability to target the pRB family member p130 for degradation.低风险和高风险人乳头瘤病毒的E7蛋白都具有将视网膜母细胞瘤家族成员p130作为降解靶点的能力。
Proc Natl Acad Sci U S A. 2006 Jan 10;103(2):437-42. doi: 10.1073/pnas.0510012103. Epub 2005 Dec 28.
5
Degradation of the retinoblastoma tumor suppressor by the human papillomavirus type 16 E7 oncoprotein is important for functional inactivation and is separable from proteasomal degradation of E7.人乳头瘤病毒16型E7癌蛋白对视网膜母细胞瘤肿瘤抑制因子的降解对于功能失活很重要，并且与E7的蛋白酶体降解可分离。
J Virol. 2001 Aug;75(16):7583-91. doi: 10.1128/JVI.75.16.7583-7591.2001.
6
Two cytodifferentiation agent-induced pathways, differentiation and apoptosis, are distinguished by the expression of human papillomavirus 16 E7 in human bladder carcinoma cells.两种细胞分化剂诱导的途径，即分化和凋亡，可通过人乳头瘤病毒16 E7在人膀胱癌细胞中的表达来区分。
Cancer Res. 1997 Jul 1;57(13):2789-98.
7
Proteasomal degradation of p130 facilitate cell cycle deregulation and impairment of cellular differentiation in high-risk Human Papillomavirus 16 and 18 E7 transfected cells.蛋白酶体降解 p130 促进高危型人乳头瘤病毒 16 和 18 E7 转染细胞的细胞周期失调和细胞分化障碍。
Mol Biol Rep. 2021 Jun;48(6):5121-5133. doi: 10.1007/s11033-021-06509-4. Epub 2021 Jun 24.
8
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.
9
Human papillomavirus type 16 E7 protein inhibits DNA binding by the retinoblastoma gene product.人乳头瘤病毒16型E7蛋白抑制视网膜母细胞瘤基因产物的DNA结合。
Mol Cell Biol. 1992 May;12(5):1905-14. doi: 10.1128/mcb.12.5.1905-1914.1992.
10
Induction of S phase and apoptosis by the human papillomavirus type 16 E7 protein are separable events in immortalized rodent fibroblasts.人乳头瘤病毒16型E7蛋白诱导永生化啮齿动物成纤维细胞进入S期和发生凋亡是可分离的事件。
Oncogene. 2000 May 4;19(19):2277-85. doi: 10.1038/sj.onc.1203570.

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The Not-So-Good, the Bad and the Ugly: HPV E5, E6 and E7 Oncoproteins in the Orchestration of Carcinogenesis.不那么好、坏和丑：HPV E5、E6 和 E7 致癌蛋白在致癌作用中的协同作用。
Viruses. 2021 Sep 22;13(10):1892. doi: 10.3390/v13101892.
2
Human Papillomavirus and Cellular Pathways: Hits and Targets.人乳头瘤病毒与细胞通路：热点与靶点
Pathogens. 2021 Feb 25;10(3):262. doi: 10.3390/pathogens10030262.
3
HPV 16E7 and 48E7 proteins use different mechanisms to target p130 to overcome cell cycle block.人乳头瘤病毒16E7和48E7蛋白利用不同机制靶向p130以克服细胞周期阻滞。
Virol J. 2016 Jan 4;13:2. doi: 10.1186/s12985-015-0460-8.
4
The Subcellular Localisation of the Human Papillomavirus (HPV) 16 E7 Protein in Cervical Cancer Cells and Its Perturbation by RNA Aptamers.人乳头瘤病毒（HPV）16 E7蛋白在宫颈癌细胞中的亚细胞定位及其受RNA适体的干扰
Viruses. 2015 Jun 26;7(7):3443-61. doi: 10.3390/v7072780.
5
The papillomavirus E7 proteins.人乳头瘤病毒 E7 蛋白。
Virology. 2013 Oct;445(1-2):138-68. doi: 10.1016/j.virol.2013.04.013. Epub 2013 May 31.
6
Cellular transformation by human papillomaviruses: lessons learned by comparing high- and low-risk viruses.人乳头瘤病毒引起的细胞转化：比较高危和低危病毒得出的经验教训。
Virology. 2012 Mar 15;424(2):77-98. doi: 10.1016/j.virol.2011.12.018. Epub 2012 Jan 27.
7
Localisation of human papillomavirus 16 E7 oncoprotein changes with cell confluence.人乳头瘤病毒 16 型 E7 癌蛋白的定位随细胞汇合度而变化。
PLoS One. 2011;6(6):e21501. doi: 10.1371/journal.pone.0021501. Epub 2011 Jun 29.
8
Nonconserved lysine residues attenuate the biological function of the low-risk human papillomavirus E7 protein.非保守赖氨酸残基削弱了低危型人乳头瘤病毒 E7 蛋白的生物学功能。
J Virol. 2011 Jun;85(11):5546-54. doi: 10.1128/JVI.02166-10. Epub 2011 Mar 16.
9
Subcellular localization of the human papillomavirus 16 E7 oncoprotein in CaSki cells and its detection in cervical adenocarcinoma and adenocarcinoma in situ.人乳头瘤病毒 16 型 E7 癌蛋白在 CaSki 细胞中的亚细胞定位及其在宫颈腺癌和原位腺癌中的检测。
Virology. 2011 Jan 5;409(1):54-68. doi: 10.1016/j.virol.2010.09.024. Epub 2010 Oct 23.
10
Low- and high-risk human papillomavirus E7 proteins regulate p130 differently.低危型和高危型人乳头瘤病毒 E7 蛋白对 p130 的调节作用不同。
Virology. 2010 May 10;400(2):233-9. doi: 10.1016/j.virol.2010.01.034. Epub 2010 Feb 26.

本文引用的文献

1
Differential expression and functionally co-operative roles for the retinoblastoma family of proteins in epidermal differentiation.视网膜母细胞瘤蛋白家族在表皮分化中的差异表达及功能协同作用。
Oncogene. 1998 Aug 27;17(8):949-57. doi: 10.1038/sj.onc.1202031.
2
The retinoblastoma gene family: cousins with overlapping interests.视网膜母细胞瘤基因家族：兴趣重叠的亲属
Trends Genet. 1998 Jun;14(6):223-9. doi: 10.1016/s0168-9525(98)01470-x.
3
Differential regulation of the pocket domains of the retinoblastoma family proteins by the HPV16 E7 oncoprotein.人乳头瘤病毒16型E7癌蛋白对视网膜母细胞瘤家族蛋白口袋结构域的差异调控
Cell Growth Differ. 1997 Dec;8(12):1277-86.
4
E2F activity is regulated by cell cycle-dependent changes in subcellular localization.E2F活性受亚细胞定位的细胞周期依赖性变化调控。
Mol Cell Biol. 1997 Dec;17(12):7268-82. doi: 10.1128/MCB.17.12.7268.
5
The human papillomavirus E7 oncoprotein can uncouple cellular differentiation and proliferation in human keratinocytes by abrogating p21Cip1-mediated inhibition of cdk2.人乳头瘤病毒E7癌蛋白可通过消除p21Cip1介导的对细胞周期蛋白依赖性激酶2（cdk2）的抑制作用，使人类角质形成细胞中的细胞分化与增殖脱钩。
Genes Dev. 1997 Aug 15;11(16):2101-11. doi: 10.1101/gad.11.16.2101.
6
Inhibition of CDK activity and PCNA-dependent DNA replication by p21 is blocked by interaction with the HPV-16 E7 oncoprotein.p21对细胞周期蛋白依赖性激酶（CDK）活性及增殖细胞核抗原（PCNA）依赖性DNA复制的抑制作用，会因与人类乳头瘤病毒16型（HPV-16）E7癌蛋白相互作用而被阻断。
Genes Dev. 1997 Aug 15;11(16):2090-100. doi: 10.1101/gad.11.16.2090.
7
Initiation of DNA synthesis by human papillomavirus E7 oncoproteins is resistant to p21-mediated inhibition of cyclin E-cdk2 activity.人乳头瘤病毒E7癌蛋白引发的DNA合成对p21介导的细胞周期蛋白E-细胞周期蛋白依赖性激酶2活性抑制具有抗性。
J Virol. 1997 Jul;71(7):5570-8. doi: 10.1128/JVI.71.7.5570-5578.1997.
8
Accumulation of human papillomavirus type 16 E7 protein bypasses G1 arrest induced by serum deprivation and by the cell cycle inhibitor p21.人乳头瘤病毒16型E7蛋白的积累绕过了血清剥夺和细胞周期抑制剂p21诱导的G1期阻滞。
J Virol. 1997 May;71(5):3451-7. doi: 10.1128/JVI.71.5.3451-3457.1997.
9
Expression and activity of the retinoblastoma protein (pRB)-family proteins, p107 and p130, during L6 myoblast differentiation.视网膜母细胞瘤蛋白（pRB）家族蛋白p107和p130在L6成肌细胞分化过程中的表达与活性
Cell Growth Differ. 1995 Oct;6(10):1287-98.
10
G1 cyclin/CDK-independent phosphorylation and accumulation of p130 during the transition from G1 to G0 lead to its association with E2F-4.在从G1期向G0期转变过程中，p130的G1期细胞周期蛋白/细胞周期蛋白依赖性激酶非依赖性磷酸化和积累导致其与E2F-4结合。
Oncogene. 1996 Jul 18;13(2):237-46.

人乳头瘤病毒16 E7在转化过程中的核内定位以及E7与Rb家族成员p130的优先结合

Intranuclear localization of human papillomavirus 16 E7 during transformation and preferential binding of E7 to the Rb family member p130.

作者信息

Smith-McCune K, Kalman D, Robbins C, Shivakumar S, Yuschenkoff L, Bishop J M

机构信息

Department of Obstetrics, Gynecology, and Reproductive Sciences, University of California, San Francisco CA 94115, USA.

出版信息

Proc Natl Acad Sci U S A. 1999 Jun 8;96(12):6999-7004. doi: 10.1073/pnas.96.12.6999.

DOI:10.1073/pnas.96.12.6999
PMID:10359828
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC22035/
Abstract

To study intracellular pathways by which the human papillomavirus 16 oncogene E7 participates in carcinogenesis, we expressed an inducible chimera of E7 by fusion to the hormone-binding domain of the estrogen receptor. The chimeric protein (E7ER) transformed rodent fibroblast cell lines and induced DNA synthesis on addition of estradiol. In coimmunoprecipitation experiments, E7ER preferentially bound p130 when compared to p107 and pRb. After estradiol addition, E7ER localization changed to a more intense intranuclear staining. Induction of E7 function was not correlated with binding to p130 or pRb but rather with intranuclear localization and modest induction of binding to p107.

摘要

为了研究人乳头瘤病毒16型癌基因E7参与致癌作用的细胞内途径，我们通过与雌激素受体的激素结合域融合表达了一种可诱导的E7嵌合体。这种嵌合蛋白（E7ER）转化了啮齿动物成纤维细胞系，并在添加雌二醇后诱导DNA合成。在免疫共沉淀实验中，与p107和pRb相比，E7ER优先结合p130。添加雌二醇后，E7ER的定位改变为更强的核内染色。E7功能的诱导与与p130或pRb的结合无关，而是与核内定位以及与p107结合的适度诱导有关。