• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

p62c-yes与多瘤病毒中间T抗原突变体的关联与转化能力相关。

Association of p62c-yes with polyomavirus middle T-antigen mutants correlates with transforming ability.

作者信息

Kornbluth S, Cheng S H, Markland W, Fukui Y, Hanafusa H

机构信息

Laboratory of Molecular Oncology, Rockefeller University, New York, New York 10021-6399.

出版信息

J Virol. 1990 Apr;64(4):1584-9. doi: 10.1128/JVI.64.4.1584-1589.1990.

DOI:10.1128/JVI.64.4.1584-1589.1990
PMID:1690822
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC249293/
Abstract

A number of mutants of polyomavirus middle T antigen (MTag) were constructed into replication-competent avian retroviruses. To assess the ability of these MTag variants to transform and to associate with the avian p60c-src and p62c-yes proto-oncogene products, we used these viruses to infect chicken embryo fibroblasts. We found that the ability of individual mutant MTags to associate with p62c-yes correlated well with the ability of these mutants to transform, as has been previously shown for the association of MTag with p60c-src. All transformation-competent mutant MTags retained the ability to complex with p62c-yes. Two transformation-defective mutants, RX67 and RX68, which could weakly associate with p60c-src, were unable to associate with p62c-yes.dl1015, a transformation-defective mutant which could associate with p60c-src and with a phosphatidylinositol kinase activity, was also able to associate with p62c-yes. Therefore, some as yet unmeasured biochemical property is defective in this mutant.

摘要

将多瘤病毒中T抗原(MTag)的多个突变体构建到具有复制能力的禽逆转录病毒中。为了评估这些MTag变体转化以及与禽p60c-src和p62c-yes原癌基因产物结合的能力,我们用这些病毒感染鸡胚成纤维细胞。我们发现,单个突变型MTag与p62c-yes结合的能力与这些突变体的转化能力密切相关,正如之前所显示的MTag与p60c-src的结合情况一样。所有具有转化能力的突变型MTag都保留了与p62c-yes形成复合物的能力。两个转化缺陷型突变体RX67和RX68,它们与p60c-src的结合较弱,无法与p62c-yes结合。dl1015是一个转化缺陷型突变体,它能与p60c-src以及一种磷脂酰肌醇激酶活性结合,也能与p62c-yes结合。因此,这个突变体中某些尚未测定的生化特性存在缺陷。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26e6/249293/f4a795b492d3/jvirol00059-0180-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26e6/249293/a6257e14b9fb/jvirol00059-0178-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26e6/249293/df6c12674554/jvirol00059-0179-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26e6/249293/9bccf16e97d5/jvirol00059-0179-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26e6/249293/99c98e74cf19/jvirol00059-0180-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26e6/249293/f4a795b492d3/jvirol00059-0180-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26e6/249293/a6257e14b9fb/jvirol00059-0178-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26e6/249293/df6c12674554/jvirol00059-0179-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26e6/249293/9bccf16e97d5/jvirol00059-0179-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26e6/249293/99c98e74cf19/jvirol00059-0180-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26e6/249293/f4a795b492d3/jvirol00059-0180-b.jpg

相似文献

1
Association of p62c-yes with polyomavirus middle T-antigen mutants correlates with transforming ability.p62c-yes与多瘤病毒中间T抗原突变体的关联与转化能力相关。
J Virol. 1990 Apr;64(4):1584-9. doi: 10.1128/JVI.64.4.1584-1589.1990.
2
Association of the polyomavirus middle-T antigen with c-yes protein.
Nature. 1987;325(7000):171-3. doi: 10.1038/325171a0.
3
Induction of tumor formation and cell transformation by polyoma middle T antigen in the absence of Src.在缺乏Src的情况下,多瘤病毒中T抗原诱导肿瘤形成和细胞转化。
Oncogene. 1993 Sep;8(9):2521-9.
4
Transformation-defective mutants of polyomavirus middle T antigen associate with phosphatidylinositol 3-kinase (PI 3-kinase) but are unable to maintain wild-type levels of PI 3-kinase products in intact cells.多瘤病毒中T抗原的转化缺陷型突变体与磷脂酰肌醇3激酶(PI 3激酶)相关联,但无法在完整细胞中维持PI 3激酶产物的野生型水平。
J Virol. 1992 Mar;66(3):1702-8. doi: 10.1128/JVI.66.3.1702-1708.1992.
5
Identification and characterization of the hamster polyomavirus middle T antigen.仓鼠多瘤病毒中T抗原的鉴定与特性分析
J Virol. 1991 Jun;65(6):3301-8. doi: 10.1128/JVI.65.6.3301-3308.1991.
6
Transformation of chicken embryo fibroblasts and tumor induction by the middle T antigen of polyomavirus carried in an avian retroviral vector.禽逆转录病毒载体携带的多瘤病毒中间T抗原对鸡胚成纤维细胞的转化及肿瘤诱导作用
Mol Cell Biol. 1986 May;6(5):1545-51. doi: 10.1128/mcb.6.5.1545-1551.1986.
7
Polyomavirus middle-T antigen associates with the kinase domain of Src-related tyrosine kinases.多瘤病毒中T抗原与Src相关酪氨酸激酶的激酶结构域相关联。
J Virol. 1996 Mar;70(3):1323-30. doi: 10.1128/JVI.70.3.1323-1330.1996.
8
The carboxy terminus of pp60c-src is a regulatory domain and is involved in complex formation with the middle-T antigen of polyomavirus.pp60c-src的羧基末端是一个调节结构域,参与与多瘤病毒中间T抗原的复合物形成。
Mol Cell Biol. 1988 Apr;8(4):1736-47. doi: 10.1128/mcb.8.4.1736-1747.1988.
9
Signaling pathways controlling trophoblast cell differentiation: Src family protein tyrosine kinases in the rat.控制滋养层细胞分化的信号通路:大鼠中的Src家族蛋白酪氨酸激酶
Biol Reprod. 1997 Dec;57(6):1302-11. doi: 10.1095/biolreprod57.6.1302.
10
Structural and functional modification of pp60c-src associated with polyoma middle tumor antigen from infected or transformed cells.与来自感染或转化细胞的多瘤病毒中间肿瘤抗原相关的pp60c-src的结构和功能修饰。
Mol Cell Biol. 1985 Oct;5(10):2647-52. doi: 10.1128/mcb.5.10.2647-2652.1985.

引用本文的文献

1
Transformation by Polyomavirus Middle T Antigen Involves a Unique Bimodal Interaction with the Hippo Effector YAP.多瘤病毒中T抗原介导的转化涉及与Hippo效应因子YAP的独特双峰相互作用。
J Virol. 2016 Jul 27;90(16):7032-7045. doi: 10.1128/JVI.00417-16. Print 2016 Aug 15.
2
Global Analysis of Mouse Polyomavirus Infection Reveals Dynamic Regulation of Viral and Host Gene Expression and Promiscuous Viral RNA Editing.小鼠多瘤病毒感染的全球分析揭示了病毒和宿主基因表达的动态调控以及混杂的病毒RNA编辑。
PLoS Pathog. 2015 Sep 25;11(9):e1005166. doi: 10.1371/journal.ppat.1005166. eCollection 2015 Sep.
3
Evidence that the middle T antigen of polyomavirus interacts with the membrane skeleton.

本文引用的文献

1
Transmission of the polyoma virus middle T gene as the oncogene of a murine retrovirus.多瘤病毒中T基因作为鼠逆转录病毒致癌基因的传递。
Nature. 1984;308(5961):748-50. doi: 10.1038/308748a0.
2
The complex of polyoma virus middle-T antigen and pp60c-src.多瘤病毒中T抗原与pp60c-src的复合物
EMBO J. 1984 Mar;3(3):585-91. doi: 10.1002/j.1460-2075.1984.tb01852.x.
3
Isolation of monoclonal antibodies that recognize the transforming proteins of avian sarcoma viruses.识别禽肉瘤病毒转化蛋白的单克隆抗体的分离
多瘤病毒中间T抗原与膜骨架相互作用的证据。
Mol Cell Biol. 1993 Aug;13(8):4703-13. doi: 10.1128/mcb.13.8.4703-4713.1993.
4
Stoichiometry of cellular and viral components in the polyomavirus middle-T antigen-tyrosine kinase complex.多瘤病毒中T抗原-酪氨酸激酶复合物中细胞和病毒成分的化学计量学。
Mol Cell Biol. 1990 Oct;10(10):5569-74. doi: 10.1128/mcb.10.10.5569-5574.1990.
5
Interleukin 2- and polyomavirus middle T antigen-induced modification of phosphatidylinositol 3-kinase activity in activated T lymphocytes.白细胞介素2和多瘤病毒中T抗原诱导活化T淋巴细胞中磷脂酰肌醇3激酶活性的改变。
Mol Cell Biol. 1991 Sep;11(9):4431-40. doi: 10.1128/mcb.11.9.4431-4440.1991.
6
Two species of human CRK cDNA encode proteins with distinct biological activities.
Mol Cell Biol. 1992 Aug;12(8):3482-9. doi: 10.1128/mcb.12.8.3482-3489.1992.
7
Interactions of polyomavirus middle T with the SH2 domains of the pp85 subunit of phosphatidylinositol-3-kinase.多瘤病毒中T抗原与磷脂酰肌醇-3-激酶pp85亚基的SH2结构域的相互作用。
J Virol. 1992 Sep;66(9):5485-91. doi: 10.1128/JVI.66.9.5485-5491.1992.
J Virol. 1983 Nov;48(2):352-60. doi: 10.1128/JVI.48.2.352-360.1983.
4
Transforming activity of polyoma virus middle-T antigen probed by site-directed mutagenesis.通过定点诱变探究多瘤病毒中T抗原的转化活性。
Nature. 1983;304(5925):456-9. doi: 10.1038/304456a0.
5
Polyoma virus transforming protein associates with the product of the c-src cellular gene.多瘤病毒转化蛋白与c-src细胞基因的产物相关联。
Nature. 1983;303(5916):435-9. doi: 10.1038/303435a0.
6
The roles of individual polyoma virus early proteins in oncogenic transformation.多瘤病毒早期蛋白个体在致癌转化中的作用。
Nature. 1982 Dec 23;300(5894):713-8. doi: 10.1038/300713a0.
7
Mutation causing premature termination of the polyoma virus medium T antigen blocks cell transformation.导致多瘤病毒中T抗原过早终止的突变会阻断细胞转化。
J Virol. 1982 Mar;41(3):1014-24. doi: 10.1128/JVI.41.3.1014-1024.1982.
8
Transformation of rat cells by an altered polyoma virus genome expressing only the middle-T protein.仅表达中T蛋白的改变的多瘤病毒基因组对大鼠细胞的转化。
Nature. 1981 Aug 13;292(5824):595-600. doi: 10.1038/292595a0.
9
Coding capacity of a 35 percent fragment of the polyoma virus genome is sufficient to initiate and maintain cellular transformation.多瘤病毒基因组35%片段的编码能力足以启动并维持细胞转化。
Proc Natl Acad Sci U S A. 1980 Jun;77(6):3278-82. doi: 10.1073/pnas.77.6.3278.
10
Middle T antigen as primary inducer of full expression of the phenotype of transformation by polyoma virus.中T抗原作为多瘤病毒转化表型完全表达的主要诱导因子。
J Virol. 1980 Jul;35(1):219-32. doi: 10.1128/JVI.35.1.219-232.1980.