• 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

在小鼠细胞与自发产生SV40的中国仓鼠细胞的体细胞杂种中“早期”和“晚期”病毒功能的表达

Expression of "early" and "late" viral functions in a somatic cell hybrid between a mouse cell and a spontaneous yielder SV 40-transformed Chinese hamster cell.

作者信息

Suarez H G, Lavialle C, Estrade C L, Stevenet J, Cassingena R

出版信息

Arch Virol. 1978;56(1-2):119-33. doi: 10.1007/BF01317287.

DOI:10.1007/BF01317287
PMID:204268
Abstract

A somatic cell hybrid (Cl. 6d) was originated from the fusion of mouse 3T3-4E) and spontaneous yielder SV 40-transformed Chinese hamster (CHK/SVLP AG) cells. During the early stages of its history, the C1. 6d hybrid underwent a rapid chromosome loss, preferentially loosing hamster chromosomes. This was not a constant tendency of the hybrid cells. As the parental CHK)SVLP AG cells, the hybrid cells were always found 100 per cent SV40 T-antigen positive. While CHK/SVLP AG cells infectious SV 40 DNA, V-antigen and virus were regularly detected, in the hybrid cells only infectious DNA was occasionally detected. This was not due either to the loww of an essential Chinese hamster gene(s) or to the presence of an inhibiting mouse cell component(s); it was apparently the consequence of inability of the cells to properly activate the resident SV 40 genome(s). After superinfection with SV 40 DNA, the hybrid cells-though capable of synthesizing SV 40 V-antigen--were unable to ensure virus assembly. Experimental evidence was obtained suggesting that SV 40 maturation is dependent of a cellular function(s).

摘要

体细胞杂种(Cl. 6d)源自小鼠3T3 - 4E细胞与自发产生SV40转化的中国仓鼠(CHK/SVLP AG)细胞的融合。在其早期阶段,Cl. 6d杂种经历了快速的染色体丢失,优先丢失仓鼠染色体。这并非杂种细胞的恒定趋势。与亲代CHK/SVLP AG细胞一样,杂种细胞总是100% SV40 T抗原呈阳性。虽然在CHK/SVLP AG细胞中可定期检测到感染性SV40 DNA、V抗原和病毒,但在杂种细胞中仅偶尔检测到感染性DNA。这既不是由于必需的中国仓鼠基因缺失,也不是由于存在抑制性小鼠细胞成分;这显然是细胞无法正确激活驻留的SV40基因组的结果。用SV40 DNA进行超感染后,杂种细胞虽然能够合成SV40 V抗原,但无法确保病毒组装。获得的实验证据表明,SV40成熟依赖于一种细胞功能。

相似文献

1
Expression of "early" and "late" viral functions in a somatic cell hybrid between a mouse cell and a spontaneous yielder SV 40-transformed Chinese hamster cell.在小鼠细胞与自发产生SV40的中国仓鼠细胞的体细胞杂种中“早期”和“晚期”病毒功能的表达
Arch Virol. 1978;56(1-2):119-33. doi: 10.1007/BF01317287.
2
Chromosomes involved in production of infectious SV40 particles in mouse/SV40-transformed Chinese hamster cell hybrids.参与小鼠/SV40转化的中国仓鼠细胞杂交体中感染性SV40颗粒产生的染色体。
Oncology. 1981;38(2):86-97. doi: 10.1159/000225529.
3
Simian virus 40-chinese hamster kidney cell interaction. II. The semipermissivity of the cell system.猿猴病毒40-中国仓鼠肾细胞相互作用。II. 细胞系统的半允许性。
Arch Virol. 1976;50(1-2):137-46. doi: 10.1007/BF01318008.
4
Assignment of the integration site for simian virus 40 to chromosome 17 in GM54VA, a human cell line transformed by simian virus 40.在经猿猴病毒40转化的人类细胞系GM54VA中,将猿猴病毒40的整合位点定位到17号染色体上。
Proc Natl Acad Sci U S A. 1977 Jan;74(1):315-8. doi: 10.1073/pnas.74.1.315.
5
Enhanced SV 40-virus replication in chinese hamster kidney cells pretreated with 5-iodo-2'-deoxyuridine.在经5-碘-2'-脱氧尿苷预处理的中国仓鼠肾细胞中增强的SV 40病毒复制。
Arch Virol. 1976;50(3):249-53. doi: 10.1007/BF01320580.
6
Characterization of defective SV40 isolated from SV40-transformed cells.从SV40转化细胞中分离出的缺陷型SV40的特性分析。
Virology. 1975 Feb;63(2):512-22. doi: 10.1016/0042-6822(75)90324-4.
7
The induction of SV40-transformed chinese hamster and mouse kidney cells by mitomycin C.
Intervirology. 1975;5(5):305-12. doi: 10.1159/000149927.
8
Induction of infectious virus DNA and virus particles by mitomycin C in SV40-transformed mouse cells.
J Gen Virol. 1978 Oct;41(1):201-5. doi: 10.1099/0022-1317-41-1-201.
9
Properties of SV40 rescued from actinomycin D-sensitive and actinomycin D-resistant transformed hamster cells. I. Lytic infection.从对放线菌素D敏感和对放线菌素D耐药的转化仓鼠细胞中拯救出的SV40的特性。I. 溶细胞感染。
Arch Gesamte Virusforsch. 1974;46(1-2):93-104. doi: 10.1007/BF01240209.
10
Tumorigenicity of mouse-human diploid hybrids in nude mice.小鼠 - 人二倍体杂种在裸鼠中的致瘤性。
Science. 1975 Dec 19;190(4220):1200-2. doi: 10.1126/science.173020.

本文引用的文献

1
Chromatin structure: deduced from a minichromosome.染色质结构:从小染色体推断出来的。
Science. 1975 Mar 28;187(4182):1202-3. doi: 10.1126/science.187.4182.1202.
2
INFECTION OF HUMAN AND SIMIAN TISSUE CULTURES WITH ROUS SARCOMA VIRUS.劳斯肉瘤病毒对人和猴组织培养物的感染
Proc Natl Acad Sci U S A. 1964 Jul;52(1):53-9. doi: 10.1073/pnas.52.1.53.
3
[SELECTIVE DEVELOPMENT IN AGAR OF HAMSTER CELLS TRANSFORMED BY THE POLYOMA VIRUS].[多瘤病毒转化的仓鼠细胞在琼脂中的选择性发育]
C R Hebd Seances Acad Sci. 1964 Apr 20;258:4171-3.
4
Clonal growth of mammalian cells in vitro; growth characteristics of colonies from single HeLa cells with and without a feeder layer.哺乳动物细胞的体外克隆生长;有无饲养层时单个海拉细胞形成的集落的生长特性。
J Exp Med. 1956 Feb 1;103(2):273-83. doi: 10.1084/jem.103.2.273.
5
Somatic cell hybrid between the established human line D98 (presumptive HeLa) and 3T3.已建立的人类细胞系D98(推测为海拉细胞系)与3T3细胞的体细胞杂交体。
Science. 1969 Feb 14;163(3868):697-8. doi: 10.1126/science.163.3868.697.
6
Activation of infectious SV40 synthesis in transformed cells.转化细胞中感染性SV40合成的激活。
Proc Natl Acad Sci U S A. 1968 Aug;60(4):1239-46. doi: 10.1073/pnas.60.4.1239.
7
"Early" virus-specific RNA may contain information necessary for chromosome replication and mitosis induced by Simian Virus 40.“早期”病毒特异性RNA可能包含猴病毒40诱导染色体复制和有丝分裂所需的信息。
Proc Natl Acad Sci U S A. 1973 Jun;70(6):1654-8. doi: 10.1073/pnas.70.6.1654.
8
Simian virus 40 deoxyribonucleic acid synthesis: the viral replicon.猴病毒40脱氧核糖核酸合成:病毒复制子。
J Virol. 1972 Oct;10(4):591-8. doi: 10.1128/JVI.10.4.591-598.1972.
9
Properties of an SV40-transformed African green monkey kidney (BSC-1) cell line.
Int J Cancer. 1972 Mar 15;9(2):324-33. doi: 10.1002/ijc.2910090210.
10
Induction of virus synthesis in polyoma-transformed cells by DNA antimetabolites and by irradiation after pretreatment with 5-bromodeoxyuridine.
Virology. 1972 Jul;49(1):12-22. doi: 10.1016/s0042-6822(72)80003-5.