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人胚胎癌细胞及其体外分化衍生物与猿猴病毒40、人7型腺病毒或副流感病毒的相互作用

Interaction of human embryonal carcinoma cells and differentiated derivatives in vitro with simian virus 40, human adenovirus type 7, or PARA.

作者信息

Bronson D L, Lanford R E, Casper J, Wians F H

机构信息

Department of Virology and Immunology, Southwest Foundation for Biomedical Research, San Antonio, Texas 78284.

出版信息

Exp Cell Res. 1990 Jan;186(1):60-5. doi: 10.1016/0014-4827(90)90210-2.

Abstract

Polyclonal antibodies were used to assay human embryonal carcinoma (EC), differentiating EC, yolk sac carcinoma, and teratoma cells for expression of viral early antigen (T-Ag) after infection with simian virus 40 (SV40). Cells of four EC lines were induced to differentiate by cultivation at low density or by exposure to retinoic acid or dimethyl sulfoxide. After infection with SV40, T-Ag was expressed by 1%, or less, of the cells (presumed to be differentiated derivatives) in only some EC cultures whereas the antigen was synthesized by a significant percentage of the yolk sac carcinoma, teratoma, and differentiating EC cells. Also, viral late proteins were produced by EC cells infected with human adenovirus type 7 (Ad7), and SV40 T-Ag was expressed by EC cells after infection with PARA, which is an Ad7-SV40 hybrid virus containing the SV40 T-Ag sequence controlled by Ad7 late regulatory sequences. Thus, T-Ag is not synthesized by the parental EC cells infected with SV40, but it is expressed in cultures of infected differentiated derivatives. The EC cells produce T-Ag, however, when expression of the viral protein is controlled by the Ad7 regulatory sequences in PARA particles. These results demonstrate that expression of T-Ag after infection with SV40 is an indicator of EC cell differentiation and also raise the possibility that, as in mouse EC cells infected with the virus, the SV40 regulatory sequences controlling T-Ag synthesis are not active in human EC cells.

摘要

使用多克隆抗体检测人胚胎癌(EC)、分化型EC、卵黄囊癌和畸胎瘤细胞在感染猿猴病毒40(SV40)后病毒早期抗原(T抗原)的表达情况。四种EC细胞系的细胞通过低密度培养或暴露于视黄酸或二甲基亚砜诱导分化。感染SV40后,仅在部分EC培养物中,1%或更少的细胞(推测为分化衍生物)表达T抗原,而卵黄囊癌、畸胎瘤和分化型EC细胞中有相当比例的细胞合成该抗原。此外,感染人7型腺病毒(Ad7)的EC细胞产生病毒晚期蛋白,感染PARA(一种含有由Ad7晚期调控序列控制的SV40 T抗原序列的Ad7 - SV40杂交病毒)后的EC细胞表达SV40 T抗原。因此,感染SV40的亲代EC细胞不合成T抗原,但在感染后的分化衍生物培养物中表达。然而,当病毒蛋白的表达受PARA颗粒中的Ad7调控序列控制时,EC细胞会产生T抗原。这些结果表明,感染SV40后T抗原的表达是EC细胞分化的一个指标,也增加了一种可能性,即与感染该病毒的小鼠EC细胞一样,控制T抗原合成的SV40调控序列在人EC细胞中不活跃。

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