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猿猴病毒40转化细胞中病毒转录和肿瘤抗原表达的调控

Regulation of viral transciption and tumor antigen expression in cells transformed by simian virus 40.

作者信息

Basilico C, Zouzias D

出版信息

Proc Natl Acad Sci U S A. 1976 Jun;73(6):1931-5. doi: 10.1073/pnas.73.6.1931.

Abstract

We have studied the expression of simian virus 40 (SV40) specific tumor antigen (T-antigen) and viral RNA in SV40-transformed mouse 3T3 cells that are temperature-sensitive for the expression of the transformed phenotype (ts SV3T3). Although transformed by wild-type SV40, ts SV3T3 cells at 32 degrees behave like standard transformants, while at 39 degrees they became arrested in G1 after reaching saturation density or under conditions of serum starvation. ts SV3T3 cells at 32 degrees or exponentially growing at 39 degrees are uniformly T-antigen positive. However, after G1 arrest at 39 degrees the majority of the cells becomes T-antigen negative. Induction of proliferation in the resting cultures results in the reappearance of T-antigen in most of the cells, concomitant with the induction of DNA synthesis. The reason for the disappearance of T-antigen from ts SV3T3 cells arrested in G1 seems to reside in a transcriptional control operating on the integrated viral DNA, since these cells contain no appreciable amounts of SV40 specific RNA. Viral RNA can be easily detected in cells growint at 32 degrees or at 39 degrees. The results suggest that transcription of the viral genome in SV40-transformed cells is cell-cycle-dependent.

摘要

我们研究了猿猴病毒40(SV40)特异性肿瘤抗原(T抗原)和病毒RNA在对转化表型表达具有温度敏感性的SV40转化小鼠3T3细胞(ts SV3T3)中的表达情况。尽管ts SV3T3细胞由野生型SV40转化而来,但在32摄氏度时其表现如同标准转化细胞,而在39摄氏度时,当达到饱和密度或处于血清饥饿条件下,它们会在G1期停滞。在32摄氏度的ts SV3T3细胞或在39摄氏度指数生长的细胞均呈T抗原阳性。然而,在39摄氏度G1期停滞之后,大多数细胞变为T抗原阴性。在静止培养物中诱导增殖会导致大多数细胞中T抗原重新出现,同时伴随着DNA合成的诱导。ts SV3T3细胞在G1期停滞时T抗原消失的原因似乎在于对整合病毒DNA起作用的转录调控,因为这些细胞不含可观量的SV40特异性RNA。在32摄氏度或39摄氏度生长的细胞中可轻易检测到病毒RNA。结果表明,SV40转化细胞中病毒基因组的转录是细胞周期依赖性的。

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