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在病毒基因表达方面存在缺陷的Friend红白血病细胞突变体。

Friend erythroleukaemia cell mutants defective in viral gene expression.

作者信息

Yokota J, Iwamoto A, Suzuki A, Yamaguchi-Tejima S, Kitamura Y, Yoshikura H

出版信息

J Gen Virol. 1984 Feb;65 ( Pt 2):429-35. doi: 10.1099/0022-1317-65-2-429.

Abstract

Cellular mutants defective in the expression of viral polypeptides were isolated from the Friend erythroleukemia cell line 745a by immunoselection with anti-ecotropic murine leukaemia virus serum in the presence of complement. The mode of appearance of the antiserum-resistant cells showed an interesting pattern which is discussed in the text. One of the mutants obtained contained no detectable gp70 or p15(E) while retaining gPr90env; defects appeared to reside in the processing of the gPr90env to gp70 and p15(E). In another type of mutant, gPr90env was not detected. All these mutants retained spleen focus-forming virus (SFFV)-specific gp55 and gag precursor Pr68gag. The mutants superinfected with the helper virus produced the helper and SFFV also, indicating that these mutations did not affect the replication of the exogenously infecting virus.

摘要

在补体存在的情况下,用抗嗜亲性鼠白血病病毒血清通过免疫选择从弗瑞德红白血病细胞系745a中分离出病毒多肽表达缺陷的细胞突变体。抗血清抗性细胞的出现模式呈现出一种有趣的格局,文中对此进行了讨论。获得的一个突变体中未检测到可检测的gp70或p15(E),但保留了gPr90env;缺陷似乎存在于gPr90env加工成gp70和p15(E)的过程中。在另一种类型的突变体中,未检测到gPr90env。所有这些突变体都保留了脾集落形成病毒(SFFV)特异性的gp55和gag前体Pr68gag。用辅助病毒超感染的突变体也产生了辅助病毒和SFFV,这表明这些突变不影响外源感染病毒的复制。

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