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经显微注射爱泼斯坦-巴尔病毒DNA后永生化的人类新生儿淋巴细胞。

Human neonatal lymphocytes immortalized after microinjection of Epstein-Barr virus DNA.

作者信息

Klein C, Raab-Traub N

出版信息

J Virol. 1987 May;61(5):1552-8. doi: 10.1128/JVI.61.5.1552-1558.1987.

Abstract

Epstein-Barr virus (EBV) is a highly efficient acute transforming agent in human cells, provided that the intact virus is used. To investigate the ability of viral DNA alone to transform cells, we introduced the EBV genome into human lymphocytes. After microinjection of EBV DNA into neonatal B lymphocytes, we established a cell line that in early passages contained multiple viral fragments. This cell line retained sequences from the short, unique (Us) region of the EBV genome and sequences from EcoRI-E. The viral sequences were not expressed; however, the cells expressed a 2.3-kilobase polyadenylated message homologous to the c-fgr oncogene, a cellular locus believed to be activated by EBV infection [M. S. C. Cheah, T. J. Ley, S. R. Tronick, and K. C. Robbins, Nature (London) 319:238-240.]. The cell line was monoclonal with rearrangement at the immunoglobulin locus and had a reciprocal translocation t(1;7)(p34;q34) and a deletion of sequences within the locus for the beta chain of the T-cell receptor. The close proximity of the translocation to the chromosomal loci for c-fgr on chromosome 1 and the T-cell receptor beta chain on chromosome 7 suggests that structural alteration of these genes was critical to this transformation event.

摘要

如果使用完整的病毒,爱泼斯坦-巴尔病毒(EBV)是人类细胞中一种高效的急性转化因子。为了研究单独的病毒DNA转化细胞的能力,我们将EBV基因组导入人类淋巴细胞。在将EBV DNA显微注射到新生B淋巴细胞后,我们建立了一个细胞系,该细胞系在早期传代时包含多个病毒片段。该细胞系保留了来自EBV基因组短独特(Us)区域的序列以及来自EcoRI-E的序列。病毒序列未表达;然而,这些细胞表达了一种与c-fgr癌基因同源的2.3千碱基多聚腺苷酸化信使,c-fgr是一个据信被EBV感染激活的细胞基因座[M. S. C. Cheah、T. J. Ley、S. R. Tronick和K. C. Robbins,《自然》(伦敦)319:238 - 240]。该细胞系是单克隆的,在免疫球蛋白基因座处发生重排,并且有一个相互易位t(1;7)(p34;q34)以及T细胞受体β链基因座内序列的缺失。该易位与1号染色体上c-fgr的染色体基因座以及7号染色体上T细胞受体β链的染色体基因座紧密相邻,这表明这些基因的结构改变对这一转化事件至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/686f/254135/9783ca5cca78/jvirol00096-0264-a.jpg

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