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劳氏肉瘤病毒src基因在禽类巨噬细胞中的表达未能引发转化细胞表型。

Expression of the Rous sarcoma virus src gene in avian macrophages fails to elicit transformed cell phenotype.

作者信息

Lipsich L, Brugge J S, Boettiger D

出版信息

Mol Cell Biol. 1984 Jul;4(7):1420-4. doi: 10.1128/mcb.4.7.1420-1424.1984.

Abstract

Infection of avian macrophages with Rous sarcoma virus does not induce any changes in the morphology, growth behavior, or expression of macrophage-specific proteins. The absence of cellular transformation does not result from a block in the synthesis of viral proteins, since infectious viruses are released from a majority of cells in the culture. In this report, we examine the synthesis, processing, and functional activity of pp60src in Rous sarcoma virus-infected macrophages to determine whether the absence of transformation is due to an alteration in the functional expression of pp60src. Although the absolute level of pp60src was reduced compared with fibroblasts, the protein exhibited the same phosphorylation pattern and subcellular distribution and was able to phosphorylate immunoglobulin in the immune complex-protein kinase assay. These results imply that the failure of Rous sarcoma virus to transform macrophage may be due to a restriction in the cellular response to a functional src protein, perhaps due to the absence of cellular products which are essential for mediating pp60src-induced transformation.

摘要

用劳氏肉瘤病毒感染禽巨噬细胞不会引起巨噬细胞形态、生长行为或巨噬细胞特异性蛋白表达的任何变化。细胞未发生转化并非由于病毒蛋白合成受阻,因为培养物中的大多数细胞都能释放出有感染性的病毒。在本报告中,我们研究了劳氏肉瘤病毒感染的巨噬细胞中pp60src的合成、加工及功能活性,以确定未发生转化是否是由于pp60src功能表达的改变所致。尽管与成纤维细胞相比,pp60src的绝对水平有所降低,但该蛋白呈现出相同的磷酸化模式和亚细胞分布,并且在免疫复合物 - 蛋白激酶试验中能够使免疫球蛋白磷酸化。这些结果表明,劳氏肉瘤病毒不能转化巨噬细胞可能是由于细胞对功能性src蛋白的反应受到限制,也许是因为缺乏介导pp60src诱导转化所必需的细胞产物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1103/368926/6afc600de19e/molcellb00149-0237-a.jpg

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