Identification of an Abelson murine leukemia virus-encoded protein present in transformed fibroblast and lymphoid cells.
Identification of an Abelson murine leukemia virus-encoded protein present in transformed fibroblast and lymphoid cells.
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鉴定存在于转化成纤维细胞和淋巴细胞中的阿贝尔森鼠白血病病毒编码蛋白。
DOI：
10.1073/pnas.75.5.2488
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发表时间：
1978
影响因子：
11.1
通讯作者：
D. Baltimore
中科院分区：
文献类型：
--
作者：
O. Witte;N. Rosenberg;M. Paskind;A. Shields;D. Baltimore
Abelson鼠白血病病毒（A-MuLV）转化的淋巴细胞和成纤维细胞系的提取物含有分子量为120，000（P120）的蛋白质。用特异性血清进行的免疫沉淀显示，P120含有与MULV gag基因复合物的5 '端片段同源的区域--p15、p12和至少部分p30--但缺乏可检测的p10、逆转录酶和包膜糖蛋白的决定簇。P120是磷酸化的，细胞内半衰期为3- 6小时。用Moloney MuLV作为辅助物，体外翻译来自A-MuLV的病毒体RNA，产生分子量为120，000的产物，其血清学反应性与细胞P120相似。翻译来自辅助细胞的RNA没有产生P120。P120在我们测试的所有被A-MuLV转化的淋巴细胞系和成纤维细胞系中表达，但在A-MuLV基因组通过感染建立但不负责转化的淋巴细胞系中检测不到。P120的表达选择性地保留在A-MuLV转化的淋巴细胞克隆中，这些淋巴细胞在辅助MuLV细胞内前体表达丧失后转化为非生产者状态。这些结果表明A-MuLV基因组的P120产物可能负责维持由病毒转化的淋巴细胞和成纤维细胞的转化表型。
Extracts from lymphoid and fibroblast cell lines transformed by Abelson murine leukemia virus (A-MuLV) contain a protein of molecular weight 120,000 (P120). Immunoprecipitation with specific sera shows that P120 contains regions homologous to the 5'-terminal segment of the MULV gag gene complex--p15, p12, and at least part of p30--but lacks detectable determinants of p10, reverse transcriptase, and the envelope glycoprotein. P120 is phosphorylated and has an intracellular half-life of 3--6 hr. In vitro translation of virion RNA from A-MuLV, with Moloney MuLV as helper, yields a product of molecular weight 120,000 with serological reactivity similar to that of the cellular P120. Translation of the RNA from the helper gave no P120. P120 is expressed in all lymphoid and fibroblastic cell lines we have tested that were transformed by A-MuLV but is not detectable in a lymphoid line in which the A-MuLV genome was established by infection but was not responsible for the transformation. Expression of P120 is selectively retained in clones of A-MuLV-transformed lymphocytes that convert to a nonproducer state after loss of expression of helper MuLV intracellular precursors. These results suggest that the P120 product of the A-MuLV genome may be responsible for maintenance of the transformed phenotype of lymphoid and fibroblast cells transformed by the virus.