N-terminal deletion in the src gene of Rous sarcoma virus results in synthesis of a 45,000-Mr protein with mitogenic activity.

D Laugier; M Marx; J V Barnier; F Poirier; P Genvrin; P Dezélée; G Calothy

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N-terminal deletion in the src gene of Rous sarcoma virus results in synthesis of a 45,000-Mr protein with mitogenic activity.

机译：在肉瘤病毒的SRC基因中缺失N末端缺失导致合成45,000-mr蛋白质，含有催乳素活性。

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Expression of the v-src gene of Rous sarcoma virus in avian embryo neuroretina cells results in transformation and sustained proliferation of these normally resting cells. Transformed neuroretina cells are also tumorigenic upon inoculation into immunodeficient hosts. We have previously described conditional mutants of Rous sarcoma virus encoding p60v-src proteins which induce proliferation of neuroretina cells in the absence of transformation and tumorigenicity. These results suggest that p60v-src is composed of functionally distinct domains which may interact with multiple cellular targets. In this study, we describe a spontaneous variant of Rous sarcoma virus, subgroup E, which carries a deletion of 278 base pairs in the 5' portion of the v-src gene but which has retained the ability to induce proliferation of quail neuroretina cells. The deleted v-src gene encodes a 45,000-molecular-weight phosphoprotein which contains both phosphoserine and phosphotyrosine, is myristylated, and possesses tyrosine kinase activity indistinguishable from that of wild-type p60v-src. Molecular cloning and sequence analysis of the mutant v-src gene have shown that this deletion extends from amino acid 33 to 126 of the wild-type p60v-src. Therefore, this portion of the v-src protein is dispensable for the mitogenic activity of Rous sarcoma virus in neuroretina cells.

机译：禽类胚胎神经遗传因子中的肉瘤病毒V-SRC基因的表达导致这些通常静息细胞的转化和持续增殖。在接种到免疫缺陷宿主时，转化的神经遗传因子细胞也是致致瘤的。我们之前描述了编码P60V-SRC蛋白的ROS SARCOMA病毒的条件突变体，其在没有转化和致瘤性的情况下诱导神经尿苷细胞的增殖。这些结果表明，P60V-SRC由功能性不同的域组成，其可以与多个蜂窝目标相互作用。在这项研究中，我们描述了一种肉瘤病毒，亚组E的自发变体，其缺失在V-SRC基因的5'部分中缺失278个碱基对，但保留了诱导鹌鹑神经内松细胞增殖的能力。缺失的V-SRC基因编码了45,000分子量的磷蛋白，其含有磷源和磷酸磷酸，是肌脲化的，并且具有与野生型P60V-SRC的酪氨酸激酶活性难以区分。突变体V-SRC基因的分子克隆和序列分析表明，该缺失从野生型P60V-SRC的氨基酸33至126延伸。因此，V-SRC蛋白的这部分可分配用于神经遗传因子细胞中的肉瘤病毒的促丝状活性。

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《Journal of Virology》 |1987年第8期|共7页
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D Laugier; M Marx; J V Barnier; F Poirier; P Genvrin; P Dezélée; G Calothy;
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1. N-terminal deletion in the src gene of Rous sarcoma virus results in synthesis of a 45,000-Mr protein with mitogenic activity. [J] . D Laugier, M Marx, J V Barnier, Journal of Virology . 1987,第8期

机译：在肉瘤病毒的SRC基因中缺失N末端缺失导致合成45,000-mr蛋白质，含有催乳素活性。
2. N-terminal deletion in the src gene of Rous sarcoma virus results in synthesis of a 45,000-Mr protein with mitogenic activity. [J] . D Laugier, M Marx, J V Barnier, Journal of Virology . 1987,第8期

机译：在肉瘤病毒的SRC基因中缺失N末端缺失导致合成45,000-mr蛋白质，含有催乳素活性。
3. Small deletion in src of Rous sarcoma virus modifying transformation phenotypes: identification of 207-nucleotide deletion and its smaller product with protein kinase activity. [J] . N Kitamura, M Yoshida Journal of Virology . 1983,第3期

机译：Sarcoma病毒改性转化表型的SRC小缺失：鉴定207核苷酸缺失及其具有蛋白激酶活性的较小产品。
4. Construction and Vaccine Studies on a Pseudorabies Virus with Deletions in Glycoprotein t and Glycoprotein E Genes [C] . Songlin Zhang, Meilin Jin, Huanchun Chen International Conference on Materials for Environmental Protection and Energy Application . 2012

机译：糖蛋白T和糖蛋白E基因缺失缺失病毒的构建和疫苗研究
5. Characterization of DNA-protein interactions involved in Marek's disease virus-mediated rous sarcoma virus long terminal repeat promoter transactivation [D] . Sun, Wei. 1997

机译：涉及马立克氏病病毒介导的肉瘤肉瘤长末端重复启动子反式激活的DNA-蛋白质相互作用的表征
6. N-terminal deletion in the src gene of Rous sarcoma virus results in synthesis of a 45000-Mr protein with mitogenic activity. [O] . D Laugier, M Marx, J V Barnier, 1987

机译：劳斯肉瘤病毒src基因的N末端缺失导致合成具有促有丝分裂活性的45000-Mr蛋白。
7. N-terminal deletion in the src gene of Rous sarcoma virus results in synthesis of a 45,000-Mr protein with mitogenic activity [O] . D Laugier, M Marx, J V Barnier, 1987

机译：在肉瘤病毒的SRC基因中N-末端缺失导致合成45,000-mR蛋白质，含有促致泌发活性

N-terminal deletion in the src gene of Rous sarcoma virus results in synthesis of a 45,000-Mr protein with mitogenic activity.

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