STUDIES OF E26 AVIAN V-ETS AND ITS CELLULAR HOMOLOGUE IN MOUSE CELLS

一种禽类急性白血病病毒的小鼠同源物E26被用来 GAG-MYB-ETS的致癌和促生长作用研究 融合癌基因及其组成成分MYB和ETS。表达式 这种病毒在部分(但不是全部)依赖IL3的小鼠造血中的作用 细胞系导致这些细胞获得在EPO上生长的潜力 (促红细胞生成素)，并表达升高的GATA-1，促红细胞生成素 受体和β-珠蛋白。执行以下操作所需的步骤和要求 获得EPO反应表型的细胞正在分析中。数据 暗示细胞需要其他步骤才能变得能够 生长在EPO上，除了GAG-MYB-ETS的表达，还有一些 效果似乎可逆地依赖于EPO的存在。 V-ETS/DNA相互作用对融合至关重要的额外证据 蛋白诱导对成纤维细胞生长因子依赖性的改变 已经获得了。ELF，一种其产物阻断ETS-表达的基因- 反应性启动子，能够抑制细胞的低血清生长 表达ME26癌基因，与早期的研究一致 表明v-ETS DNA结合域的缺失使 病毒诱导3T3细胞低血清增殖能力的研究 成纤维细胞。

A murine homolog of the avian acute leukemia virus, E26, was used to study the oncogenic and growth-altering potential of the gag-myb-ets fusion oncogene and its constituent myb and ets components. Expression of this virus in some, but not all, IL3-dependent murine hematopoietic cell lines leads to these cells acquiring the potential to grow on epo (erythropoietin), and to express elevated levels of GATA-1, the epo receptor, and beta-globin. The steps and requirements necessary for a cell to acquire an epo-responsive phenotype are being analyzed. The data suggests that additional steps are required for a cell to become able to grow on epo, in addition to gag-myb-ets expression, and that some of the effects appear to be reversibly dependent on the presence of epo. Additional evidence that v-ets/DNA interactions are essential for fusion protein induction of changes in fibroblast growth factor dependence has been obtained. ELF, a gene whose product blocks the expression of ets- responsive promoters, is able to inhibit the low-serum growth of cells expressing the ME26 oncogene, consistent with earlier studies which indicated that deletion of the v-ets DNA-binding domain inactivated the capacity of the virus to induce low-serum proliferation of 3T3 fibroblasts.