Cook W D, Fazekas de St Groth B, Miller J F, MacDonald H R, Gabathuler R
Mol Cell Biol. 1987 Jul;7(7):2631-5. doi: 10.1128/mcb.7.7.2631-2635.1987.
Abelson murine leukemia virus (A-MuLV) carries the gene v-abl, one of a group of oncogenes with structural and functional (tyrosine kinase) homology to three growth factor receptors. Work in this and other laboratories has shown that A-MuLV infection can render myeloid and lymphoid cells independent of the growth factors interleukin 3 and granulocyte-macrophage colony-stimulating factor. We have now shown that v-abl can also relieve interleukin 2 (IL-2) dependence in T cells. We infected a cloned IL-2-dependent antigen-specific cell line. Transformed cells were generated which were factor independent and tumorigenic. The transformants each bore unique v-abl DNA inserts and expressed v-abl mRNA. No elevation of expression of either IL-2 or its receptor could be detected in these cells. Thus, A-MuLV can short-circuit the dependence of hematopoietic cells on IL-2, IL-3, and possibly granulocyte-macrophage colony-stimulating factor, none of whose receptors are known to be of the tyrosine kinase type.
阿贝尔逊鼠白血病病毒(A-MuLV)携带v-abl基因,它是一组癌基因之一,与三种生长因子受体在结构和功能(酪氨酸激酶)上具有同源性。本实验室及其他实验室的研究表明,A-MuLV感染可使髓系和淋巴系细胞不依赖生长因子白细胞介素3和粒细胞-巨噬细胞集落刺激因子。我们现在已经证明,v-abl也能解除T细胞对白细胞介素2(IL-2)的依赖。我们感染了一个克隆的依赖IL-2的抗原特异性细胞系。产生了不依赖因子且具有致瘤性的转化细胞。每个转化体都带有独特的v-abl DNA插入片段并表达v-abl mRNA。在这些细胞中未检测到IL-2或其受体表达的升高。因此,A-MuLV可以绕过造血细胞对IL-2、IL-3以及可能的粒细胞-巨噬细胞集落刺激因子的依赖,而这些因子的受体均不属于酪氨酸激酶类型。