Raptis L, Lamfrom H, Benjamin T L
Mol Cell Biol. 1985 Sep;5(9):2476-86. doi: 10.1128/mcb.5.9.2476-2486.1985.
Polyoma middle T antigen (mT) was expressed in rat F-111 cells under control of the dexamethasone-regulatable mouse mammary tumor virus promoter. Graded phenotypic responses to levels of mT induction by the hormone were seen, with morphological transformation, focus formation, and anchorage-independent growth requiring increasing levels of mT expression. The ability of different clones to form tumors reflected their maximum level of induction of mT-associated kinase and their ability to grow in soft agar. Expression of transformation parameters and tumorigenicity correlates with the level of mT phosphorylated by pp60c-src in immune complexes and not with the total amount of mT determined by metabolic labeling. We suggest that cellular factors regulate mT activity by forming a kinase-active fraction of mT molecules that controls the transformed state.
多瘤病毒中T抗原(mT)在可地塞米松调节的小鼠乳腺肿瘤病毒启动子控制下,在大鼠F-111细胞中表达。观察到对激素诱导的mT水平的分级表型反应,形态转化、集落形成和不依赖贴壁生长需要增加的mT表达水平。不同克隆形成肿瘤的能力反映了它们对mT相关激酶的最大诱导水平以及它们在软琼脂中生长的能力。转化参数和致瘤性的表达与免疫复合物中由pp60c-src磷酸化的mT水平相关,而与代谢标记测定的mT总量无关。我们认为细胞因子通过形成控制转化状态的mT分子的激酶活性部分来调节mT活性。