Nichols E J, Manger R, Hakomori S, Herscovics A, Rohrschneider L R
Mol Cell Biol. 1985 Dec;5(12):3467-75. doi: 10.1128/mcb.5.12.3467-3475.1985.
The effect of glycosylational-processing inhibitors on the synthesis, cell surface expression, endocytosis, and transforming function of the v-fms oncogene protein (gp140fms) was examined in McDonough feline sarcoma virus-transformed Fischer rat embryo (SM-FRE) cells. Swainsonine (SW), a mannosidase II inhibitor, blocked complete processing, but an abnormal v-fms protein containing hybrid carbohydrate structures was expressed on the cell surface. SW-treated SM-FRE cells retained the transformed phenotype. In contrast, two glucosidase I inhibitors (castanospermine [CA] and N-methyl-1-deoxynojirimycin [MdN]) blocked carbohydrate remodeling at an early stage within the endoplasmic reticulum and prevented cell surface expression of v-fms proteins. CA-treated SM-FRE cells reverted to the normal phenotype. Neither SW, CA, nor MdN affected either endocytosis or the tyrosine kinase activity associated with the v-fms gene product in vitro. These results demonstrate the necessity of carbohydrate processing for cell surface expression of the v-fms gene product and illustrate the unique ability to modulate the transformed state of SM-FRE cells with the glycosylational-processing inhibitors CA and MdN.
在麦克多诺猫肉瘤病毒转化的费舍尔大鼠胚胎（SM-FRE）细胞中，研究了糖基化加工抑制剂对v-fms癌基因蛋白（gp140fms）的合成、细胞表面表达、内吞作用及转化功能的影响。甘露糖苷酶II抑制剂苦马豆素（SW）阻断了完整加工过程，但含有杂合碳水化合物结构的异常v-fms蛋白在细胞表面表达。经SW处理的SM-FRE细胞保留了转化表型。相比之下，两种葡糖苷酶I抑制剂（栗精胺[CA]和N-甲基-1-脱氧野尻霉素[MdN]）在内质网内的早期阶段阻断了碳水化合物重塑，并阻止了v-fms蛋白的细胞表面表达。经CA处理的SM-FRE细胞恢复为正常表型。SW、CA和MdN在体外均不影响内吞作用或与v-fms基因产物相关的酪氨酸激酶活性。这些结果证明了碳水化合物加工对于v-fms基因产物细胞表面表达的必要性，并说明了利用糖基化加工抑制剂CA和MdN调节SM-FRE细胞转化状态的独特能力。
