Cohen A, Leung C, Thompson E
J Cell Physiol. 1985 Jun;123(3):431-4. doi: 10.1002/jcp.1041230320.
A mutant clone (NT-1) of a T-cell lymphoma was selected for its ability to grow in HAT medium (hypoxanthine, aminopterin and thymidine) in the presence of the nucleoside transport inhibitor P-nitrobenzyl-6-mercaptoinosine (NBMI). NT-1 cells contain half the number of NBMI binding sites present on the parental S49 cells and are partially able to transport nucleosides in the presence of the transport inhibitor (NBMI). These observations suggest that the mutant cells are heterozygous for nucleoside transport proteins and contain two types of transport proteins: the first protein can both bind and is inhibited by NBMI similar to the wild type phenotype, and the second is an altered protein. The altered transport protein apparently lost its NBMI binding sites without a parallel loss of nucleoside transport ability suggesting that the nucleoside transported sites are separate from the binding sites of the transport inhibitor.
选择一种T细胞淋巴瘤的突变克隆（NT-1），因其在核苷转运抑制剂对硝基苄基-6-巯基肌苷（NBMI）存在的情况下能够在HAT培养基（次黄嘌呤、氨基蝶呤和胸腺嘧啶核苷）中生长。NT-1细胞所含的NBMI结合位点数量是亲代S49细胞的一半，并且在转运抑制剂（NBMI）存在的情况下能够部分转运核苷。这些观察结果表明，突变细胞对于核苷转运蛋白是杂合的，并且包含两种类型的转运蛋白：第一种蛋白既能结合NBMI又会被其抑制，类似于野生型表型，第二种是一种改变了的蛋白。这种改变了的转运蛋白显然失去了其NBMI结合位点，而核苷转运能力并未相应丧失，这表明核苷转运位点与转运抑制剂的结合位点是分开的。
