Characterization of mouse lymphoma cells with altered nucleoside transport
Characterization of mouse lymphoma cells with altered nucleoside transport
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核苷转运改变的小鼠淋巴瘤细胞的表征
DOI：
10.1002/jcp.1041230320
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发表时间：
1985
影响因子：
5.6
通讯作者：
E. Thompson
中科院分区：
文献类型：
--
作者：
A. Cohen;Changyee Leung;E. Thompson
选择T细胞淋巴瘤的突变克隆（NT-1），因为其在核苷转运抑制剂对硝基苄基-6-巯基肌苷（NBMI）存在下在HAT培养基（次黄嘌呤、氨基蝶呤和胸苷）中生长的能力。NT-1细胞含有亲本S49细胞上存在的一半数量的NBMI结合位点，并且在存在转运抑制剂（NBMI）的情况下能够部分转运核苷。这些观察结果表明，突变细胞是杂合的核苷转运蛋白，并含有两种类型的转运蛋白：第一种蛋白质可以结合，并抑制NBMI类似于野生型表型，第二种是一个改变的蛋白质。改变的转运蛋白显然失去了NBMI结合位点，而没有核苷转运能力的平行损失，这表明核苷转运位点与转运抑制剂的结合位点是分开的。
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.