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首页> 外文期刊>Molecular and Cellular Biology >Incomplete nucleoside transport deficiency with increased hypoxanthine transport capability in mutant T-lymphoblastoid cells.
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Incomplete nucleoside transport deficiency with increased hypoxanthine transport capability in mutant T-lymphoblastoid cells.

机译：不完全核苷传输缺乏，突变体T淋巴细胞细胞中的缺氧嘌呤输送能力增加。

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From a mutagenized population of wild-type mouse (S49) T-lymphoma cells, a clone, 80-5D2, was isolated in a single step by virtue of its ability to survive in 80 nM 5-fluorouridine. Unlike previously isolated nucleoside transport-deficient cell lines (A. Cohen, B. Ullman, and D. W. Martin, Jr., J. Biol. Chem. 254:112-116, 1979), 80-5D2 cells were only slightly less sensitive to growth inhibition by a variety of cytotoxic nucleosides and were capable of proliferating in hypoxanthine-amethopterin-thymidine-containing medium. The molecular basis for the phenotype of 80-5D2 cells was incomplete deficiency in the ability of the mutant cells to translocate nucleosides across the plasma membrane. Interestingly, mutant cells were more capable than wild-type cells of transporting the nucleobase hypoxanthine. Residual transport of adenosine into 80-5D2 cells was just as sensitive to inhibition by nucleosides and more sensitive to inhibition by hypoxanthine than that in wild-type cells, indicating that the phenomena of ligand binding and translocation can be uncoupled genetically. The 80-5D2 cells lacked cell surface binding sites for the potent inhibitor of nucleoside transport p-nitrobenzylthioinosine (NBMPR) and, consequently, were largely resistant to the physiological effects of NBMPR. However, the altered transporter retained its sensitivity to dipyridamole, another inhibitor of nucleoside transport. The biochemical phenotype of the 80-5D2 cell line supports the hypothesis that the determinants that comprise the nucleoside carrier site, the hypoxanthine carrier site, the NBMPR binding site, and the dipyridamole binding site of the nucleoside transport function of mouse S49 cells are genetically distinguishable.
机译：从诱变的野生型小鼠（S49）T淋巴瘤细胞中，克隆，80-5d2在单一的阶梯中分离出一种逐步分离，其能够在80nm 5-氟氨氨酰胺中存活。与先前分离的核苷传输缺乏细胞系（A.Cohen，B. Ullman和DW Martin，Jr.，J.Biol.Chem.254：112-116,1979），80-5d2细胞仅略微不太敏感通过各种细胞毒性核苷的生长抑制，并且能够在余生 - 氨基丙氨酸胸苷培养基中增殖。 80-5d2细胞表型的分子基础在突变细胞在血浆膜上翻译核苷的能力不完全缺乏。有趣的是，突变细胞比运输核碱基脱氧核苷酸的野生型细胞更有能力。腺苷将腺苷分为80-5d2细胞对核苷的抑制性和对缺氧的抑制性比在野生型细胞中更敏感，表明配体结合和易位的现象可以遗传地绕过。 80-5D2细胞缺乏用于核苷输送p-硝基苄基喹啉（NBMPR）的有效抑制剂的细胞表面结合位点，因此，基本上耐受NBMPR的生理作用。然而，改变的转运蛋白保留了其对双嘧达莫的敏感性，其另一个核苷输送抑制剂。 80-5d2细胞系的生化表型支持该假设：包含核苷载体部位，缺氧载体部位，NBMPR结合位点和小鼠S49细胞的核苷传输功能的二嘧达咪胶结合位点的决定蛋白是遗传可区分的。

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