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氟脱氧尿苷对X染色体脆性位点的诱导作用:叶酸和胸苷抑制机制的证据

FUdR induction of the X chromosome fragile site: evidence for the mechanism of folic acid and thymidine inhibition.

作者信息

Glover T W

出版信息

Am J Hum Genet. 1981 Mar;33(2):234-42.

Abstract

Experiments designed to illuminate the mechanism by which folic acid and thymidine inhibit expression of the Xq28 fragile site in human lymphocytes are described. The fragile site is induced by 5-fluorodeoxyuridine (FUdR), a potent inhibitor of thymidylate synthetase, in the presence of otherwise inhibiting concentrations of folic acid but not in the presence of thymidine. These results indicate that the fragile site is expressed because of depletion of deoxythymidine monophosphate (dTMP) available for DNA synthesis.

摘要

本文描述了旨在阐明叶酸和胸苷抑制人类淋巴细胞中Xq28脆性位点表达机制的实验。脆性位点是由胸苷酸合成酶的强效抑制剂5-氟脱氧尿苷(FUdR)在存在抑制性浓度叶酸的情况下诱导产生的,但在有胸苷存在时则不会诱导产生。这些结果表明,脆性位点的表达是由于可用于DNA合成的脱氧胸苷一磷酸(dTMP)耗竭所致。

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