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抗肿瘤药物L-(αS,5S)-α-氨基-3-氯-4,5-二氢-5-异恶唑乙酸(AT-125)使谷氨酰胺酰胺转移酶失活的机制

Mechanism of inactivation of glutamine amidotransferases by the antitumor drug L-(alpha S, 5S)-alpha-amino-3-chloro-4,5-dihydro-5-isoxazoleacetic acid (AT-125).

作者信息

Tso J Y, Bower S G, Zalkin H

出版信息

J Biol Chem. 1980 Jul 25;255(14):6734-8.

PMID:6993476
Abstract

L-(alphaS, 5S)-alpha-Amino-3-chloro-4,5-dihydro-5-isoxazoleacetic acid (AT-125), an antitumor drug isolated from Streptomyces sviceus, is an active site-directed affinity analog of glutamine. It selectively inactivates the glutamine-dependent activities of two bacterial glutamine amidotransferases, anthranilate synthase and glutamate synthase. A reversible noncovalent complex is formed prior to irreversible enzyme modification. Inactivation of anthranilate synthase results from incorporation of approximately 1 eq of AT-125/enzyme protomer. Active site cysteine-83 in Serratia marcescens anthranilate synthase Component II is the residue alkylated by AT-125. Anthranilate synthase is rapidly inactivated by AT-125 IN S. marcescens cells. In vivo inactivation is by the same mechanism as in vitro.

摘要

L-(αS,5S)-α-氨基-3-氯-4,5-二氢-5-异恶唑乙酸(AT-125)是从淡紫链霉菌中分离出的一种抗肿瘤药物,是谷氨酰胺的活性位点定向亲和类似物。它选择性地使两种细菌谷氨酰胺酰胺转移酶(邻氨基苯甲酸合酶和谷氨酸合酶)的谷氨酰胺依赖性活性失活。在不可逆的酶修饰之前会形成可逆的非共价复合物。邻氨基苯甲酸合酶的失活是由于每分子酶原掺入了约1当量的AT-125。粘质沙雷氏菌邻氨基苯甲酸合酶组分II中的活性位点半胱氨酸-83是被AT-125烷基化的残基。在粘质沙雷氏菌细胞中,邻氨基苯甲酸合酶会被AT-125迅速失活。体内失活机制与体外相同。

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