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3-羟基-3-甲基戊二酰辅酶A合酶缺陷的哺乳动物细胞突变体的分离与鉴定

Isolation and characterization of a mammalian cell mutant defective in 3-hydroxy-3-methylglutaryl coenzyme A synthase.

作者信息

Schnitzer-Polokoff R, von Gunten C, Logel J, Torget R, Sinensky M

出版信息

J Biol Chem. 1982 Jan 10;257(1):472-6.

PMID:6118375
Abstract

A somatic cell mutant of the Chinese hamster ovary (CHO)-K1 cell auxotrophic for mevalonic acid has been isolated by means of the bromodeoxyuridine-visible light technique. This mutant can incorporate labeled mevalonate but not labeled acetate into cholesterol and, thus, is apparently defective in mevalonate biosynthesis. The mutant is recessive with respect to the parental cell phenotype. Assessment of the in vitro activities of the enzymes responsible for mevalonate biosynthesis under varying growth conditions indicates that the mutant, Mev-1, is defective in 3-hydroxy-3-methylglutaryl coenzyme A synthase.

摘要

利用溴脱氧尿苷-可见光技术分离出了中国仓鼠卵巢(CHO)-K1细胞的一种体细胞突变体,该突变体对甲羟戊酸营养缺陷。这种突变体能够将标记的甲羟戊酸掺入胆固醇中,但不能将标记的乙酸盐掺入胆固醇中,因此,其甲羟戊酸生物合成显然存在缺陷。该突变体相对于亲本表型是隐性的。在不同生长条件下对负责甲羟戊酸生物合成的酶的体外活性进行评估表明,突变体Mev-1在3-羟基-3-甲基戊二酰辅酶A合酶方面存在缺陷。

相似文献

1
Isolation and characterization of a mammalian cell mutant defective in 3-hydroxy-3-methylglutaryl coenzyme A synthase.3-羟基-3-甲基戊二酰辅酶A合酶缺陷的哺乳动物细胞突变体的分离与鉴定
J Biol Chem. 1982 Jan 10;257(1):472-6.
2
Transfection of the ketogenic mitochondrial 3-hydroxy-3-methylglutaryl-coenzyme A synthase cDNA into Mev-1 cells corrects their auxotrophy for mevalonate.
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Analysis of regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase in a somatic cell mutant auxotrophic for mevalonate.对甲羟戊酸营养缺陷型体细胞突变体中3-羟基-3-甲基戊二酰辅酶A还原酶的调控分析。
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Analysis of the coordinate expression of 3-hydroxy-3-methylglutaryl coenzyme A synthase and reductase activities in Chinese hamster ovary fibroblasts.中国仓鼠卵巢成纤维细胞中3-羟基-3-甲基戊二酰辅酶A合酶与还原酶活性的协同表达分析。
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Regulation of cytosolic acetoacetyl coenzyme A thiolase, 3-hydroxy-3-methylglutaryl coenzyme A synthase, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and mevalonate kinase by low density lipoprotein and by 25-hydroxycholesterol in Chinese hamster ovary cells.低密度脂蛋白和25-羟基胆固醇对中国仓鼠卵巢细胞中胞质乙酰乙酰辅酶A硫解酶、3-羟基-3-甲基戊二酰辅酶A合酶、3-羟基-3-甲基戊二酰辅酶A还原酶和甲羟戊酸激酶的调节
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Further characterization of a somatic cell mutant defective in regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase.3-羟基-3-甲基戊二酰辅酶A还原酶调节缺陷的体细胞突变体的进一步表征。
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Regulation of cholesterol synthesis in rat adrenal gland through coordinate control of 3-hydroxy-3-methylglutaryl coenzyme A synthase and reductase activities.通过对3-羟基-3-甲基戊二酰辅酶A合酶和还原酶活性的协同控制来调节大鼠肾上腺中的胆固醇合成。
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Regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase synthesis by a non-sterol mevalonate-derived product in Mev-1 cells. Apparent translational control.非甾醇甲羟戊酸衍生产物对Mev-1细胞中3-羟基-3-甲基戊二酰辅酶A还原酶合成的调控。明显的翻译控制。
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Isolation and characterization of cells resistant to ML236B (compactin) with increased levels of 3-hydroxy-3-methylglutaryl coenzyme A reductase.对3-羟基-3-甲基戊二酰辅酶A还原酶水平升高且对ML236B(美伐他汀)耐药的细胞进行分离与鉴定。
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Regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase and lipid metabolism in a concanavalin A-resistant Chinese hamster ovary cell line.刀豆球蛋白A抗性中国仓鼠卵巢细胞系中3-羟基-3-甲基戊二酰辅酶A还原酶的调节与脂质代谢
Arch Biochem Biophys. 1986 Feb 1;244(2):502-16. doi: 10.1016/0003-9861(86)90619-3.

引用本文的文献

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Biomolecules. 2025 Apr 14;15(4):580. doi: 10.3390/biom15040580.
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Contribution of steroidogenic factor 1 to the regulation of cholesterol synthesis.类固醇生成因子1对胆固醇合成调节的作用。
Biochem J. 2000 Sep 15;350 Pt 3(Pt 3):785-90.
3
Mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase: a control enzyme in ketogenesis.线粒体3-羟基-3-甲基戊二酰辅酶A合酶:酮体生成中的一种调控酶。
Biochem J. 1999 Mar 15;338 ( Pt 3)(Pt 3):569-82.
4
Loss of transcriptional activation of three sterol-regulated genes in mutant hamster cells.突变仓鼠细胞中三个固醇调节基因转录激活的丧失。
Mol Cell Biol. 1993 Sep;13(9):5175-85. doi: 10.1128/mcb.13.9.5175-5185.1993.
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Defective macromolecule biosynthesis and cell-cycle progression in a mammalian cell starved for mevalonate.在缺乏甲羟戊酸的哺乳动物细胞中,大分子生物合成和细胞周期进程存在缺陷。
Proc Natl Acad Sci U S A. 1985 May;82(10):3257-61. doi: 10.1073/pnas.82.10.3257.
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J Cell Biol. 1990 May;110(5):1489-99. doi: 10.1083/jcb.110.5.1489.