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具有异常嘌呤代谢的中国仓鼠细胞突变体的生化遗传学:磷酸核糖氨基咪唑合成酶活性缺陷突变体的分离与鉴定

Biochemical genetics of Chinese hamster cell mutants with deviant purine metabolism: isolation and characterization of a mutant deficient in the activity of phosphoribosylaminoimidazole synthetase.

作者信息

Irwin M, Oates D C, Patterson D

出版信息

Somatic Cell Genet. 1979 Mar;5(2):203-16. doi: 10.1007/BF01539161.

DOI:10.1007/BF01539161
PMID:483121
Abstract

A new purine-requiring mutant of Chinese hamster ovary cells (CHO-Kl) is described. This mutant, Ade-G, grows on aminoimidazole carboxamide, hypoxanthine, or adenine. It complements all eight of our other previously described Ade- mutants. Biochemical analysis of de novo purine synthesis in whole cells suggests that Ade-G is capable of the first four reactions of de novo purine biosynthesis and that it synthesizes and accumulates phosphoribosylformylglycinamidine (FGAM). Direct enzyme assay in cell-free extracts confirms that Ade-G is defective in phosphoribosylaminoimidazole synthetase activity and does not convert FGAM to phosphoribosylaminoimidazole (AIR), the next intermediate in the de novo biosynthetic pathway.

摘要

本文描述了中国仓鼠卵巢细胞(CHO-K1)的一种新的嘌呤需求型突变体。该突变体Ade-G可在氨基咪唑甲酰胺、次黄嘌呤或腺嘌呤上生长。它能与我们之前描述的其他8种Ade-突变体互补。对全细胞中嘌呤从头合成的生化分析表明,Ade-G能够进行嘌呤从头生物合成的前四个反应,并且它能合成并积累磷酸核糖甲酰甘氨脒(FGAM)。无细胞提取物中的直接酶活性测定证实,Ade-G在磷酸核糖氨基咪唑合成酶活性方面存在缺陷,无法将FGAM转化为磷酸核糖氨基咪唑(AIR),而AIR是从头生物合成途径中的下一个中间产物。

相似文献

1
Biochemical genetics of Chinese hamster cell mutants with deviant purine metabolism: isolation and characterization of a mutant deficient in the activity of phosphoribosylaminoimidazole synthetase.具有异常嘌呤代谢的中国仓鼠细胞突变体的生化遗传学:磷酸核糖氨基咪唑合成酶活性缺陷突变体的分离与鉴定
Somatic Cell Genet. 1979 Mar;5(2):203-16. doi: 10.1007/BF01539161.
2
Biochemical genetics of Chinese hamster cell mutants with deviant purine metabolism: characterization of Chinese hamster cell mutants defective in phosphoribosylpyrophosphate amidotransferase and phosphoribosylglycinamide synthetase and an examination of alternatives to the first step of purine biosynthesis.嘌呤代谢异常的中国仓鼠细胞突变体的生化遗传学:磷酸核糖焦磷酸酰胺转移酶和磷酸核糖甘氨酰胺合成酶缺陷的中国仓鼠细胞突变体的特征以及嘌呤生物合成第一步替代途径的研究
Somatic Cell Genet. 1977 Nov;3(6):561-77. doi: 10.1007/BF01539066.
3
Biochemical genetics of Chinese hamster cell mutants with deviant purine metabolism III. Isolation and characterization of a mutant unable to convert IMP to AMP.中国仓鼠细胞嘌呤代谢异常突变体的生化遗传学III. 一个无法将肌苷酸转化为腺苷酸的突变体的分离与鉴定
Somatic Cell Genet. 1976 Jan;2(1):41-53. doi: 10.1007/BF01539241.
4
Biochemical genetics of Chinese hamster cell mutants with deviant purine metabolism. IV. Isolation of a mutant which accumulates adenylosuccinic acid and succinylaminoimidazole carboxamide ribotide.嘌呤代谢异常的中国仓鼠细胞突变体的生化遗传学。IV. 一种积累腺苷酸琥珀酸和琥珀酰氨基咪唑甲酰胺核苷酸的突变体的分离。
Somatic Cell Genet. 1976 May;2(3):189-203. doi: 10.1007/BF01538958.
5
Biochemical genetics of Chinese hamster cell mutants with deviant purine metabolism: isolation, selection, and characterization of a mutant lacking hypoxanthine-guanine phosphoribosyltransferase activity by nutritional means.具有异常嘌呤代谢的中国仓鼠细胞突变体的生化遗传学:通过营养手段分离、筛选和鉴定缺乏次黄嘌呤-鸟嘌呤磷酸核糖基转移酶活性的突变体。
Somatic Cell Genet. 1976 Sep;2(5):429-39. doi: 10.1007/BF01542723.
6
Expression of a human cDNA encoding a protein containing GAR synthetase, AIR synthetase, and GAR transformylase corrects the defects in mutant Chinese hamster ovary cells lacking these activities.编码一种包含甘氨酰胺核糖核苷酸(GAR)合成酶、5-氨基咪唑核糖核苷酸(AIR)合成酶和GAR转甲酰基酶的蛋白质的人互补DNA(cDNA)的表达可纠正缺乏这些活性的突变型中国仓鼠卵巢细胞中的缺陷。
Somat Cell Mol Genet. 1991 Jul;17(4):411-20. doi: 10.1007/BF01233066.
7
Genetic and metabolomic analysis of AdeD and AdeI mutants of de novo purine biosynthesis: cellular models of de novo purine biosynthesis deficiency disorders.从头嘌呤生物合成中 AdeD 和 AdeI 突变体的遗传和代谢组学分析:从头嘌呤生物合成缺陷疾病的细胞模型。
Mol Genet Metab. 2013 Mar;108(3):178-189. doi: 10.1016/j.ymgme.2013.01.002. Epub 2013 Jan 12.
8
Biochemical genetics of Chinese hamster cell mutants with deviant purine metabolism: biochemical analysis of eight mutants.具有异常嘌呤代谢的中国仓鼠细胞突变体的生化遗传学:八个突变体的生化分析
Somatic Cell Genet. 1975 Jan;1(1):91-110. doi: 10.1007/BF01538734.
9
Characterization of a guanine-sensitive mutant defective in adenylo-succinate synthetase activity.腺嘌呤琥珀酸合成酶活性缺陷的鸟嘌呤敏感突变体的特性分析。
J Cell Physiol. 1978 Jul;96(1):123-32. doi: 10.1002/jcp.1040960115.
10
A gene correcting the defect in the CHO mutant Ade -H, deficient in a branch point enzyme (adenylosuccinate synthetase) of de novo purine biosynthesis, is located on the long arm of chromosome 1.一个纠正中国仓鼠卵巢细胞(CHO)突变体Ade-H缺陷的基因位于1号染色体长臂上,该突变体缺乏从头嘌呤生物合成的一个分支点酶(腺苷酸琥珀酸合成酶)。
Genomics. 1991 Feb;9(2):322-8. doi: 10.1016/0888-7543(91)90260-l.

引用本文的文献

1
Mutations in the Chinese hamster ovary cell GART gene of de novo purine synthesis.新生嘌呤合成的中国仓鼠卵巢细胞甘氨酰胺核糖核苷酸转甲酰基酶基因中的突变。
Gene. 2009 Jan 15;429(1-2):23-30. doi: 10.1016/j.gene.2008.10.007. Epub 2008 Oct 21.
2
Demonstration, by somatic cell genetics, of coordinate regulation of genes for two enzymes of purine synthesis assigned to human chromosome 21.通过体细胞遗传学证明,定位于人类21号染色体上的嘌呤合成途径中两种酶的基因存在协同调控。
Proc Natl Acad Sci U S A. 1981 Jan;78(1):405-9. doi: 10.1073/pnas.78.1.405.
3
Selective transfer of individual human chromosomes to recipient cells.
将人类个体染色体选择性转移至受体细胞。
Mol Cell Biol. 1985 Jan;5(1):140-6. doi: 10.1128/mcb.5.1.140-146.1985.