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磷酸核糖焦磷酸减少作为人淋巴母细胞氨基酸饥饿期间嘌呤合成减少的基础。

Decreased phosphoribosylpyrophosphate as the basis for decreased purine synthesis during amino acid starvation of human lymphoblasts.

作者信息

Boss G R

出版信息

J Biol Chem. 1984 Mar 10;259(5):2936-41.

PMID:6199353
Abstract

Rates of de novo and salvage purine synthesis decrease by approximately 80 and 60%, respectively, when normal human lymphoblasts are starved 3 h for an essential amino acid (Boss, G. R., and Erbe, R. W. (1982) J. Biol. Chem. 257, 4242-4247). Amino acid starvation decreased the intracellular phosphoribosylpyrophosphate (PP-Rib-P) and ribose 5-phosphate concentrations by approximately 40%, but neither the specific activities of PP-Rib-P synthetase and glutamine amidophosphoribosyltransferase nor the intracellular concentrations of purine nucleotides and inorganic phosphate changed significantly. In mutant cells with either an increased capacity to generate PP-Rib-P (superactive PP-Rib-P synthetase), or an increased PP-Rib-P concentration (inosinate-guanylate:pyrophosphate phosphoribosyltransferase deficiency), the intracellular PP-Rib-P concentration decreased by less than 15% during amino acid starvation and de novo purine synthesis decreased significantly less than in normal cells. When normal cells were treated with drugs that simultaneously decreased feed-back inhibition by purine nucleotides and increased the intracellular concentration of ribose 5-phosphate and PP-Rib-P rates of de novo purine synthesis were stimulated 3-fold in nonstarved cells and more than 8-fold in starved cells. This greater stimulation in the starved cells appeared to be from the increased PP-Rib-P production; moreover, in starved cells in which the increase of the PP-Rib-P concentration by the drugs was impaired because of purine nucleoside phosphorylase deficiency, rates of de novo purine synthesis increased only 3.5-fold. The data suggest that amino acid starvation decreases purine synthesis by decreasing the generation of PP-Rib-P from glucose.

摘要

当正常人淋巴母细胞缺乏必需氨基酸3小时时,从头合成和补救嘌呤合成的速率分别下降约80%和60%(博斯,G.R.,和厄尔贝,R.W.(1982年)《生物化学杂志》257,4242 - 4247)。氨基酸饥饿使细胞内磷酸核糖焦磷酸(PP - Rib - P)和5 - 磷酸核糖浓度降低约40%,但PP - Rib - P合成酶和谷氨酰胺磷酸核糖焦磷酸转酰胺酶的比活性以及嘌呤核苷酸和无机磷酸盐的细胞内浓度均无显著变化。在具有增加生成PP - Rib - P能力(超活性PP - Rib - P合成酶)或增加PP - Rib - P浓度(次黄苷酸 - 鸟苷酸:焦磷酸磷酸核糖基转移酶缺乏)的突变细胞中,氨基酸饥饿期间细胞内PP - Rib - P浓度降低不到15%,从头嘌呤合成的下降明显少于正常细胞。当正常细胞用同时降低嘌呤核苷酸反馈抑制并增加5 - 磷酸核糖和PP - Rib - P细胞内浓度的药物处理时,在未饥饿细胞中从头嘌呤合成速率提高3倍,在饥饿细胞中提高超过8倍。饥饿细胞中这种更大的刺激似乎来自PP - Rib - P产量的增加;此外,在因嘌呤核苷磷酸化酶缺乏而药物增加PP - Rib - P浓度受损的饥饿细胞中,从头嘌呤合成速率仅增加3.5倍。数据表明,氨基酸饥饿通过减少葡萄糖生成PP - Rib - P来降低嘌呤合成。

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