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多胺营养缺陷型细胞系中鸟氨酸脱羧酶和S-腺苷甲硫氨酸脱羧酶的调控

Regulation of ornithine decarboxylase and S-adenosylmethionine decarboxylase in a polyamine auxotrophic cell line.

作者信息

Svensson F, Persson L

机构信息

Department of Physiology, University of Lund, Sweden.

出版信息

Mol Cell Biochem. 1996 Sep 20;162(2):113-9. doi: 10.1007/BF00227537.

DOI:10.1007/BF00227537
PMID:8905633
Abstract

In the present study we have examined the regulation of the polyamine biosynthetic pathway in a cell line deficient in ornithine decarboxylase (ODC) activity. These cells were unable to grow unless polyamines were provided in their growth medium. Seeding the cells in the absence of polyamines rapidly resulted in a cellular depletion of putrescine and spermidine. Although the cells were devoid of ODC activity they were demonstrated to express an inactive ODC which was feedback regulated by polyamines in a normal manner. Cells seeded in the absence of polyamines exhibited a marked increase in ODC synthesis rate which was not correlated with an equal change in the ODC mRNA level. The synthesis of S-adenosylmethionine decarboxylase (AdoMetDC) was also increased in the cells seeded in the absence of polyamines. However, this increase was essentially explained by a change in the amount of AdoMetDC mRNA. The addition of putrescine to the growth medium appeared to stimulate the conversion of AdoMetDC proenzyme into its two subunits, indicating a physiological role of putrescine in the regulation of AdoMetDC expression.

摘要

在本研究中,我们检测了鸟氨酸脱羧酶(ODC)活性缺陷的细胞系中多胺生物合成途径的调控。除非在生长培养基中提供多胺,这些细胞无法生长。在没有多胺的情况下接种细胞会迅速导致细胞内腐胺和亚精胺的消耗。尽管这些细胞缺乏ODC活性,但它们被证明表达一种无活性的ODC,该ODC以正常方式受多胺的反馈调节。在没有多胺的情况下接种的细胞,其ODC合成速率显著增加,这与ODC mRNA水平的同等变化无关。在没有多胺的情况下接种的细胞中,S-腺苷甲硫氨酸脱羧酶(AdoMetDC)的合成也增加。然而,这种增加基本上是由AdoMetDC mRNA量的变化所解释的。向生长培养基中添加腐胺似乎刺激了AdoMetDC酶原转化为其两个亚基,表明腐胺在AdoMetDC表达调控中具有生理作用。

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本文引用的文献

1
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Eur J Biochem. 1993 Jun 15;214(3):671-6. doi: 10.1111/j.1432-1033.1993.tb17967.x.
2
Development of resistance to hydroxyurea during treatment of human myelogenous leukemia K562 cells with alpha-difluoromethylornithine as a result of coamplification of genes for ornithine decarboxylase and ribonucleotide reductase R2 subunit.在使用α-二氟甲基鸟氨酸治疗人髓性白血病K562细胞过程中,由于鸟氨酸脱羧酶和核糖核苷酸还原酶R2亚基基因的共扩增而产生对羟基脲的耐药性。
Cancer Res. 1993 Nov 1;53(21):5262-8.
3
Rapid and regulated degradation of ornithine decarboxylase.鸟氨酸脱羧酶的快速且受调控的降解
Biochem J. 1995 Feb 15;306 ( Pt 1)(Pt 1):1-10. doi: 10.1042/bj3060001.
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Polyamines as targets for therapeutic intervention.多胺作为治疗干预的靶点。
Annu Rev Pharmacol Toxicol. 1995;35:55-91. doi: 10.1146/annurev.pa.35.040195.000415.
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